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COVID-19 Immunopathology, Particle Pollution, and Iron Balance

Authors:
  • Florida Department of Health in Monroe County
  • Transdyne Corporation, California

Abstract and Figures

The coronavirus (COVID-19) pandemic exploded into a world already reeling from climate change, degradation of natural systems, and pandemics of air pollution and noncommunicable diseases. These pandemics are interrelated; air pollution, the world’s biggest killer, is a major contributor to noncommunicable disease. Air pollution is a probable cofactor in the spread and severity of COVID-19. There are shared mechanisms of injury by the emerging COVID-19 immunopathology, ultrafine air pollutants, and chronic degenerative disease. A key feature of each is oxidative stress, including that caused by iron dysregulation. Exogenous combustion-derived magnetite nanoparticles found in human brains and hearts are strongly implicated in the development of cardiometabolic and neurogenerative disease. Altered iron balance favoring excess reactive or misplaced iron is probably the most important predisposing condition for severe COVID-19 infection. Ultrafine-particle/nanoparticle toxicity and COVID-19 immunopathology on the subcellular level are both characterized by iron dysregulation, mitochondrial dysfunction, and endoplasmic reticulum stress. Primary sources of the most damaging ultrafine pollution particles are fossil fuel combustion, vehicle emissions, and coal fly ash utilized in undisclosed tropospheric aerosol geoengineering. The same ultrafine particles when emitted or placed into the troposphere alter the world’s cloud layers and reduce atmospheric convection, directly contributing to climate change and global warming. Pandemics can only be tackled by international cooperation. Immediate steps that must be taken include monitoring and control of ultrafine particulate air pollution, and prompt cessation of geoengineering operations.
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*Corresponding author: E-mail: mherndon@san.rr.com;
Journal of Advances in Medicine and Medical Research
32(18): 43-60, 2020; Article no.JAMMR.61789
ISSN: 2456-8899
(Past name: British Journal of Medicine and Medical Research, Past ISSN: 2231-0614,
NLM ID: 101570965)
COVID-19 Immunopathology, Particle Pollution, and
Iron Balance
Mark Whiteside
1
and J. Marvin Herndon
2*
1
Florida Department of Health in Monroe County, 1100 Simonton Street, Key West, FL 33040, USA.
2
Transdyne Corporation, 11044 Red Rock Drive, San Diego, CA 92131, USA.
Authors’ contributions
This work was a joint effort between both authors that is part of an ongoing collaboration aimed at
providing scientific, medical, public health implications and evidence related to COVID-19, iron
balance, and particulate pollution, especially, aerosolized coal fly ash including its use in the near-
daily, near-global covert geoengineering activity. Author MW was primarily responsible for medical
and public health considerations. Author JMH was primary responsible for mineralogical and
geophysical considerations. Both authors read and approved the final manuscript.
Article Information
DOI: 10.9734/JAMMR/2020/v32i1830654
Editor(s):
(1)
Dr. Ashish Anand, G. V. Montgomery Veteran Affairs Medical Center, University of Mississippi Medical Center and
William Carey School of Osteopathic Medicine, USA.
(2)
Dr. Chan-Min Liu, Xuzhou Normal University, China.
(3)
Dr. Salomone Di Saverio, S. Orsola Malpighi University Hospital, Italy.
Reviewers:
(1) Jomin Jose, Sumandeep Vidhyapeeth, India.
(2)
Amit Gupta, Graphic Era (Deemed to be University), India.
(3)
Ahmed Raheem Rayshan, University of Al-Qadisiyah, Iraq.
(4)
S. Venkat Rao, Adikavi Nannaya University, India.
(5) Manveen Kaur Lall, Institute of Medical Sciences and Research, India.
Complete Peer review History:
http://www.sdiarticle4.com/review-history/61789
Received 21 September 2020
Accepted 02 October 2020
Published 10 October 2020
ABSTRACT
The coronavirus (COVID-19) pandemic exploded into a world already reeling from climate change,
degradation of natural systems, and pandemics of air pollution and noncommunicable diseases.
These pandemics are interrelated; air pollution, the world’s biggest killer, is a major contributor to
noncommunicable disease. Air pollution is a probable cofactor in the spread and severity of
COVID-19. There are shared mechanisms of injury by the emerging COVID-19 immunopathology,
ultrafine air pollutants, and chronic degenerative disease. A key feature of each is oxidative stress,
including that caused by iron dysregulation. Exogenous combustion-derived magnetite
nanoparticles found in human brains and hearts are strongly implicated in the development of
Review Article
Whiteside and Herndon; JAMMR, 32(18): 43-60, 2020; Article no.JAMMR.61789
44
cardiometabolic and neurogenerative disease. Altered iron balance favoring excess reactive or
misplaced iron is probably the most important predisposing condition for severe COVID-19
infection. Ultrafine-particle/nanoparticle toxicity and COVID-19 immunopathology on the subcellular
level are both characterized by iron dysregulation, mitochondrial dysfunction, and endoplasmic
reticulum stress. Primary sources of the most damaging ultrafine pollution particles are fossil fuel
combustion, vehicle emissions, and coal fly ash utilized in undisclosed tropospheric aerosol
geoengineering. The same ultrafine particles when emitted or placed into the troposphere alter the
world’s cloud layers and reduce atmospheric convection, directly contributing to climate change
and global warming. Pandemics can only be tackled by international cooperation. Immediate steps
that must be taken include monitoring and control of ultrafine particulate air pollution, and prompt
cessation of geoengineering operations.
Keywords: Virology; pandemic; cardiology; hematology; aerosols; coal fly ash; particulate air
pollution; magnetite; nanoparticles; geoengineering.
1. INTRODUCTION
Since its 2019 emergence in China, the
coronavirus SARS-CoV-2, also known as
COVID-19, has wrought illness, suffering, death,
financial disaster, and much human misery. Like
the unprovoked attack on Pearl Harbor,
December 7, 1941, [1] its consequence was to
awaken a sleeping giant, not only in America, but
throughout the world.
Understanding in a more fundamental way how
the virus attacks and alters the human body, one
of the moral imperatives awakened by the
COVID-19 Pandemic, is one purpose of this
Review.
The former Director-General of the World Health
Organization recently pointed out that the simple
act of breathing is killing seven million people a
year and injuring billions more, and stated [2]:
No one, rich or poor, can escape air pollution.
Despite this epidemic of needless, preventable
deaths and disability, a smog of complacency
pervades the planet.” Some might say smog of
compliancy” as few individuals have been willing
to question policies that not only allow, but
greatly augment air pollution. That may change
now.
Another of the moral imperatives awakened by
the COVID-19 Pandemic is to understand in a
more fundamental way the spectrum of
bodily harm caused by pollution, and especially,
its role in spreading the virus, and
exacerbating the severity of its attack on human
populations.
This review explores the emerging
immunopathology of COVID-19 and shows how
the pandemics of air pollution, noncommunicable
disease (NCD) and COVID-19 are interrelated.
Air pollution, the world’s greatest killer, is a major
cause of noncommunicable diseases (NCD’s).
Age and chronic disease (NCD’s) predispose to
more severe COVID-19 disease. Air pollution,
COVID-19, and many NCD’s share common
features of iron dysregulation, inflammation, and
subcellular organelle toxicity. The universal
exposure to combustion-derived UFP’s and
nanoparticles in human cells and tissue produces
very similar pathological features. The ultrafine
fraction of air pollution in the troposphere is
related to climate change and global
warming.
2. THE PANDEMIC
The COVID-19 pandemic has become the most
important infectious disease problem of the
century and one of the greatest challenges to
ever face mankind. The novel coronavirus,
SARS-CoV-2, which emerged in China in 2019,
was found to be responsible for the disease.
SARS-CoV-2, now known as COVID-19, has
rapidly circled the globe and affected every
continent except Antarctica. COVID-19 follows
outbreaks of two other deadly Beta-
coronaviruses, severe acute respiratory virus
syndrome (SARS) in 2003 and Middle East
respiratory syndrome (MERS) in 2012 [3].
COVID-19 is likely to cause immense human
suffering and death in a world already racked by
climate change and rapid global warming,
pollution, ozone layer depletion, and the
decimation of ecosystems and wildlife.
Ecosystem degradation from anthropogenic
activities has greatly accelerated outbreaks of
emerging and zoonotic infectious diseases in the
past century, The COVID-19 pandemic should be
considered an indirect consequence of these
environmental changes [4].
Whiteside and Herndon; JAMMR, 32(18): 43-60, 2020; Article no.JAMMR.61789
45
3. COVID-19 AND ITS EMERGING
IMMUNOPATHOLOGY
The pandemic poses vast health, economic,
environmental, and social challenges to the
human population [5]. The COVID-19
pandemic is bound to have a devastating effect
on the world’s economy, in part because of pre-
existing global wealth disparity, imposed
austerity, and deterioration of public health.
Although the future severity of the
pandemic is difficult to predict and quantify, there
will almost certainly be a vicious downward
spiral of illness and impoverishment.
Global cooperative efforts based on sound
scientific and public health principles will be
necessary to bring the COVID-19 pandemic
under control [6].
Coronaviruses are enveloped, positive stranded
RNA viruses which infect both man and animals.
The majority of known human coronaviruses
cause mild respiratory disease. SARS, MERS,
and COVID-19 belong to the group of beta
coronaviruses that can cause severe lower
respiratory infection and sometimes fatal severe
respiratory syndrome [7]. COVID-19 is highly
transmissible person-to-person, by virus-
containing droplets, secretions, and aerosolized
particles [8].
Coronaviruses bind to receptors to enter and
infect cells. COVID-19 uses its spike protein to
bind to the peptidase angiotensin-converting
enzyme 2, or ACE2. The interaction between
COVID-19 and ACE2 in part determines tissue
tropism and progression from mild to severe
disease. ACE2 is highest in nasal epithelial cells
with lesser amounts in lung epithelial cells,
consistent with disease pathology. Breakdown of
the lung epithelial-endothelial barrier in
susceptible persons might trigger viral
dissemination and widespread or systemic
disease. The strategies of most of the vaccine
candidates, convalescent plasma, and
monoclonal antibodies are aimed at preventing
the binding of COVID-19 spike protein to the
ACE2 receptor [9].
The body’s defense against coronavirus includes
not only cellular and humoral (i.e. antibody)
immunity, but also the production of
proinflammatory cytokines. Effector cytokines like
interferon reduce viral replication and promote
antigen recognition, thereby contributing to viral
containment. However, SARS-CoV-2 has the
potential to sabotage the host’s immune
response. Infection of certain immune cells by
the virus can inhibit or counteract interferon [10].
Impaired clearance of virus due to both host and
pathogen factors can lead to an “over-reaction”
of the immune system characterized by cellular
infiltration and apoptosis (programmed cell
death), and a proliferation of inflammatory
mediators released by effector cells.
Severe COVID-19 disease is characterized by
“cytokine storm” and macrophage activation
syndrome [11]. An excessive inflammatory
response is thought to be a major cause of
disease severity and death in patients with
COVID-19 infection, and is associated with high
levels of circulating cytokines, profound
lymphopenia (lymphocyte depletion), and
mononuclear white blood cell infiltration into the
lungs, heart, spleen, lymph nodes and kidney
[12]. Findings in critical ill patients with COVID-
19, including fever/confusion, high ferritin, LDH,
IL-6, C-reactive protein, and coagulation
abnormalities, suggest cytokine storm syndrome
[13].
While most healthy persons survive the initial
phase of COVID-19 replication and associated
inflammation, a small percentage of individuals
have a secondary inflammatory response to the
virus after they have already developed IgG
antibodies to the virus [14]. This delayed
response is likely due to antibody dependent
enhancement (ADE), which occurs with other
viruses including dengue and influenza [15, 16].
Early and/or non-neutralizing antibodies bind to
virus and the resulting virus-containing immune
complexes are taken up by Fc receptors on
monocytes and macrophages. This kind of viral
uptake can result in persistent viral replication in
immune cells and virus-antibody (that is, immune
complex)-mediated inflammation and tissue
damage [17]. Blood vessel occlusion and
infarction during COVID-19 infection show
features of immune complex vasculitis [18], and
the COVID multisystem poly-inflammatory
syndrome (MIS-C) in children resembles
Kawasaki, which is most likely an immune
complex disease [19]. Both the quality and
quantity of antibodies dictate the functional
outcomes of ADE [20]. Clinical support for ADE
immunopathology comes for the observation that
severe SARS/COVID disease often occurs after
2 weeks of illness, when viral loads are declining,
but antibodies are rising. Antibody-dependent
SARS coronavirus enhanced infection is
mediated by antibodies against spike protein
[21].
Whiteside and Herndon; JAMMR, 32(18): 43-60, 2020; Article no.JAMMR.61789
46
The emerging paradigm of COVID-19
immunopathology involving ADE and immune
complexes has vast implications for testing
strategies, viral persistence, re-infection, vaccine
development, and therapeutics. The detection of
SARS-CoV-2 by IgM and IgG antibodies along
with viral PCR/antigen tests provides the basis
for diagnosis. However, early production and
higher titers of IgG antibody are often associated
with more severe COVID-19 disease, consistent
with ADE [22]. Experience with SARS and MERS
show that some antibodies directed against the
spike protein of the virus can facilitate uptake by
Fc receptors on human monocyte and
macrophages; these cells do not normally
express ACE2 receptors. For both viruses, this
process is dependent on antibody concentration.
Vaccines against SARS and MERS in animal
studies have not been effective, with a number of
these vaccines triggering immunopathology and
severe lung disease upon challenge with the
virus. Monoclonal antibodies and convalescent
serum must be carefully tested for ADE effects
[23]. It has been shown that highly diluted anti-
sera against SARS-CoV-2 enhances SARS-CoV
infectivity [24]. COVID-19 not only induces
immune responses but produces uncontrolled
inflammation and cytokine release in severe
disease. There is a strong association between
SARS-CoV-2 induced immunopathology and
poor survival of patients. Antivirals, steroids, and
immunoglobulin treatment have limited efficacy in
persons with severe COVID-19 disease.
However, targeting the specific COVID-19
immune profiles, such as by enhancing innate
immunity or inhibiting inflammation, can be useful
treatment strategies for more severe cases [25].
It is becoming evident that COVID-19 can lead to
significant morbidity and residual effects in many
“recovered” patients. In this regard, a hallmark of
immune complex disease is viral persistence
[26].
4. CENTRAL ROLE OF IRON IN HEALTH
AND ILLNESS
Iron is crucial to basic biological functions
including DNA/RNA synthesis, mitochondrial
function, and production of ATP. Viruses depend
on intracellular iron in order to replicate. Both
host and pathogen require iron in the
evolutionary process, so the innate immune
response must control iron metabolism to limit its
availability during infection [27].
Systemic iron homeostasis is controlled by the
hepcidin-ferroportin axis and cellular iron uptake
is mediated by interactions between iron-bound
transferrin and transferrin receptors on cells. The
transferrin receptor (TfR) is a common portal for
many viruses to enter cells, although not yet
studied in the case of COVID-19 [27, 28]. Iron
metabolism is tightly regulated by iron absorption
in the gut, iron storage in the liver and spleen,
iron transport in blood, iron utilization (primarily in
bone marrow for erythropoiesis), and iron
recycling by macrophages [29]. Tissue resident
macrophages regulate local iron availability and
modulate the tissue microenvironment,
supporting proper cellular and tissue function
[30].
Increasing evidence suggests that inflammation,
oxidative stress, and altered iron homeostasis
are linked at the systemic level. Ferritin is the
main iron-storage protein in the body. Iron in
ferritin is normally bound and released in a
controlled manner. During infection, increases in
ferritin may deprive pathogens of iron and protect
immune function. Conversely, ferritin may be a
key regulator of immune dysregulation,
especially in situations of extremely high levels of
ferritin (hyperferritinemia) via direct immune
suppression and pro-inflammatory effects.
Certain conditions of hyperferritemia (with
disruption of ferritin and reactive iron release)
identify patients at high risk of severe disease or
even death while its resolution predicts recovery
[31]. Shifting of immunoregulatory balances
caused by iron excess can lead to deleterious
physiological effects. Disease states
characterized by high body stores of iron
increase virus replication and complicate clinical
management [32].
5. IRON DYSREGULATION AND COVID-
19
Although COVID-19 has been considered an
infectious/inflammatory disease primarily
affecting the lungs, there is growing recognition
that this virus can affect multiple organ systems
by using different pathways of injury. Uptake of
the virus into monocytes and macrophages by Fc
receptors with subsequent dissemination
throughout the body is one such pathway.
Hemoglobinopathy with associated hypoxemia
and iron dysregulation appears to be a feature of
more severe disease with COVID-19 [33]. During
the cytokine storm produced by COVID-19, high
levels of IL-6 are produced, which stimulates
ferritin and the synthesis of hepcidin. Hepcidin
sequesters iron in macrophages, leading to
Whiteside and Herndon; JAMMR, 32(18): 43-60, 2020; Article no.JAMMR.61789
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increased intracellular ferritin and reduced iron
efflux from cells. Excess intracellular iron creates
reactive oxygen species and impairs
mitochondrial function. Damage to the cell can
result in ferroptosis, a type of programmed cell
death caused by iron excess [34].
When ferritin is released from damaged cells, it
loses part of its inner iron content giving rise to
high levels of “free” or reactive iron. Free iron
worsens inflammation by the production of
reactive oxygen species (ROS’s) and can induce
a marked pro-coagulant effect. Oxidative stress
on red blood cells produced by reactive iron
predisposes to dense clots that can produce
stroke [35]. Iron laden macrophages are
observed in tissue (e.g. bone marrow) of persons
who died from severe COVID-19 disease. In
humans with HIV immunodeficiency and/or
hepatitis C virus infection, iron overload is
associated with more pronounced disease, with
evidence that the virus itself may enhance
macrophage iron loading [36]. Iron disrupts the
balance between M1 (pro-inflammatory) and M2
(anti-inflammatory) macrophage phenotype
populations [37].
During the past century, research has shown that
excessive or misplaced iron in specific tissues,
cells, and subcellular sites can produce a wide
array of acute and chronic diseases. Iron excess
is recognized as a risk factor for infection,
neoplasm, metabolic disease, cardiopulmonary
disease, and neurodegenerative disease [38].
The most important co-morbidities associated
with severe COVID-19 infection include
metabolic disease, e.g. obesity and diabetes,
cardiovascular disease (including hypertension),
respiratory disease (including COPD and
asthma), cancer, and chronic liver and kidney
disease [39]. Altered iron homeostasis is a
common risk factor linking many of these co-
morbidities to increased morbidity and mortality
from COVID-19 infection.
Epidemiological evidence strongly supports the
association of iron dysregulation with diabetes
and heart disease [40]. Iron imbalance affects
chronic metabolic diseases, glucose and lipid
metabolism, fatty liver disease, and obesity. Iron
excess increases lipid peroxidation that in turn
modifies the fatty acid profile of cell membranes,
leads to damage of cellular organelles, and
impairs mitochondrial function [41]. Increased
serum ferritin predicts the development of
hypertension in men [42], and arterial stiffness is
associated with increased ferritin and deposition
of iron in vessels walls [43]. The high rate of
cardiomyopathy in persons with hemosiderosis
and transfusion iron overload suggests that iron
build-up in the heart has an important role in the
development of heart failure [44].
Obesity is a major risk factor for COVID-19.
Increased dietary availability of iron through
fortification of processed food is a factor related
to the global epidemic of obesity [45]. Iron
dysregulation is common in obesity [46], chronic
liver disease [47], chronic kidney disease [48],
and many cancers [49]. Heavy alcohol usage
and smoking cigarettes can worsen iron excess
in the body [50].
In summary, altered iron balance favoring excess
reactive or catalytic iron may be the single most
important underlying pathological process
predisposing to severe COVID-19 infection and
associated inflammation and immunopathology.
6. AIR POLLUTION THE WORLD’S
LEADING KILLER
The modern plague of air pollution is the greatest
killer of our age. Air pollution is the leading
environmental cause of disease (morbidity) and
death (mortality) in the world. [51, 52]. Air
pollution particulates penetrate deeply into the
lungs and systemic circulation; contributing to
stroke and neurodegenerative disease [53, 54]
heart disease [55-57], lung cancer [56, 57],
COPD [58, 59], and respiratory infections [60].
Air pollution is thus one of the main contributors
to yet another global pandemic; that of
noncommunicable diseases. Air pollution causes
both acute and chronic disease, potentially
affecting every organ system in the body. Tissue
damage can result directly from toxic particles
that gain access to organ systems, or indirectly
by systemic inflammation. Oxidative stress
caused by air pollution activates pro-
inflammatory signaling which sets off a cascade
of events that impact distant organ systems.
Oxidative stress in cells and tissues is a central
mechanism by which PM exposure leads to
injury, disease, and mortality. The damage from
particle pollution is cumulative over time [61].
Ambient air pollution is a leading cause of excess
mortality and loss of life expectancy (LLE),
especially caused by cardiovascular disease.
Globally, the loss of life and life expectancy from
air pollution exceeds, by a large margin, that of
infectious disease and many other causes.
Whiteside and Herndon; JAMMR, 32(18): 43-60, 2020; Article no.JAMMR.61789
48
Although air pollution affects everyone, it causes
more severe disease in those with
the most exposure and greater susceptibility. The
fraction of preventable loss of life expectancy
(LLE) from anthropogenic air pollution
attributable to fossils fuels is nearly two-thirds
(2/3) globally, and up to 80% in high-income
nations [62].
7. HORRORS OF TROPOSPHERIC
AEROSOL GEOENGINERING
A deliberate form of air pollution and existential
threat to the biosphere is posed by tropospheric
aerosol geoengineering. For decades, several
countries and entities including the U.S. military
have been co-opted into the aerial spraying or
injecting particulates into areas where clouds
form for purposes of weather modification,
climate intervention, communication systems,
weather warfare or defense, etc. [63]. There is no
truthful public disclosure concerning these
operations, despite the obvious particulate trails
observed overhead.
Disinformation claiming that the particulate trails
represent harmless ice-crystal “contrails” stands
in conflict with direct observation, and is disputed
by scientific evidence [64]. Aircraft contrails form
only briefly in cold, humid atmospheric
conditions, unlike the particulate trails that
spread out into cirrus-type clouds or even a white
haze [65]. Particulate pollution emplaced into the
troposphere traps heat that would otherwise be
removed by convection [66]. These aerosols alter
natural weather patterns, often creating either
“drought or deluge” [67], poison the environment
[68], damage the protective ozone layer [69],
cause global warming [66, 70], and are toxic to
nearly all biota [71-74].
Several independent lines of evidence point to
coal fly ash as the main particulate that is being
sprayed into the atmosphere to alter Earth’s
natural environment [75]. When coal is burned,
the heavy ash settles, while the light ash, coal fly
ash (CFA), forms above the burner and would
exit the smokestack if not electrostatically
trapped and collected as is required in Western
nations. Readily available throughout the world,
CFA is inexpensive and requires little processing
before being deployed in aerosolized form in the
atmosphere. Primary components of CFA include
aluminum silicates and an iron-bearing fraction
which includes magnetite (Fe
3
O
4
). CFA
contains numerous toxic trace elements,
unconsumed carbon, and even radionuclides.
Concentrations of these trace elements in CFA
are typically higher than those found in the
Earth’s crust, soil, or even solid coal [76]. CFA
makes atmospheric water more electrically
conductive because of the many dissolved,
ionized elements [63].
8. ROLE OF AIR POLLUTION IN SPREAD
AND SEVERITY OF COVID-19
Airborne transmission has been identified as the
primary route of spread of COVID-19 on a global
basis. Several lines of evidence now point to
particulate pollution as a possible co-factor in the
COVID-19 pandemic, specifically, as a potential
means of viral transport, exacerbating
susceptibility and severity of the disease, and
altering the immune response to the virus [77].
During the outbreak of severe acute respiratory
syndrome (SARS-Co-1) in 2003, patients from
areas with high air pollution indices (API’s)
showed a 200% increased relative risk of death
compared to people from areas with a low API
[78]. SARS-CoV-2 RNA has been isolated from
particulate matter (PM) in a study conducted in
Northern Italy, suggesting that PM in air pollution
may act as a vector for transmission of COVID-
19 [79].
Coal fly ash with its many fine and ultrafine
particles, and notably with hollow cavities [80, 81]
(Fig. 1), has been suggested as a possible
carrier of respiratory viruses [82]. It has been
shown that long-term exposure to the gaseous
pollutant NO
2
in air pollution may be one of the
most important contributors to fatal COVID-19
infections in many regions of the world [83].
Another study showed that exposure to PM
2.5
,
particulate matter less than 2.5µm across, is a
significant predictor of the number of new
COVID-19 cases and related hospital admissions
[84].
A newly published study from Italy showed new
cases of COVID-19 are positively related to PM
and Air Quality Index, that dry air supports
COVID-19 transmission, and that outdoor
airborne aerosols are possible routes of COVID-
19 diffusion [85]. Air pollutants increase host
susceptibility to viral respiratory infections by
increasing epithelial cells permeability to viral
receptors and reducing host defense, thus
impairing macrophage function and
phagocytosis, antigen processing, and the
expression of natural killer and cytotoxic T-cells.
Pollutants may also increase the virulence of
COVID-19 [86].
Whiteside and Herndon; JAMMR, 32(18): 43-60, 2020; Article no.JAMMR.61789
49
Coal is the most abundant fossil fuel. Because of
the rapid growth of coal-fired power plants and
industries, the emissions of particulates (coarse,
fine, and ultrafine) from these activities are of
great concern. There is a direct relationship
between human morbidity and mortality and air
pollution produced from these kinds of particles
[87]. Fine particulate matter derived from
combustion sources delivers the most potent and
harmful elements of air pollution. The most
adverse effects are caused by the combustion-
derived ultrafine particles and nanoparticles that
contain reactive organic particles and transition
metal components [88].
One of the mechanisms for particle-related
infections is an accumulation of iron by surface
functional groups of PM. Since iron correlates
with the presence of surface functional groups,
the risk of infection continues while the particle is
retained [89]. Coarse particles (10 µm or less,
PM
10
) induce innate immune responses via toll-
like receptors, while fine (2.5 µm or less, PM
2.5
)
and ultrafine particles (0.1 µm or less, UFP)
induce reactive oxygen species in alveolar
macrophages by transition metals and/or
polyaromatic hydrocarbons (PAH’s) [90].
There are similarities between inflammation
caused by particulate matter and inflammation
caused by COVID-19. For example, particulate
matter induces cytokine expression in human
bronchial cells [91], angiotensin II (ACE2) can be
a molecular target of particulate matter [92],
ambient PM accelerates coagulation via the
cytokines like IL-6 [93] and PM
2.5
affects
macrophage M1 polarization [94]. Abnormal
macrophage responses and macrophage
activation syndrome can be induced by SARS-
Co-V [12] and air pollution particulates [95].
9. MAGNETITE AND HUMAN DISEASE
Magnetite (Fe
3
O
4
) is an iron oxide mineral
occurring naturally in Earth’s surface rocks and
sand [96] and industrially-produced in coal fly
ash [97]. Biogenic magnetite crystals occur in the
bodies of a wide variety of organisms including
man. Magnetite likely has several vital life
functions, as for example, the detection of
magnetic fields [98]. Analysis of human tissue
shows the presence of ferromagnetic, fine-
grained magnetically interacting particles
including the heart, liver, and spleen [99].
Magnetite biomineralization in the human brain
was first described in the 1990’s [100].
Brain tissue contains biogenic magnetite
between 5 and 100 million single-domain crystals
per gram. These biogenic ferrimagnetic particles
are known to be exquisitely sensitive to external
electromagnetic fields via a resonance/vibrational
(vs. thermal) mechanism [101]. Human biogenic
magnetite nanoparticles tend to be single domain
size, high chemical and crystalline purity,
arranged in chains or clusters and associated
with lipid coatings near the cell membrane [102].
In 2016 Maher et al. [103] showed there were
two types of magnetite in brains of persons with
cognitive deficits from highly polluted areas:
euhedral biogenic particles and spherical
exogenous particles most likely arising from air
pollution. Fig. 2 presents a morphological
comparison of spherical magnetite particles in
amyloid cores of Alzheimer’s disease, from
Plascencia-Villa et al. [104] with spherical coal fly
ash magnetic particles from Vu et al. [105].
Fig. 1. SEM image of coal fly ash hollow cenosphere. From Yoriya and Tepsri [80]
Whiteside and Herndon; JAMMR, 32(18): 43-60, 2020; Article no.JAMMR.61789
50
Fig. 2. High-resolution analytical imaging of spherical magnetite particles in amyloid cores of
Alzheimer’s disease, upper left plus lower left. EDX mapping of iron, upper center, and oxygen,
upper right, from [104]. Note morphological similarity with spherical magnetic particles from
coal fly ash, lower right, from [105]
More recently, similar combustion and friction-
derived magnetic air pollution nanoparticles were
found in hearts of persons from highly polluted
areas. The organelles and cellular structures
associated with these pollution particles showed
significant abnormalities.
The health impact of up to 22 billion exogenous
magnetic particles per gram of heart tissue is
likely to reflect surface charge, ferrimagnetism,
redox activity and associated oxidative stress.
Exposure to iron-rich combustion-derived
nanoparticles, including children and young
people, is almost certainly a major risk factor for
the development of cardiovascular disease [106].
While biogenic magnetite in tissue serves
essential life functions, magnetite in excess from
exogenous sources causes harm and disease
[107].The findings of countless combustion-
derived magnetic spherical nanoparticles in both
human brains and hearts is irrefutable evidence
of the near-universal contamination of humanity
by the iron oxide/magnetite fraction of air
pollution [108]. Furthermore, these spherical
particles precisely match the iron/magnetite
nanoparticles in coal fly ash and certain
combustion/diesel fumes [108, 109].
Ultrafine particles (UFP’s) and nanoparticles, that
fraction of particulates less than 0.1 µm, are the
most abundant air pollutants from anthropogenic
sources. Ultrafine (0.1-1 µm) particles and
nanometer-sized particles (< 100 nm) are both
found in coal fly ash. Transmission electron
microscopy reveals that the ultrafine fraction of
CFA is a rich source of magnetite nanoparticles
[110].
There are a growing number of reports of
pulmonary toxicity from the inhalation of
magnetite nanoparticles. Size fractionated
magnetite effects on lung epithelial cells include
cytotoxicity, genotoxicity, and increased reactive
oxygen species [111]. Lung epithelial cells
Whiteside and Herndon; JAMMR, 32(18): 43-60, 2020; Article no.JAMMR.61789
51
treated with different concentrations of magnetic
iron oxide nanoparticles showed magnetite-
treated vs. control cells induced oxidative stress,
depleted antioxidant levels, and increased
apoptosis [112].
Iron oxide nanoparticles alter macrophage
phenotype, iron metabolism, and stimulate
migration and invasion [113]. Iron oxide
nanoparticles can affect both cellular immunity
[114], and humoral (antibody system) immunity
[115]. UFP’s are the most toxic particles based
on their greater surface-to-mass ratio, their larger
content of redox active compounds, and their
ability to penetrate cell walls [116].
Once deposited deep into the lung, UFP’s, unlike
larger particles, can gain access to the blood
circulation and affect distant organ systems,
including both the heart and brain [117]. In
addition to penetration of UFP’s through lung
tissue into circulating cells like red blood cells,
these particles can be phagocytized by
macrophages and dendritic cells and carried
throughout the lymphatic system. The deposition
of UFP’s into tissue like heart and brain is
cumulative over time, gradually increasing
oxidative stress [118].
10. TOXICITY OF ULTRAFINE
PARTICLES IN HUMAN TISSUE
Translocation of inhaled nanoparticles into
systemic circulation and accumulation at sites of
vascular inflammation provides a direct
mechanism that can explain the link between
environmental nanoparticles and cardiovascular
disease [119]. Iron is usually the dominant metal
species in the solid fraction of UFP’s that is
produced and emitted by combustion sources.
In heart tissue iron-rich pollution nanoparticles
are concentrated in intracellular structures and
organelles including endoplasmic reticulum (ER)
and mitochondria. Iron-driven mitochondrial
dysfunction with increased reactive oxygen
species are thought to play an important role in
the initiation and progression of cardiovascular
disease [120].
In the brain, magnetic combustion-derived
nanoparticles are deposited in cells including
microglia and neurons and they too are found in
and produce abnormalities of mitochondria,
endoplasmic reticulum, and mitochondrial-ER
contacts (MERC’s). These highly oxidative
particles are a source of mitochondrial
dysfunction and accumulation of misfolded
proteins including tau, B-amyloid, and synuclein,
which are early hallmarks of cognitive deficits
and dementia [121].
Recently, high resolution scanning/transmission
electron microscopy revealed abundant nano-
sized aggregates containing carbon and iron rich,
ferrimagnetic pollution-derived particles in human
placentas. The inhaled, metal-bearing air
pollution-derived particulate matter was taken up
by macrophage-enriched placental cells. Thus
the human placenta and presumably the fetus
appear to be a target for these same particles
[122].
Endoplasmic reticulum is a crucial organelle
involved in proper protein folding. Reactive
oxygen species produced in the mitochondria
and ER lead to a misfolding of proteins and
apoptosis, which likely contributes to various
degenerative diseases [123]. A variety of
nanoparticles (NP), especially metal based NP’s,
induce this ER-stress mediated pathway in vitro
and in-vivo. These studies suggest that ER
stress could be a primary mechanism
responsible for NP-induced intracellular toxicity
[124].
Note the endoplasmic reticulum-mitochondrial
junction is required for iron homeostasis [125].
The coronavirus spike protein induces
endoplasmic reticulum stress and triggers innate
immune responses [126]. Accumulating evidence
indicates that induction of ER stress and
unfolded protein response (UPR) constitutes a
major component of coronavirus-host interaction
[127].
11. AEROSOL PARTICLES MAJOR
EFFECT ON CLIMATE AND PUBLIC
HEALTH
Recently, abundant exogenous nanoparticles
were found in human serum (healthy subjects)
and pleural fluid (from patients with various
diseases) [128]. These nanoparticles showed a
wide diversity of chemical species, concentration,
and morphology. Via chemical multi-
fingerprinting (including elemental fingerprints,
high-resolution structural fingerprints, and stable
iron isotopic fingerprints) of NP’s, the sources
were found to be abiogenic, and mostly of
combustion-derived particulate emission. The
nanoparticles included many magnetite
nanoparticles highly resembling the pollution
particles previously found in heart and lungs.
Whiteside and Herndon; JAMMR, 32(18): 43-60, 2020; Article no.JAMMR.61789
52
Amorphous spherical Si, O, and C NP’s showed
an elemental fingerprint of coal fly ash, while Hg-
bearing crystal NP’s also suggested this source
[128].
Ultrafine particles from coal are rich in Si, Al, Fe,
Na, K, Mg, Ca, TI, Mn, Co, Ni, Zn, V, Cr, Cu, Sb,
As, Se, S, and Cl. UFP’s from coal combustion
are more toxic and reactive to human tissue for
the following reasons: (1) Higher concentrations
of toxic and volatile compounds are adsorbed in
the UFP’s than the coarse or fine fractions (with
enrichments up to 50-fold), (2) Iron oxides in the
UFP fraction are highly reactive and increase
oxidative stress, and (3) There is unburned
carbon in the UFP’s, and carbonaceous content
correlates with particle toxicity, possibly related
to the oxygenated functional groups on the
surface [129].
Most official regulations and air quality standards
are focused on PM
10
and PM
2.5
and there are no
widely standardized UFP-specific
measurements, reporting method, or emission
standards. There are limited scientific studies of
the human effects of ultrafine particles
[130]. Ultrafine particles from smokestacks
generate excessive numbers of tiny cloud
condensation nuclei, rather than forming large
aerosols. Concurrent reduction of cloud droplet
size modes by the introduction of excessive
UFP’s into the atmosphere results in diverse
undesirable effects, such as causing either
drought or flooding. These particles affect both
climate change and the global hydrological cycle,
thus affecting public health both directly and
indirectly [130-132].
12. ELECTRO-POLLUTION, IRON AND
COVID-19
Electro-pollution likely plays a role in the toxicity
of exogenous magnetite pollution particles which
are deposited in human cells and tissues. Both
biogenic and exogenous magnetite pollution
particles absorb and transduce a variety of man-
made electromagnetic frequencies. Mechanically
sensitive ion channels can open or close from
the movement of magnetite in response to
external electromagnetic fields. This transient
opening of membrane pores allows calcium and
other ions to enter cells [101].
It is well-known that electromagnetic fields can
produce their non-thermal biological effects by
activation of voltage-gated calcium channels
[133]. Voltage-gated calcium channels are also
an alternative route for iron entry into neuronal
cells under conditions that promote cellular iron
overload toxicity [134]. In the heart, L-type
calcium channels (LTCC) are high capacity
pathways of ferrous iron (Fe
2+
) uptake into
cardiomyocytes, especially under iron overload
conditions [135].
Recently it was shown that radiofrequency
(RF) waves activate ferritin-tagged channels via
a biochemical pathway. Radiofrequency
waves interact with ferritins, increasing the levels
of free iron, which produce reactive
oxygen species and oxidize membrane lipids
[136]. Since cytokine storm and inflammation are
both linked to iron dysregulation in
severe COVID-19 infection, this
immunopathology could be enhanced in the
extremely high EMF environment of the hospital
intensive care unit.
13. HIGHLIGHTS AND PRINCIPLES
1. COVID-19 is the most important infectious
disease of the past century and one of the
greatest challenges to ever face mankind.
2. Viral uptake by virus-containing immune
complexes by Fc receptors on immune cells
is a pathway of immunopathology in COVID-
19 infections.
3. There is an emerging paradigm of severe
COVID-19 infection as a multi-system,
antibody and immune complex-mediated,
and possibly persistent viral disease
4. The probability of antibody-dependent
enhancement of infection associated with
serious COVID infections makes the
prospect of a safe and effective vaccine and
the ultimate eradication of the virus much
less likely.
5. COVID-19, like other viruses, depends on
intracellular iron to replicate. Disease states
characterized by high body stores of iron
increase virus replication.
6. Iron dysregulation is a key feature of severe
COVID-19 infection. Altered iron balance
favoring excess reactive iron may be the
most important underlying pathological
process predisposing to severe COVID-19
infection.
7. Air pollution is the greatest environmental
health threat and one of the most important
causes of the global pandemic of
noncommunicable disease.
8. There is growing evidence that particulate
air pollution is a potential means of
transmission of COVID-19, and that it
Whiteside and Herndon; JAMMR, 32(18): 43-60, 2020; Article no.JAMMR.61789
53
exacerbates susceptibility and severity of
the disease.
9. There are many similarities between
inflammation caused by particulate matter in
air pollution and inflammation caused by
COVID-19.
10. Fine particulate matter derived from
combustion sources deliver the most potent
and harmful elements of air pollution. The
most adverse effects are due to reactive
organic particles and transition metals like
iron.
11. The recent finding of countless
magnetic combustion-derived spherical
nanoparticles in human brains,
hearts, and placentas is definitive proof of
the universal contamination of humanity by
the iron oxide/magnetite fraction of air
pollution.
12. The combustion-derived magnetic particles
found in human tissue and cells match the
iron-magnetite ultrafine particles in coal fly
ash and diesel fumes.
13. The main sources of magnetite
nanoparticles are from coal combustion,
vehicle emissions, and coal fly ash utilized
in global covert, undisclosed tropospheric
aerosol geoengineering.
14. Magnetic combustion-derived nanoparticles
in tissue and cells cause oxidative stress
and mitochondrial dysfunction. They
contribute to the development and
progression of cardiovascular and
neurologic disease.
15. Magnetite nanoparticles affect both cellular
and humoral immunity.
16. The intracellular toxicity of iron oxide and
other nanoparticles may be related to
mitochondrial dysfunction and endoplasmic
reticulum stress.
17. Coronavirus spike protein also produces
endoplasmic reticulum stress.
18. Exogenous magnetite nanoparticles
interact with external electromagnetic fields.
19. Exposure to nanoparticulate iron is “womb
to tomb,” and cumulative over time.
20. Diseases characterized by iron
excess/dysregulation including obesity,
cardiovascular disease, and diabetes are
among the most important co-morbid
conditions predisposing to severe COVID-
19 infection.
21. Ultrafine pollution particles from combustion
sources have recently been found in human
sera and pleural fluid.
22. The same fine and ultrafine particles that
adversely affect human health are key
elements of climate change and global
warming.
23. Climate change, air pollution, and
noncommunicable disease are the greatest
threats to human and environmental health,
and they are all intertwined and interrelated.
24. The global spread of COVID-19 is linked to
these same factors. The control of COVID-
19 will depend not only on global public
health initiatives and therapeutics, but
environmental measures as well.
14. CONCLUSIONS
Iron is necessary for DNA/RNA synthesis and it
is an essential element for all organisms
including viruses. However, free (non-bound),
reactive iron within cells and tissue is responsible
for iron’s redox toxicity. For these reasons
complex systemic and intracellular mechanisms
are needed for proper iron handling, storage,
transfer, and metabolism. There is limited
excretion of iron, whereas iron can be loaded by
ingestion, transfusions, disease states, and
exogenous sources. Iron excess and iron
dysregulation are associated with a wide variety
of acute and chronic human diseases.
There is an emerging paradigm of severe
COVID-19 infection as a multi-system, antibody
and immune complex-mediated disease. There is
evidence of antibody-dependent enhancement
(ADE) of infection with COVID-19, suggesting
that low (affinity) quality or quantity of antibodies
will worsen rather than protect against the
disease. Iron dysregulation is a key feature of
severe COVID-19 infections. Covid-19
immunopathology is characterized by iron
dysregulation. The most common co-morbid
conditions associated with severe COVID-19
infection, for example, obesity, hypertension, and
diabetes are related to iron overload or
dysfunction.
Air pollution is the world’s leading killer, and the
smallest particulate matter derived from
combustion sources contains the most harmful
elements. It has been previously shown that
countless exogenous magnetic combustion-
derived spherical pollution nanoparticles
accumulate in brains and hearts of children and
adults from highly polluted areas. These particles
are associated with heart disease and
neurodegeneration. Diverse ultrafine particles
including magnetite (Fe
3
O
4
) have also been
found in human sera and pleural fluid.
Collectively, these findings are consistent with
Whiteside and Herndon; JAMMR, 32(18): 43-60, 2020; Article no.JAMMR.61789
54
near-universal contamination of human tissue
and cells with combustion-derived ultrafine and
nanoparticles.
In human cells nanoparticles like magnetite tend
to concentrate in organelles including
mitochondria and endoplasmic reticulum.
Reactive oxygen species and oxidative stress in
these structures lead to miscommunication
between mitochondria and ER, misfolding of
proteins, and eventually cell breakdown and
apoptosis. Ultrafine particles most likely produce
toxicity by mitochondrial dysfunction and ER
stress. Endoplasmic reticulum stress is
recognized as a major contributor to various
degenerative diseases. The mitochondrial-ER
junction is involved in iron homeostasis, and
COVID-19 attacks these same areas.
Growing evidence suggests that air pollution is a
cofactor in the spread and severity of COVID-19.
Ultrafine particles have major effects on the
world’s cloud layer, the hydrological cycle,
climate change, and global warming. Magnetic
particles in human tissue match those found in
coal fly ash and certain diesel emissions. While
traffic-related air pollution (TRAP) contributes to
the particle load, this fraction is presumably
eclipsed by coal fly ash from industrial sources,
coal-fired power plants, and aerosolized coal fly
ash used in tropospheric aerosol
geoengineering. Climate change and global
warming linked to particle pollution. Pandemics
of air pollution, noncommunicable disease, and
COVID-19 are interrelated and intertwined. They
share the common feature of nanoparticle toxicity
and iron dysregulation. Altogether these
converging catastrophes pose an existential
threat to human and environmental health.
The global nature of these problems shows they
can only be tackled by international cooperation.
Complacency about the dangers of air pollution
and the deadly “code of silence”, specifically, the
subject of ongoing, “covert” geoengineering and
“climate intervention” must be broken if the world
is to have a realistic chance of controlling these
public health emergencies. Immediate steps to
be taken include:
1. There must be international study,
quantification, and regulation of emissions
of ultrafine air pollution
2. The “hidden in plain sight” tropospheric
aerosol geoengineering operations must
halt.
3. Small particle pollution from all sources
including coal fired power plants, vehicle
emissions, fuel additives, and industrial
sources must be curbed.
4. Full public disclosure as to the sources,
nature, and extent of air-polluting activities.
5. Universal public health mandates (e.g.
masks/face coverings) must remain in place
until the COVID-19 crisis is brought under
control.
These and other actions constitute a moral
imperative if humanity, even our children, is to
have a healthy or even viable future.
CONSENT
It is not applicable.
ETHICAL APPROVAL
No human or animal subjects were involved.
COMPETING INTERESTS
Authors have declared that no competing
interests exist.
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