Low dosage Sarin gas was tested on the New York subway system more than a decade ago. People got sick. We believe that test and others along with studies listed below and information from Senate hearings provides sufficient backdrop to support what everyone is coming to see.
It isn’t just Italy, New York is an epicenter too and it isn’t simply CV 19 but chemical weapons that mimic the disease, according to highest level intelligence sources.
Defense experts are seeing a targeted biowar on China, Italy, Spain, Iran and left-leaning political regions of the US. We will now discuss our findings.
In advanced nations, the overall death rate compared to those identified as infected averages under 1%. In Italy and Iran the rate is many times that and the reasons given are fake. Both nations have very advanced medical capability.
Then we look at Spain, China’s best friend in Europe and, of course, China.
Moreover, reporting on CV19 includes concocted conspiracies that trace to Israeli intelligence and the CIA, spread by Trump and Pompeo, which are impossibly absurd and hide a multifaceted operation thoroughly evidence in US Army studies on bio-warfare that our sources say are in motion now.
The US has been relocating Global Hawk aircraft to Sicily, ostensibly to be used to spy on Russia through missions over the Black Sea. However, other missions have been flown, Northern Italy, or across Northern Iran. We know the US and Israel have developed the capability of dropping microdrones, with a self destruct capability that can spread diseases like SARS, Swine Flu and the various strains of Bird Flu and crop diseases. We also have evidence such devices have been used against China on 6 or more occasions. We now have a new and far more sinister report.
We have a report from Russian intelligence that says the US is using low dose Sarin gas to mimic pandemic diseases. They say they have evidence that in Iran and Italy sarin gas in extremely small concentrations have been in the food, water and environment in minuscule concentrations.
These concentrations cause, over a two week period, the onset of pneumonia and a respiratory disorder. Larger concentrations cause heart disease and mimic heart failure.
Starting in 1996 and then ramping up to an extreme level in 2006, the US financed studies on various nerve agents and halucogens which could be dropped by drones, now by micro-drones such as Israel has developed.
Parallel studies were made on crop diseases but most included diseases that could move from livestock to humans, giving a ‘cover and deception’ cause that could be explained away through controlled press assets, which means ‘all of them.’
We will also add that we have found extensive CIA and Mossad/Shen Bet complicity in media manipulation. Worse is the recent, March 19, 2020, piece by Mitch Prothero in Business Insider. Prothero is a “go to” guy for reliable propaganda from the CIA.
and Business Insider regularly launders CIA promoted conspiracy theories to the “unwashed.” It is, in fact, one of their most successful operations. The article we refer to is an attempt to “close the barn door after the horse has run off” scheme involving the CIA’s bioweapons/Sarin lab in Tbilisi, Georgia that has been busted time and time again for leaking Swine Flu into the community near the facility and making Sarin gas to be used in Syria.
Here’s another one worse than the others, check the bio of the author, a food service worker. The site was 2 years of short posts on prison reform, 50 words or so, then this showed up, which ended up on Trump’s desk as a manifesto for his blame China policy. Ultra-curious:
An investigative team from VT/New Eastern Outlook and Russia24 not only got plans for the weapons facility but was eventually allowed in to film. The result was devastating to the US bio-war capability in the region which has since recovered.
We also know the CIA has repeatedly tested both chemical and biological weapons, often in New York City, on the subway, according to a New York Times article that covers the Senate hearings on this. (below/archival)
We also know the CIA tested low dose Sarin gas on the New York Subway in 2008, releasing gas at the Bowling Green station near midnight, along with other stations that were “end of the line.” Some dropped immediately, others struggled up the steps and recovered in minutes while some suffered longterm illness (perhaps worse).
This program, documented by the Senate, was the precursor to the CV 19 augmentation exercises, Italy, Spain, Iran and China. Greece may well soon be targeted as well, based on geopolitical analysis and the pattern we have seen thus far.
We might also add that medical evidence from Italy and China shows far too many patients that don’t respond to treatments, far too many anecdotal deaths, than fall within baseline parameters for typical respiratory patients.
Someone will write a paper on this if not “accidented” first.
The nerve agents are a group of particularly toxic chemical warfare agents. They were developed just before and during World War II and are related chemically to the organophosphorus insecticides. The principle agents in this group are:
- GA – tabun
- GB – sarin
- GD – soman
- GF – cyclosarin
- VX – methylphosphonothioic acid
The “G” agents tend to be non-persistent whereas the “V” agents are persistent. Some “G” agents may be thickened with various substances in order to increase their persistence, and therefore the total amount penetrating intact skin. At room temperature GB is a comparatively volatile liquid and therefore non-persistent. GD is also significantly volatile, as is GA though to a lesser extent. VX is a relatively non-volatile liquid and therefore persistent. It is regarded as presenting little vapor hazard to people exposed to it. In the pure state nerve agents are colorless and mobile liquids. In an impure state nerve agents may be encountered as yellowish to brown liquids. Some nerve agents have a faint fruity odor.
In 1996, a US Army study examined the question:
Are there observable long-term health effects associated with exposure to Sarin (GB) and mustard at concentrations below that needed to cause acute signs, symptoms, or injury?
Here are the findings of that study (emphasis added):
GB is a nerve agent and is chemically known as isopropyl methyl phosphonofluoridate. It is a colorless and odorless liquid when pure; the vapor is also colorless. GB evaporates at approximately the same rate as water. Like other nerve agents (soman, tabun, VX), GB is a highly toxic organophosphate which irreversibly binds to acetylcholinesterase. As a result, acetylcholine accumulates at neuromuscular junctions and causes a loss of function at these junctions. This interferes with the fundamental mechanism required for the normal function of the central nervous system and the peripheral nervous system, that is, transmission of a nerve impulse. While the great majority of effects are due to the anticholinesterase actions of GB, not all effects are related to this characteristic.
Marrs, Maynard, and Sidell (1996) categorize the signs and symptoms of GB intoxication into three groups, muscarinic, nicotinic and central. The muscarinic signs and symptoms result from increased activity of the parasympathetic system and include miosis, dim vision, salivation, bradycardia, lacrimation, abdominal cramps, diarrhea and rhinorrhea. Nicotinic effects include pallor, tachycardia , hypertension, muscle fasciculation and weakness. Central nervous system effects include headache, anxiety, difficulty concentrating, restlessness, confusion, convulsions, and respiratory depression or paralysis, which can lead to death.
Signs and symptoms can be observed regardless of exposure route, but the intensity and sequence is influenced by the route of exposure. Skin exposure may cause localized sweating and fasciculations first. Vapor exposure where the eyes and respiratory tract may come into contact with GB first, may result in miosis, rhinorrhea, and tightness of chest first. Respiratory exposure appears to result in symptoms faster than skin exposure.
During vapor exposure studies and unintentional vapor exposures, the first signs and symptoms are usually miosis, rhinorrhea and/or chest tightness (Sidell, 1992). In fact, early studies often defined an individual as “exposed” when that person had at least one of these symptoms. Persons in the same area, without any health complaints, were not considered exposed or “hit.” This is the first of a multitude of methodologic problems related to the question at hand. Only those who had clinical signs or symptoms would be studied and documented. Anyone else, even if they were in the same area, would not be considered exposed and would not be examined.
The amount of GB necessary to cause initial clinical signs and symptoms is debatable, but has been estimated to be approximately 2-3 mg-min/m3. This is known as the Ct, or the concentration of agent vapor in air as milligrams per cubic meter times the time of exposure in minutes (Sidell, 1992). McKee and Woolcott (1949) report that a single exposure to a Ct of 3.3 mg-min/m3 (for 40 minutes) is the minimal dosage necessary to produce effects in men. However, they also state that chemical analysis of the agent indicated that the concentration actually given was approximately 75% of the intended dose, therefore the Ct would actually be approximately 2.5 mg-min/m3. When the exposure time was reduced by 50% (20 minutes, Ct approximately 1.2 mg-min/m3), a single dose did not produce symptoms, but the same report indicated that exposure to a Ct of 0.6mg-min/m3 (1 minute) also caused detectable symptoms. It appears that a single exposure of man to a very small amount of GB will produce observable acute signs and/or symptoms. It is also important to note that an exposure with a Ct derived over a longer period of time (e.g. 240 minutes vs 20 minutes) will cause fewer or less severe signs and symptoms since there is some detoxification that occurs during the longer period of exposure.
As will be described below, there are essentially no controlled human studies in which men were exposed to doses calculated to avoid symptoms and where these men were followed over extended periods of time. Several studies utilizing doses that did cause acute symptoms, several unintentional high level exposure investigations, and animal studies can be used to make general suggestions regarding the long-term health risks associated with low-level exposure to GB.
So, in 1996, there was no data on low-dose exposure to Sarin, therefore studies would need to be conducted to gather such data. The US Army came to the same conclusion (emphasis added):
Sarin, or GB is a highly toxic organophosphate nerve agent that can cause mild, reversible signs and symptoms at low doses, and death at doses that are not too much greater. There is no scientific information that directly answers the entire question: Are there observable long-term health effects associated with exposure to Sarin (GB) at concentrations below that needed to cause acute signs, symptoms, or injury?
Extrapolation from a variety of sources, not designed to answer this particular question, was utilized. Some studies are clearly negative for a particular health effect at higher doses than that of concern to this question. These provide confidence that there is no increased specific health risk at the low doses under question.
GB does not have carcinogenic or mutagenic properties. While the teratology literature is less clear, it appears that GB is not a teratogen. Therefore, no increase in birth defects or cancer would be expected from low-dose, short duration exposure to GB. Follow-up of a cohort of men exposed to GB found no significant increase in hospitalizations, reported health problems, mortality, or other measured end point.
There remains some question as to the validity of concerns regarding changes in EEG patterns long after GB exposure. Also, it is unclear what such changes really mean regarding the function of the soldier if those long-term EEG changes actually occur.
It is prudent to suggest that further research into the long-term effects of low dose GB exposure (including doses that do not result in acute signs or symptoms) on the EEG of primates be undertaken.
The two key sentences:
There is no scientific information that directly answers the entire question: Are there observable long-term health effects associated with exposure to Sarin (GB) at concentrations below that needed to cause acute signs, symptoms, or injury?
They don’t know what the effects of low-dosage sarin exposure are.
It is prudent to suggest that further research into the long-term effects of low dose GB exposure (including doses that do not result in acute signs or symptoms) on the EEG of primates be undertaken.
So they recommend carrying out studies.
The Army unit responsible for such studies is based at the Aberdeen Proving Ground in Maryland:
United States Army Medical Research Institute of Chemical Defense (USAMRICD) the nation’s leading science and technology laboratory in the area of medical chemical countermeasures research and development. With sophisticated laboratories located at Aberdeen Proving Ground, Maryland, USAMRICD manages a diversified portfolio of medical chemical warfare agent research projects for the Department of Defense and other Federal Agencies.
The USAMRICD did indeed carry out a study into low-dose Sarin exposure and published the results in 2006:
2006 Sep 1;215(2):119-34. Epub 2006 Mar 23.
The effects of repeated low-dose sarin exposure.
Shih TM*, Hulet SW, McDonough JH.
- Pharmacology Branch, Research Division, U.S Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, MD 21010-5400, USA. [email protected]
This project assessed the effects of repeated low-dose exposure of guinea pigs to the organophosphorus nerve agent sarin. Animals were injected once a day, 5 days per week (Monday-Friday), for 2 weeks with fractions (0.3x, 0.4x, 0.5x, or 0.6x) of the established LD(50) dose of sarin (42 microg/kg, s.c.). The animals were assessed for changes in body weight, red blood cell (RBC) acetylcholinesterase (AChE) levels, neurobehavioral reactions to a functional observational battery (FOB), cortical electroencephalographic (EEG) power spectrum, and intrinsic acetylcholine (ACh) neurotransmitter (NT) regulation over the 2 weeks of sarin exposure and for up to 12 days postinjection. No guinea pig receiving 0.3, 0.4 or 0.5 x LD(50) of sarin showed signs of cortical EEG seizures despite decreases in RBC AChE levels to as low as 10% of baseline, while seizures were evident in animals receiving 0.6 x LD(50) of sarin as early as the second day; subsequent injections led to incapacitation and death. Animals receiving 0.5 x LD(50) sarin showed obvious signs of cholinergic toxicity; overall, 2 of 13 animals receiving 0.5 x LD(50) sarin died before all 10 injections were given, and there was a significant increase in the angle of gait in the animals that lived. By the 10th day of injection, the animals receiving saline were significantly easier to remove from their cages and handle and significantly less responsive to an approaching pencil and touch on the rump in comparison with the first day of testing. In contrast, the animals receiving 0.4 x LD(50) sarin failed to show any significant reductions in their responses to an approaching pencil and a touch on the rump as compared with the first day. The 0.5 x LD(50) sarin animals also failed to show any significant changes to the approach and touch responses and did not adjust to handling or removal from the cage from the first day of injections to the last day of handling. Thus, the guinea pigs receiving the 0.4 and 0.5 x LD(50) doses of sarin failed to habituate to some aspects of neurobehavioral testing. Spectral analysis of EEG data suggested that repeated sarin exposure may disrupt normal sleeping patterns (i.e., lower frequency bandwidths). While these EEG changes returned to relative normalcy 6 days after the last injection in animals receiving 0.4 x LD(50) sarin, these changes were still observed in the animals that received 0.5 x LD(50) sarin. Ten to twelve days after the last sarin injection (in 0.4 x LD(50) group only), neurochemical data showed that striatal choline levels were reduced in comparison to the saline group. At this time, atropine sulfate (5 mg/kg, i.p.) challenge resulted in a transient elevation in striatal ACh levels in animals exposed to repeated 0.4 x LD(50) sarin as well as in control animals. No evidence of brain or heart pathology was found in any guinea pig that survived all 10 sarin injections.
The sequence of symptoms varies with the route of exposure. While respiratory symptoms are generally the first to appear after inhalation of nerve agent vapor, gastrointestinal symptoms are usually the first after ingestion. Tightness in the chest is an early local symptom of respiratory exposure. This symptom progressively increases as the nerve agent is absorbed into the systemic circulation, whatever the route of exposure. Following comparable degrees of exposure, respiratory manifestations are most severe after inhalation, and gastrointestinal symptoms may be most severe after ingestion.
Naval Air Station Sigonella, just outside Catania on the Italian island of Sicily.
It is a 1,000km 2 hour flight to Milan for a Global Hawk drone flying from Sigonella
Northrop Grumman RQ-4 Block 40 Global Hawk, which entered service with the US Air Force in September 2013. This latest variant of the drone has synthetic-aperture radar and ground-moving target indicators. Five of these unmanned craft are based at Sigonella.
The Five RQ-4D drones based at Sigonella became operation at the end of 2019 with the NATO AGS (Alliance Ground Surveillance).
WASHINGTON, Sept. 18 (2016)—Army scientists secretly spread simulated biological poison on two subway lines in Manhattan in the mid nineteen‐sixties to test the vulnerability of the New York subway system to a biological warfare attack, a Department of Defense engineer testified today.
Charles Senseney, a project engineer who developed weapons such as an electric poison dart gun and a system to spread biological poison from a fluorescent bulb, told the Senate Select Committee on Intelligence that he took part in the New York “vulnerability study” as one of many such efforts aimed at testing the dangers of biological warfare.
His account provided the first substantial details of the subway project, which was disclosed Tuesday in testimony and documents submitted to the Senate panel by William E. Colby, the Director of Central Intelligence.
Mr. Senseney said the studies. conducted by the staff of the Army laboratories at Fort Detrick, Md., had been performed on behalf of the Army and the Central Intelligence Agency. They included tests at the, White House, the Pentagon, a Food and Drug Administration building in Washington and McGuire Air Force Base in New Jersey.
In a meeting with reporters after today’s hearing, Mr. Senseney gave this account of the New York City subway experiments:
Possibly in 1966 or 1967, Mr. Senseney and 20 other Fort Detrick employes were sent to New York for the two‐week test. The “operator” of the test threw “bulbs” of a simulated biological poison on the tracks of two subway lines. He said he believed, but could not be sure, they they were the Sixth and Eighth Avenue lines in Manhattan.
The bulbs burst and the wind of the passing subway trains spread the simulated poison along the tracks. He said that in the short time it took for two trains to pass the simulated poison was spread from 15th Street to 58th Street.
Mr. Senseney said his role in the experiment was as a “sampler.” He and part of the team rode the subways with a sampling device t,o test the spread of the simulated poison. His was kept on his belt with the appearnce of a photographic‐light meter, he said.
City Officials Not Told
He said the other detection devices had been hidden in pocketbooks and other camouflages so the subway possengers would not know what was being done. He said that to his knowledge — and Senate committee documents appear to confirm this —neither the New York City government nor the Transit Authority officials were aware that such a test was being conducted.