by Hildegarde Staninger, Ph.D., RIET-1, Industrial Toxicologist/IH & Doctor of Integrative Medicine. Integrative Health Systems, LLC, 415 3/4th N. Larchmont Blvd., Los Angeles, CA 90004 Tel: 323-466-2599 Fax: 323-466-2774e-Mail: ihs-drhildy@sbcglobal.net © September 7, 2009 Presented at the 2009 National Registry of Environmental Professionals Conference Oct 5-6th, 2009, Des Plaines, IL. Published NREP Journal of Environment and Sustainability.
ABSTRACT:
Cholinesterase inhibition has been associated with exposure to oranophosphate and carbamate pesticides, since their creation during World War I and II. Traditionally, they cause severe neurological disorders that can paralyze not only insects but humans. Individuals are usually exposed by misuse of pesticide applications or through aerial spraying. The cholinesterase inhibition effects for chronic exposure or multiple acute exposures are expressed in acetyl cholinesterase, enzyme (AChE) activities inhibition. The integration of nano particulates in various nano composite materials, such as aerial hydrogels and other similar materials used in aerial vector sprays, weather modification and sensor grids, resulted in the individual having as high as 96.2 % cholinesterase inhibition and detectable readings of nano composite materials present. Confirming Ocean University, China’s findings in the June 2009 issue of Chemical Sensitivities, that nano particles are 100 times more toxic than a single molecule of a pesticide, such as Malathion, propoxopur or benomyl.
Background:
During the summer of 2007 in Phoenix, Arizona, a female age 51 was exposed to aerial spraying for weather modification and vector control (mosquito) as performed through G-1 requirements and Project Earth Scope1. She was at home and had her windows open and went outside of her home to see what was happening. She immediately felt a burning and tingling sensation and became ill. After numerous analytical testing and physician evaluations, it was determined she was exposed at a minimum to nano composite material and Sencil™1 technology due to specimens of the materials taken from her body appeared to be hair follicles, but were not upon laboratory analysis. The sample melted at 650o C, while human hair melts at just above 135oC and synthetic hair melts at approximately 2250 C.
Discussion:
Primary concern was individual’s symptoms, which coincided with chronic acetyl cholinesterase (AChE) enzyme inhibition in the circulating red blood cells that are depository regulators for the various soft tissue organs within the body.2 Once the levels of the red blood cell values become very high they trigger the release of plasma cholinesterase to replenish any future inhibition roller coastering effects. The roller coastering affects can be very sudden or gradual; all depending upon the amount of recovery of the enzyme into the organ systems and the trigger points of specific sensor modulating factors within the cell membranes and nuclear membrane.
A comprehensive toxicological analysis of the results using the standard mathematical calculations to determine the percent (%) inhibition of acetylcholinesterase was determined from initial testing in 2008 to present 2009 values. The values were calculated and based upon the most current cholinesterase value for red blood cells and plasma to show a linear time relationship and medically observations by her treating physician/naturopath and toxicologist from the chronic effects of cholinesterase inhibition and its toxicological neurological mechanisms of action.
On August 15, 2009 her individual value for cholinesterase, plasma 2019 and RBC 5774 IUs. A comparative table is stated below, based on each date’s value and compared to August 15, 2008 (note exactly one year from initial testing).
Table 1 -1: Date vs. Value Level (IU) and Calculated % Inhibition of
Cholinesterase
Plasma
08/15/2008 07/21/2009 08/11/2009
2019 4928 4581
% Inhibition Base Value (BV) 59% 7.57%
NOTE: BV to Most Resent Test Value % Inhibition is 55.92% inhibition of Plasma Cholinesterase over a 1 year period.
RBC
08/15/2008 07/21/2009 08/11/2009
5774 2080 L 15,092
% Inhibition Base Value (BV) 96.4% 86.2%
NOTE: BV to Most Resent Test Value % Inhibition is 61.74% inhibition of RBC Cholinesterase over a 1 year period. Another individual exposed to nano composite and nanoparticulate via water; female age 50 had 76.2 % RBC AChe inhibition. Control male age 70 had 0.3 % RBC Ache inhibition and no exposure to advanced nano microbic materials of any type. The control’s value is within standard deviation of <= 2% inhibition value.
The US Federal Government’s standard for chronic cholinesterase inhibition was set by the US EPA Agency in EPA Recognition and Management of Pesticide Poisonings, 4th Edition, US Governmental Printing Office, Washington, D.C. March 1989 EPA-0540/9-88-001 that a 10 % or more inhibition factor is a result of chronic pesticide poisoning. A number of advanced nano microbic materials are made from composite material that contains mixtures of dragon protein, carbamates, and microbivores each containing specific chemicals that are known to cause cholinesterase inhibition.
The difference between a regular chemical and/or pesticide exposure and nano advanced materials is that the nano materials are able to penetrate the cell membrane and attach to the cellular membrane as G protein/C-reactive protein with chemical interactions on the nuclear membrane, which would result in measurable value of antinuclear antibody immunoglobulins.2 Because of this primary factor of entering the cytoplasma, organelles and nuclear membrane nano materials are cytotoxic and cause cellular dysfunction, injury and initiate toxicological mechanisms of disease patterns. This is further complicated with previous exposure to childhood viruses (measles and chicken pox) and current aerial testing emissions for DARPA under DARPA’s Unconventional Pathogen Countermeasure Program and Project Earth Scope.3, 4
The individual had specific tests performed on ionic bath samples and “pseudo hair” samples, which revealed exposure to – nano composite material- that came out of her body. This material was sent to Applied Consumer Services, Inc. for advance materials analysis and Morris Consulting, Inc. both laboratories are governed by GPL standards within the laboratory.
Recent studies conducted by the College of Environmental Sciences and Engineering, Ocean University of China, Qingdao, China (Z. Wang, et.al.)5,6 have shown that manufactured nanoparticles can be toxic via interactions with proteins (precursor’s amino acids) and enzymes. Acetylcholinesterase (AChE) is a key enzyme present in the brain, blood and nervous system. Therefore, absorption and inhibition of AChE by specific nanoparticles, SiO2, TiO2, Al2O3, Al, Cu, and Cu-C (carbon coated copper), multi-walled carbon nanotubes (MWCNT) and single-walled carbon nanotubes (SWCNT) had the following results:
• Carbon nanotubes had high affinity for AChE absorption. SWCNT (94%),
Nano SiO2 and Al2O3 showed the lowest absorption.
• Cu(2+) release in Cu and Cu-C nanoparticle suspensions caused 40% and 45% of AChE activity reduction, respectively AChE inhibition by bulk Cu and
activated carbon particles were also measured for comparison, showing that the inhibition by bulk particles was lower than their counterpart nanoparticles.
• Bulk Cu particles, AChE inhibition was primarily caused by dissolved ions, but mainly absorption for activated charcoal.
• AChE inhibition by Cu, Cu-C, MWCNT and SWCNT had dose-response relationships, and their median inhibitory concentrations (IC 50) were 7, 17, 156 and 96 mg/L-1, respectively, showing that these nanoparticales may have neurotoxicity and AChE may have potential to be used as a biomarker for nanoparticle exposure.
The primary toxicological mechanisms of action of the nanoparticles used in nanocomposite materials are mainly due to cholinesterase inhibition. Three main biochemical reactions are responsible for these toxicological effects.
1. Inhibition of cholinesterase activity.
2. Inhibition of neuropathy target esterase (NTE) and development of delayed neuropathy.
3. Release of alkyl groups attached to the phosphorous atom and alkylation’s of macromolecules including RNA and DNA.
On August 2008 Antinuclear Antibody Tests were performed on individual and her result was 25 AU/ml. The ANA test confirms antibodies forming on the cell nuclear membrane. Reviewing the table illustrating the various % cholinesterase inhibitions from initial base line values for the individual, it was determined she had been suffering from severe chronic AChE toxicity as compared to her original baseline functional values for both plasma and RBC parameters. It must be noted, when both values of Plasma and RBC % inhibition are high the individual experiences highly aggressive behavior and when extremely low depression and suicide. The individual has had as high as 59 % cholinesterase inhibition for plasma and 96.4 % for RBC, with a 55.92% annual plasma inhibition value and 61.74 % RBC. Her value from just 3 weeks from July 21, 2009 to August 11, 2009 was 86.2 % cholinesterase inhibition.
During this time period the individual experienced several unique bowel movements that would be diagnosed as fecal incontinence. Thus, confirming as nanoparticles from nano composite materials are broken down and released through FIR Radiant Heat Therapy and appropriate custom nutritional supplementations, AChE values will become a high inhibitory factor. The ANA value, which should be repeated would confirm the alkylation’s of macromolecules of DNA, since ANA is specifically measuring antibodies on the nuclear membrane and the same individual’s had previous genetic testing under toxicogenomics, which showed less Basque values that control groups, which are known to have thicker cellular membranes, thus more superoxide dismutase enzyme would be needed to neutralize neurotoxins. Many of the new nanotubes and nano composite materials would need SOD to neutralize Cu, Cu-C nano contamination via Zn/Cu SOD-1 reactions.
It is important to note that in the formulation of Dragon protein adiptic acid a precursor to aspartame with isoleucine, leucine, lysine and arginine will react with phenylanaline esters.6, 7 Dragon protein has been used as a universal protein to blend DNA plasmids into hydrogels and nanocomposite materials. The individual had measurable amounts of phenylanaline amino acid present in her previous urine tests. The chemical name for aspartame is N-L-alpha-aspartyl-L-phenylalaine-1-methyl ester. Aspartame and its isomers are 160 times sweeter than table sugar.
It is a dipeptide that is prepared from N-benzoyldiester. When this compound is allowed to react with a phenylanaline ester as a food additive or component in many nano synthetic proteins, a displacement of a more reactive compound occurs which is p-nitrophenyl ester? P-nitrophenyl ester is a known excitatory neurotransmitter just as the L-form of aspartic acid is a primary ingredient in the manufacture of aspartame.
Neurotransmitters known to propagate nerve impulses in the receiving neuron are called excitatory neurotransmitters.8 These compounds are synthesized in the nerve’s cell body (the soma) and migrate down the axon to the pre-synaptic terminals. Here they are stored in little packets called vesicles, which fuse with the synaptic membrane like a chain of firecrackers linked to a single fuse. When a depolarizing current (the action potential) is received, these vesicles release their contents into the synaptic cleft.
Phenylalanine is a precursor to the catecholamine neurotransmitters in the brain. Elevated levels in the brain have been associated with seizures and risk of hemorrhagic stroke (when it forms phenyl propanolamine and mixed with aspartame). Aspartic acid can lower seizure thresholds making a seizure more likely in the future. This additive effect of aspartic acid and phenylalanine would significantly increase the likelihood of a seizure, especially under hypoglycemic conditions.
Many different substances effect the transmission of nerve impulse across the synapse and many are falsely called neurotransmitters. Some examples of true excitatory neurotransmitters that relate to an individual exposure are:
• Acetylcholine – peripheral and sensory nerves parasympathetic (maintenance, Diffuse Modulatory excitory forebrain, general excitability, sleep/wake cycle, learning and memory. Disease: Alzheimer’s and multiple sclerosis. MS is increased if an HLA gene mutation exists and Vitamin D deficiency.
• Norepinephrine – sympathetic (stress), Diffuse Modulatory pons, excitory, arousal of brain during interesting external events, increased responsiveness, alarm, attention, readiness, pain, reward, mood, brain metabolism, sleep/wake cycle, and memory. Disease: ADD, ADHA and depression.
• Dopamine – Diffuse Modulatory substantial Nigra, voluntary movement VTA,
Assign value to adaptive behaviors, and attention reward system. Disease:
Schizophrenia, Wain’s cats, novelty seeking, Parkinson’s, and reflective-orderly disorder.
• Serotonin – Diffuse Modulatory inhibition Raphe Nuclei, modulate pain-relief, mood, emotional behavior, satiety, self-esteem, balance, things are OK, sleep/wake, sleep stages, arousal. Disease: bipolar and synesthesia.
• Peptides – opioid; 4-joy, analgesia, and breathing. Disease: Autism.
• Glutamate – 70% of brain neurons, learning, and memory. Disease: epilepsy and nerve cell death.7
Carboxyhemoglobin values and ammonia levels were present. These materials are the degradation products of silicon nanotube/composites and the coatings applied to them as found in Acrylin™ and silicon nanotubes.
It is very important to note that excessive quantities of AChE as shown in the individual’s baseline comparative values accumulate at peripheral ganglionic and central nerve endings (synapses in effector organs, elevated concentrations occur in plasma and intestinal fluid. The intoxication effects connected with the excitement of M- and N-choline receptors (present on nerve terminals of effector organs) are as follows:
• Muscarine effect due to postganglionic cholinergic nerve impulses exciting the M-choline receptors of the lungs, gastrointestinal system, heart, kidneys, sweat glands, pupils and muscles.
• Nicotinic effect on the receptors of ganglionic synapses and motoric plates, the medular part of glandular subrenalis, and carotic nodules.
• Central effect of AChE due to nerve cells or AChE accumulation directly impacting the choline receptors, with parallel inhibition of other enzymes by nano particles or specific cholinesterase inhibitors (pesticides and polymers)
Such as lipase, cholesterol esterase, proteinase, monoaminooxidase, and other nonspecific esterase.
The duration of symptoms depends partly on the rate of AChE reactivation. Spontaneous reactivation depends on the chemical structure attached to the enzyme. The reactivation of the inhibited enzyme can be facilitated considerably by special compounds (oxymes). Several of these compounds have become important antidotes in the treatment of pesticide poisonings.
The inhibition enzyme may also be transformed into a state where no spontaneous reactivation occurs and where oximes are no longer capable of reactivating it. The phenomenon is called “aging” and is characterized by removal of one of the alkyl groups form the phosphoryl groups attached to the enzymes. The rapidity of inhibited AChE aging depends on the chemical nature of the phosphorylating materials. It must be noted that in the materials previously found by other patients exposed to advance nanomicrobic materials/nano particles phosphorus was present in other exposed individuals.
Over the last year the individual has experienced the following classical AChE symptoms with the appropriate site of action (target organ system):
Site of Action Signs and Symptoms
Eyes Increased lacrimation, slight myosis (occasional unequal, later
marked, blurred vision, eye pain when focusing, frontal headaches,
conjunctive hyperemia.
Respiratory System Rhinorrhea, hyperemia (local exposure), tightness in chest,
Prolonged wheezing, bronchoconstriction, increased secretion,
dispnea (not enough air), slight chest pain, cough, edema of the
lung.
Gastrointestinal System Increased salivation, anorexia, vomiting, abdominal
Cramps, epigastric and substernal tightness (cardiospasm) with
“heartburn” and eructation, diarrhea, tenesumus, involuntary
defection (fecal incontinence).
Sweat Glands Increased sweating.
Striated Muscles Easy fatigue, mild weakness, twitching, fasciculation’s (more
Pronounced at the side of exposure), cramps, generalized weakness
including respiratory muscles, dispnea, cyanosis.
Central Nervous System Giddiness, tension, anxiety, tremor, restlessness,
emotional labiality, excessive dreaming, insomnia, nightmares,
headache, tremor, apathy, withdrawal, and depression, slow wave
burst of elevated voltage in EEG (especially on hyperventilation),
drowsiness, concentration difficulty, slow recall, confusion, slurred
speech, ataxia, generalized weakness, coma with absence of reflexes,
Cheyne-Strokes respiration, convulsions, respiratory and circulatory
centers depression, dispnea, fall in blood pressure.
Circulatory System Brandycardia, decreased cardiac output, cardiac arrest,
vasomotor center paralysis.
The clinical symptoms of the different grades of AChE values are based upon reduction of AChE not inhibition.
Mild (60%) reduction of AChE) results in weakness, headache, dizziness, diminished vision, salivation, lacrimation, nausea, vomiting, lack of appetite, stomach-ache, restlessness, myosis, moderate bronchial spasm, convalescence in several days for pesticides and for nano particles unknown.
Moderate (60 to 90% reduction of AChE) Abruptly expressed general weakness, headache, visual disturbance, excess salivation, sweating, vomiting, diarrhea, brandycardia, hypertonia, stomach-ache, twitching of facial muscles, tremor of hand, head, and other body parts, increased excitement, disturbed gait, and feeling of fear, myosis nystagmus, chest pain, difficult respiration, cyanosis of the mucous membrane, chest crepitation; convalescence in 1 to 2 weeks for pesticides and for nano particles unknown.
Severe (90 to 100% reduction of AChE) Abrupt tremor, generalized convulsions, psyhic disturbances, intensive cyanosis of the mucous membrane, edema of the lung, coma, death from respiratory cardiac failure for pesticides and for nanoparticles.8
If CD 57 +/CD3+/CD+8 values were performed and they were “high”, indicating specific immunochemical reactions as demonstrated by the inhibition and reduction of AChE on the nervous system as a result of exposure to nanoparticles, which have been found to be more toxic to the cell than a regular molecule. It is important to note anti-myelin antibody tests were not performed, and if “positive” anitibody was present, it would confirm the binding of the particles to the nerve as a primary factor vs. embedding into the nerve as reported in viral particles embedding into the myelin sheath.
Also, one must take into account the coating of the nano particles which use antimicrobic agents, such as Aegis Microbic Shield, which is made up of silane and decomposes to silicone, carbon monoxide, carbon dioxide and silica upon exposure to oxygen. Silica is removed by exposure to Dr. Willard’s Water (CAW). The majority of all nano particles and other nano composite materials are coated with an antimicrobial agent, especially if used internally as in the new Nano Medicine and Gene Therapy.9, 10, 11, 12
Conclusion:
The female individual was exposed to advanced nano microbic materials that resulted in the production of fibers, nano composites, and nano particles in her body that reacted to her organ systems as previous stated in this paper.
In conclusion, the individual has suffered from severe chronic AChE inhibition, reduction and poisoning from nano particulates. These materials can interfere with her metabolic processes and primarily her gastrointestinal track, heart, lungs, and kidneys.
Previous clinical histories confirm the exposure to childhood viral vectors including the inoculation of polio vaccine as a child. Viral vectors and adenoviral protein envelops are precursors to the interaction of Vitamin D for the later factor, with SEVERE AChE Inhibition from exposure to nanoparticles, which are more toxic than regular chemical/pesticides within the cell and its organelles defense systems.
Aerial emission levels of strontium are monitored by the US Forestry Office. Strontium will interact with the metabolites of vitamin D and cause toxicological mechanisms that will result in vitamin D deficiencies. Nano tubes have been made of silicon-carbon and strontium. Strontium is the element of choice due to its use as a sensor material for sending and receiving for nano antenna advanced materials design. Further studies will be necessary for the determination of NO Effect Level from exposure to nano particulates and composites. Mankind is at the initiation point of determining the toxicological mechanisms from exposure to advanced nano microbic materials. We need to know the exact level, that they do not pose a threat to the health and safety of a human being as well as to the environment and its inhabitants. Especially, since a major risk from exposure is through aerial emissions over land and sea.
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