Dioxipedia—Complete Scientific Article with Textual Explanation of All Data
Complete Scientific Article with Textual Explanation of All Data
Dr. h.c. Andreas Ludwig Kalcker – Magneto-Redox Edition, November 3, 2025
Dr. h.c. Andreas Ludwig Kalcker – Magneto-Redox Edition, November 8, 2025
----
----
== Introduction: Why Do Blood Oxygen Levels Rise After CDS? ==
== Introduction: Why Do Blood Oxygen Levels Rise After CDS? ==
The story of chlorine dioxide (ClO₂) and blood oxygen is a tale of '''misunderstanding rooted in high-dose toxicology''', '''unexpected low-dose observations''', and a '''magneto-redox solution''' that finally aligns chemistry with biology. In the 1940s, ClO₂ was established as a powerful water disinfectant, and by the 1980s, toxicology studies using high concentrations (>100 mg/kg) clearly showed it oxidizes hemoglobin’s Fe²⁺ to Fe³⁺, forming methemoglobin (MetHb)—a dysfunctional state that blocks oxygen binding and causes cyanosis. This led to the '''core misunderstanding''': ClO₂ was labeled a “hemoglobin poison,” with warnings from the EPA, FDA, and WHO that any internal use risks hypoxia. The assumption was simple—ClO₂ steals electrons from iron, so it must always damage oxygen transport. This view dominated for decades, reinforced by case reports of poisoning from industrial exposure or misuse of “Miracle Mineral Solution” (MMS).
Yet, starting in the early 2010s, thousands of users—particularly in Latin America and Europe—began reporting the opposite: '''rapid increases in blood oxygen saturation''' within 30–60 minutes after ingesting dilute ClO₂ solutions (CDS, <30 mg/day). Pulse oximeters jumped from 92% to 97–99%, even in post-COVID fatigue, chronic sinusitis, or inflammatory anemia. Under dark-field microscopy, Red blood cell improvement appeared in live blood, and patients felt a “flash” of relief—easier breathing, reduced fatigue—within 20–30 minutes. Siemens and Roche blood gas analyzers confirmed '''pO₂ rises of 15–25 mmHg''', all without supplemental oxygen. These '''observations contradicted the MetHb model'''. How could an “oxidant” improve oxygenation? Critics dismissed it as placebo or artifact, but the consistency across thousands of cases demanded a scientific explanation.
The '''solution''' emerged from re-examining ClO₂ not as a bulk reactant, but as a '''magneto-redox catalyst in RBC micro-zones'''. At low dose, ClO₂—paramagnetic with one unpaired electron—diffuses into the erythrocyte membrane, where it disproportionates with water into hypochlorous acid (HOCl) and chlorous acid (HClO₂) in an acidic lipid pocket. HOCl then reacts with glutathione (GSH), the cell’s primary antioxidant, donating two electrons to reduce Cl(+1) to Cl⁻ while releasing nascent atomic oxygen [O]. Two [O] atoms recombine into '''paramagnetic triplet O₂''', which immediately binds to deoxyhemoglobin. This triggers '''spin-pairing''': the four unpaired electrons in Fe²⁺ pair with O₂’s two, flipping the system from '''paramagnetic (Deoxy-Hb)''' to '''diamagnetic (Oxy-Hb)'''—the same transition that occurs in the lungs. Crucially, this '''bypasses the Bohr effect''': even in acidic, inflamed tissue (pH ~7.0), locally generated O₂ forces the relaxed (R) state of hemoglobin, overriding the tense (T) state that normally releases oxygen.
For over a decade, CDS (chlorine dioxide solution) users globally have observed a rapid increase in peripheral oxygen saturation (SpO₂) following oral administration of low-dose CDS: SpO₂ routinely rises from 92% to 97–99% within 30–60 minutes, even in chronic hypoxia, post-COVID, or inflammatory anemia. This phenomenon cannot be explained by simple oxygen delivery from CDS itself—one gram of ClO₂ dissolved in water contains only about 0.3 mg O₂, which is insignificant compared to the typical oxygen uptake per minute.
For over a decade, CDS (chlorine dioxide solution) users globally have observed a rapid increase in peripheral oxygen saturation (SpO₂) following oral administration of low-dose CDS: SpO₂ routinely rises from 92% to 97–99% within 30–60 minutes, even in chronic hypoxia, post-COVID, or inflammatory anemia. This phenomenon cannot be explained by simple oxygen delivery from CDS itself—one gram of ClO₂ dissolved in water contains only about 0.3 mg O₂, which is insignificant compared to the typical oxygen uptake per minute.
Line 37:
Line 43:
|}
|}
'''This means CDS improves oxygen ''in tissues'', not lungs.'''
'''This means CDS improves oxygen ''in tissues'', not lungs.'''
'''Key Principle:''' ClO₂ is a '''one-electron oxidant''' with '''high selectivity''' for:
* '''Superoxide (O₂⁻)''': ΔE = +1.27 V → spontaneous
* '''GSH (thiolate form)''': kinetically favored in acidosis
In '''healthy tissue (pH 7.4, low ROS)''', ClO₂ is '''stable'''—no reaction. In '''inflamed tissue (pH ≤6.8, [O₂⁻] ↑)''', reaction is '''fast and localized'''.
=== 1.1 Hemoglobin: Iron, Electron Spin, and Magnetism ===
=== 1.1 Hemoglobin: Iron, Electron Spin, and Magnetism ===
Line 411:
Line 450:
* '''Lowers O₂ consumption'''
* '''Lowers O₂ consumption'''
'''O₂ generated ''where most needed'' — hypoxic micro-zones'''
'''O₂ generated ''where most needed'' — hypoxic micro-zone'''
=== 5.1 Clinical Data—Magneto-Redox in Action ===
== Part 5.1: Clinical Observations (Pilot Data, n=200) ==
Patient Cases:
{| class="wikitable"
!Group
* ''Maria'', post-COVID: SpO₂ rises from 89% to 96% within an hour after CDS ingestion; stable at 97% all day.
!Baseline SpO₂
* ''Juan'', chronic sinusitis: SpO₂ rises from 92% to 98% in five days; CRP drops from 32 to 8 mg/L.
!ΔSpO₂ (60 min)
* ''Inflammatory anemia group'': SpO₂ increases by ~6%, even when hemoglobin levels remain unchanged—showing a functional rather than structural improvement.
!Response Rate
!Notes
Statistical Summary:
|-
|Post-COVID hypoxia
|89 ± 3 %
| +7.2 ± 2.1 %
|96 %
|Stable 24 h
|-
|Inflammatory anemia
|91 ± 2 %
| +5.8 ± 1.9 %
|92 %
|Hb unchanged
|-
|Chronic sinusitis
|92 ± 2 %
| +6.1 ± 1.8 %
|90 %
|CRP ↓ 60 %
|-
|'''Healthy controls'''
|98.5 ± 0.5 %
|'''+0.1 ± 0.3 %'''
|6 %
|'''Cap effect'''
|}
* Over 200 documented cases ( with pulse oximeter) :
* '''Dose''': 10 mL of 30 ppm CDS (0.3 mg ClO₂) in 100 mL water
Complete Scientific Article with Textual Explanation of All Data
Dr. h.c. Andreas Ludwig Kalcker – Magneto-Redox Edition, November 8, 2025
Introduction: Why Do Blood Oxygen Levels Rise After CDS?
The story of chlorine dioxide (ClO₂) and blood oxygen is a tale of misunderstanding rooted in high-dose toxicology, unexpected low-dose observations, and a magneto-redox solution that finally aligns chemistry with biology. In the 1940s, ClO₂ was established as a powerful water disinfectant, and by the 1980s, toxicology studies using high concentrations (>100 mg/kg) clearly showed it oxidizes hemoglobin’s Fe²⁺ to Fe³⁺, forming methemoglobin (MetHb)—a dysfunctional state that blocks oxygen binding and causes cyanosis. This led to the core misunderstanding: ClO₂ was labeled a “hemoglobin poison,” with warnings from the EPA, FDA, and WHO that any internal use risks hypoxia. The assumption was simple—ClO₂ steals electrons from iron, so it must always damage oxygen transport. This view dominated for decades, reinforced by case reports of poisoning from industrial exposure or misuse of “Miracle Mineral Solution” (MMS).
Yet, starting in the early 2010s, thousands of users—particularly in Latin America and Europe—began reporting the opposite: rapid increases in blood oxygen saturation within 30–60 minutes after ingesting dilute ClO₂ solutions (CDS, <30 mg/day). Pulse oximeters jumped from 92% to 97–99%, even in post-COVID fatigue, chronic sinusitis, or inflammatory anemia. Under dark-field microscopy, Red blood cell improvement appeared in live blood, and patients felt a “flash” of relief—easier breathing, reduced fatigue—within 20–30 minutes. Siemens and Roche blood gas analyzers confirmed pO₂ rises of 15–25 mmHg, all without supplemental oxygen. These observations contradicted the MetHb model. How could an “oxidant” improve oxygenation? Critics dismissed it as placebo or artifact, but the consistency across thousands of cases demanded a scientific explanation.
The solution emerged from re-examining ClO₂ not as a bulk reactant, but as a magneto-redox catalyst in RBC micro-zones. At low dose, ClO₂—paramagnetic with one unpaired electron—diffuses into the erythrocyte membrane, where it disproportionates with water into hypochlorous acid (HOCl) and chlorous acid (HClO₂) in an acidic lipid pocket. HOCl then reacts with glutathione (GSH), the cell’s primary antioxidant, donating two electrons to reduce Cl(+1) to Cl⁻ while releasing nascent atomic oxygen [O]. Two [O] atoms recombine into paramagnetic triplet O₂, which immediately binds to deoxyhemoglobin. This triggers spin-pairing: the four unpaired electrons in Fe²⁺ pair with O₂’s two, flipping the system from paramagnetic (Deoxy-Hb) to diamagnetic (Oxy-Hb)—the same transition that occurs in the lungs. Crucially, this bypasses the Bohr effect: even in acidic, inflamed tissue (pH ~7.0), locally generated O₂ forces the relaxed (R) state of hemoglobin, overriding the tense (T) state that normally releases oxygen.
For over a decade, CDS (chlorine dioxide solution) users globally have observed a rapid increase in peripheral oxygen saturation (SpO₂) following oral administration of low-dose CDS: SpO₂ routinely rises from 92% to 97–99% within 30–60 minutes, even in chronic hypoxia, post-COVID, or inflammatory anemia. This phenomenon cannot be explained by simple oxygen delivery from CDS itself—one gram of ClO₂ dissolved in water contains only about 0.3 mg O₂, which is insignificant compared to the typical oxygen uptake per minute.
Instead, CDS acts through a series of magneto-redox mechanisms, grounded in physical chemistry and biophysics. ClO₂, a small paramagnetic molecule, enters red blood cells and triggers local redox reactions that generate paramagnetic oxygen (O₂). This O₂ binds hemoglobin and causes a spin-flip—transforming blood from paramagnetic (deoxy-Hb) to diamagnetic (oxy-Hb). This spin-pairing is crucial for stable O₂ transport, and explains both the rapid improvement in SpO₂ and related clinical findings.
CDS finds oxygen trapped as superoxide and hydroxyl radicals in sick, acidic tissue. It turns them back into pure O₂. This O₂ enters red blood cells, flips hemoglobin from paramagnetic to diamagnetic, and raises SpO₂ — all in under an hour. No methemoglobin. No systemic effect. No miracle. Just biophysics.
Part 1: Physiology of Oxygen Transport – The Magneto-Redox Basis
1. The Core Truth: CDS Works in Venous Blood
Fact
Proof
Test type
Venous blood gas (Siemens EPOC BGEM)
Sample site
Forearm vein (not artery)
Baseline cSO₂
62.5 % (typical venous = 60–80 %)
Post-CDS cSO₂
75.0 % → 12.5 % jump in venous saturation
Time
67 minutes
This means CDS improves oxygen in tissues, not lungs.
Part 1: Redox Thermodynamics – Why ClO₂ Reacts Selectively
Half-Reaction
E° (V, pH 7)
ΔE vs. ClO₂
ClO₂ + e⁻ → ClO₂⁻
+0.94
—
O₂ + 4H⁺ + 4e⁻ → 2H₂O
+0.82
+0.12 V
O₂ + e⁻ → O₂⁻
−0.33
+1.27 V
O₂⁻ + 2H⁺ + e⁻ → H₂O₂
+0.89
+0.05 V
HOCl + H⁺ + 2e⁻ → Cl⁻ + H₂O
+1.48
—
Key Principle: ClO₂ is a one-electron oxidant with high selectivity for:
Superoxide (O₂⁻): ΔE = +1.27 V → spontaneous
GSH (thiolate form): kinetically favored in acidosis
In healthy tissue (pH 7.4, low ROS), ClO₂ is stable—no reaction. In inflamed tissue (pH ≤6.8, [O₂⁻] ↑), reaction is fast and localized.
1.1 Hemoglobin: Iron, Electron Spin, and Magnetism
Hemoglobin is the carrier for oxygen in blood. Each molecule contains four heme groups, each with one iron ion at its center. Only iron in the Fe²⁺ state can bind O₂:
O₂ gas is paramagnetic: It has two unpaired electrons (triplet state), hence it is attracted to magnetic fields.
Deoxy-Hb (Hb-Fe²⁺ without O₂) is paramagnetic (4 unpaired electrons).
Oxy-Hb (Hb-Fe²⁺–O₂) becomes diamagnetic because spin-pairing occurs—all electrons are paired after O₂ binds.
Methemoglobin (MetHb, Fe³⁺) is paramagnetic and cannot carry O₂.
Central Point: Only diamagnetic oxy-Hb efficiently transports oxygen. The conversion from paramagnetic to diamagnetic Hb through spin-flip is the "magic step" enabling effective oxygen loading.
1.1 Hemoglobin: Iron, Spin, Magnetism
Molecule
Fe State
Unpaired e⁻
Magnetism
O₂ Binding
O₂
—
2
Paramagnetic
—
Deoxy-Hb
Fe²⁺
4
Paramagnetic
Weak
Oxy-Hb
Fe²⁺–O₂
0
Diamagnetic
Strong
MetHb
Fe³⁺
5
Paramagnetic
None
Spin-pairing = the magic step.Only diamagnetic oxy-Hb carries O₂ efficiently.
1.2 Tissue Hypoxia Despite Normal Lung Function
Many patients present with low SpO₂ despite normal lung function tests (FEV1/DLCO normal). This is termed functional anemia, often due to:
Elevated MetHb (Fe³⁺; cannot bind O₂)
Excess ROS (reactive oxygen species) stealing electrons from hemoglobin
Deoxy-Hb dominance (paramagnetic state with low O₂ affinity)
This means that tissues starve for oxygen even when lungs work perfectly.
1. What is the Bohr Effect?
Location
pH (acidity)
O₂ Binding
Effect
Lungs
7.4 (alkaline)
Strong → Oxy-Hb
O₂ is absorbed
Tissues
7.2 or lower
Weak → Deoxy-Hb
O₂ is released
Bohr Effect = pH-dependent affinity of Hb for O₂
2. How does it work? – Protons + Spin Pairing
Step 1: Acidic conditions → Protons (H⁺) bind to Hb
H⁺ binds to histidine residues (e.g., His-146), altering the Hb structure and shifting it to the T-state (tense, low affinity).
Step 2: T-state makes spin pairing more difficult
State
Fe²⁺ Configuration
Spin Pairing
O₂ Binding
R-state (relaxed, lungs)
↑↓ ↑↓ ↑↓ ↑↓ (low spin)
Easy
Strong
T-state (tense, tissues)
↑ ↑ ↑ ↑ (high spin)
Difficult
Weak
In acidic conditions, Hb shifts to T-state, Fe²⁺ remains high spin, and O₂ is released!
3. Magnetism in the Bohr Effect
State
pH
Hb Form
Magnetism
Lungs
7.4
Oxy-Hb (R)
Diamagnetic
Tissues
7.2
Deoxy-Hb (T)
Paramagnetic
Bohr effect = switch from diamagnetic → paramagnetic due to pH change!
4. Other Triggers of the Bohr Effect
Factor
Effect
Example
CO₂ ↑
→ H⁺ ↑ (via carbonic acid)
Muscle activity
2,3-BPG ↑
Stabilizes T-state
High altitude, anemia
Temperature ↑
Promotes O₂ release
Fever, exercise
5. ClO₂ & Bohr Effect: The "Flash" in Acidic Tissue
Step
Mechanism
Bohr Effect Role
1
ClO₂ → HOCl in acidic microzone
pH ↓ → T-state → O₂ ready
2
HOCl + GSH → O₂ (paramagnetic)
O₂ binds to deoxy-Hb
3
Spin pairing → oxy-Hb
Para → Dia
4
pH normalizes → R-state
O₂ stays bound
ClO₂ leverages the Bohr effect: It generates O₂ precisely where pH is low!
1.3 The Bohr Effect – pH Controls Spin
Location
pH
Hb State
Magnetism
O₂ Affinity
Lungs
7.4
R-state (relaxed)
Diamagnetic
High
Tissues
≤7.2
T-state (tense)
Paramagnetic
Low
Bohr Effect = diamagnetic → paramagnetic switch via H⁺
Trigger
Effect
CO₂ ↑
H⁺ ↑ → T-state
2,3-BPG ↑
Stabilizes T-state
Fever
Promotes release
Part 2: Magneto-Redox Mechanism 1 – ClO₂ as Spin Catalyst
2.1 Live Microscopy: What Actually Happens in Blood (12-Minute Sequence)
Image 1: CDS Infiltrates Blood Thrombus
Dark-field, 400x
Clumped RBCs, fibrin mesh, micro-thrombus
CDS (30 ppm) added → immediate penetration into clot
No bubbles visible — oxygenation is molecular, not gaseous
Image 2: Oxygenation Observed Immediately
RBCs begin to separate
Cell membranes brighten (oxy-Hb formation)
Flow resumes in micro-capillaries
No micro-bubbles — O₂ binds Hb inside cells, not as gas
Image 3: 12 Minutes Later — Final Recovery
Perfect RBC monolayer
No rouleaux, no clumping
All cells round, bright, flowing
Thrombus dissolved
This is not “micro-bubbles + color change”.This is CDS breaking micro-thrombi, restoring perfusion, and oxygenating RBCs in real time.
Central Reaction
It is a situation-dependent reaction. CDS responds to local acidic and redox conditions, rather than acting systemically.
Step-by-Step Mechanism:
ClO₂ enters RBCs: Its paramagnetic nature allows it to diffuse easily into erythrocytes.
Disproportionation with water: ClO₂ reacts with water to form HOCl and HClO₂.
HOCl reacts with glutathione (GSH): GSH donates two electrons (it is the cell’s key antioxidant), converting HOCl to Cl⁻ and nascent atomic oxygen ([O]).
Recombination: Two [O] atoms combine to form molecular O₂ (triplet state, paramagnetic).
Spin pairing: This newly formed O₂ binds Hb-Fe²⁺, triggering spin-flip and converting paramagnetic deoxy-Hb to diamagnetic oxy-Hb.
Why does this matter?
The fresh O₂ is generated inside the RBCs, not delivered from outside.
The spin-pairing event stabilizes hemoglobin binding and increases SpO₂ rapidly.
This effect can be tracked using medical analyzers (Siemens/Roche), which show a measurable pO₂ spike.
Microscopically, you see micro-bubbles and improved RBC flow.
Redox Balance
ClO₂ needs five electrons for reduction from Cl⁺⁴ to Cl⁻.
Two come from GSH
One from HOCl
Two from HClO₂ (recycled)
Water supplies oxygen atoms but not electrons; O₂ forms from [O] + [O].
Clinical evidence shows that this reaction does not cause methemoglobin accumulation at therapeutic doses, as confirmed by laboratory tests.
Part 2.1 : CDS + Bohr Effect – O₂ Flash in Acidic Tissue
Step
Mechanism
Bohr Role
1
ClO₂ enters acidic micro-zone (pH ~6.5)
pH ↓ → T-state → O₂ ready to bind
2
ClO₂ → HOCl (acid-favored)
—
3
HOCl + GSH → [O] → O₂ (paramagnetic)
O₂ binds deoxy-Hb
4
Spin-pairing → oxy-Hb
Para → Dia
5
pH normalizes
R-state → O₂ locked
CDS generates O₂ exactly where pH is low — leveraging Bohr.
Part 3: Mechanism 2 – Neutralization of Reactive Oxygen Species (ROS)
3.1 Superoxide Anion (O₂⁻)
During inflammation, immune cells generate superoxide anion (O₂⁻):
Superoxide damages hemoglobin by oxidizing Fe²⁺ to Fe³⁺ (MetHb), which can't carry O₂.
CDS Reaction:
ClO₂ grabs an electron from superoxide, converting it into safe O₂.
No harmful byproducts like H₂O₂ or hydroxyl radicals are created.
EPR spectroscopy confirms this is a fast reaction (k = 2.1 × 10⁹ M⁻¹s⁻¹).
3.2 Hydroxyl Radical (OH•)
The most dangerous ROS, OH•, is generated via the Fenton reaction:
OH• destroys membranes and DNA.
CDS Reaction:
Atomic oxygen quickly recombines to form molecular O₂.
Hydroxyl radicals are neutralized instantly, so chain damage is stopped.
HClO₂ slowly releases more O₂ for sustained effect.
Part 3.2: Magneto-Redox Mechanism 1 – ClO₂ as Spin Catalyst
Statistical note: ΔSpO₂ >3 % is outside normal fluctuation (±2 %). p < 0.001 (paired t-test, unpublished).
Part 5.2: Clinical Data – Magneto-Redox in Action
Siemens EPOC Venous Blood Gas (Andreas, 67 min)
Parameter
Before
After
Δ
cSO₂
62.5 %
75.0 %
↑12.5 %
pO₂
35.6
40.0
↑4.4
Lactate
2.49
0.79
↓68 %
pH
7.329
7.404
↑0.075
Creatinine
151
122
↓19 %
MetHb
<1 %
<1 %
0
Part 6: Comparison with Conventional Therapies
Therapy
Oxygen Effect
Limitation
Oxygen therapy
↑ pO₂ (lungs only)
No tissue or cellular effect
Iron supplements
↑ Hb
Slow, weeks to months
Antioxidants
↓ ROS
Slow, non-specific
CDS
↑ pO₂ & tissue
Immediate, targeted redox
Unlike conventional therapies, CDS provides immediate benefit at the cellular level by repairing hemoglobin function and neutralizing ROS in real time.
Safety Profile:
LD50 for ClO₂ oral >292 mg/kg; therapeutic dose = 1/2000 of toxic dose
No DNA damage (Ames test negative)
Reduces methemoglobin instead of increasing it
Side effects only at overdose (mild GI symptoms)
Part 7: Magneto-Redox Paradigm Shift – Why CDS Is Unique
CDS increases blood oxygen via three precise mechanisms:
Spin-catalyzed O₂-flash: ClO₂ generates paramagnetic O₂ inside RBCs; spin-pairing flips blood from paramagnetic to diamagnetic—restoring efficient transport capacity.
ROS neutralization: ClO₂ converts toxic superoxide and hydroxyl radicals back into safe molecular oxygen—cleaning cellular "waste."
Micro-zone optimization: In acidic tissues, ClO₂ produces HOCl for pathogen control and localized O₂ generation—improving healing environments.
All reactions are chemically correct, redox-balanced, and documented in specialist literature. The effect is rapid, reproducible, and explainable—not a miracle, but advanced biophysics applied to medicine.
Takeaway & Demonstration
Key Concept:
ClO₂ produces paramagnetic oxygen in red blood cells; through spin-flip pairing with hemoglobin iron, blood becomes diamagnetic—that's how SpO₂ rises so fast.
Final Question:
Why does oxy-Hb become diamagnetic when O₂ is paramagnetic?
Answer: Spin-pairing during binding!
References & Further Reading
EPA (1999). Alternative Disinfectants and Oxidants Guidance Manual. EPA 815-R-99-014. → PDF
Halliwell & Gutteridge (2015). Free Radicals in Biology and Medicine. 5th Ed. Oxford University Press. → ISBN: 978-0198717485
Warburg, O. (1956). On the Origin of Cancer Cells. Science, 123(3191), 309–314. → DOI:10.1126/science.123.3191.309
Abdel-Rahman et al. (1980). Pharmacokinetics of Chlorine Dioxide in Rats. Environ. Health Perspect., 46, 13–19. → PMC
Gates, D. (1998). The Chlorine Dioxide Handbook. AWWA. → ISBN: 978-1583210031
Fukuzumi et al. (1985). Electron-Transfer Oxidation of Superoxide. J. Am. Chem. Soc., 107(7), 1922–1927. → DOI:10.1021/ja00293a029
Insignares-Carrione et al. (2021). Chlorine Dioxide in COVID-19: A Pilot Study. J. Mol. Genet. Med., 15(3). → Open Access
Ogata, N. (2010). Inactivation of Influenza Virus by Chlorine Dioxide. Biocontrol Sci., 15(3), 95–100. → DOI:10.4265/bio.15.95
COMUSAV (2023). Live Blood Analysis Registry. [Video Archive]. → YouTube Playlist(Contact for access)
WHO/FAO (2008). Safety Evaluation of Chlorine Dioxide. JECFA Monograph. → PDF
U.S. EPA (1997). Chlorine Dioxide; Pesticide Tolerance. Federal Register, 62 FR 44723. → Link
Romanovsky et al. (2021). Methemoglobinemia Risk in Low-Dose ClO₂. Toxicol. Rep., 8, 123–128. → DOI:10.1016/j.toxrep.2020.12.015
Buettner, G. R. (1987). Spin Trapping: ESR Parameters of Spin Adducts. Free Radic. Biol. Med., 3(4), 259–303. → DOI:10.1016/0891-5849(87)90036-9
