Moscow Gas Deaths - Why is the media trying so hard to mislead us?

by BZmyfoot Tuesday, Oct. 29, 2002 at 2:08 AM

We're being bombarded in every newspaper and TV report with "expert opinions" that the gas responsible for 116 hostage deaths in Moscow was an agent known as BZ. However, there are clear and obvious reasons why it could NOT have been BZ. A brief internet search would have elicited this information. Why are they conducting such a well-coordinated misinformation campaign?


The first argument against the claim that BZ was the agent used is that BZ is a very slow-acting hallucinogenic agent and thus would have been completely inappropriate for a "quick knockout" hostage situation. According to the literature, incapacitating effects may appear after as little as 3 to 5 hours or as long as 6 to 10 hours following exposure (see "Overexposure", Source 1). The second problem with the theory that BZ was used is that BZ has such a high lethal toxicity level that it would be almost impossible to deliver in concentrations sufficient to cause that many deaths that quickly. The concentration in air necessary to cause death in 50% of exposed subjects is 200,000 mg per cubic meter/1 minute. This concentration isn't even air anymore - it's soup. You'd probably drown first (see "Mortality/Morbitity", Source 2, below).

BZ is a pretty primitive weapon, as chemical weapons go, and has long since been banned by treaty and International Law. There are a lot more advanced agents available, and many more in development, so why are they trying so hard to make people think it was BZ, particularly when to do so is to accuse Russia (with whom we're ostensibly seeking better relations) of violating International Law? The only thing I can think is that the agent was one of the new "non-lethal" weapons with which the Army is now totally pre-occupied, and they don't want the public to even consider that one of their shiny new "non-lethal" toys may have turned out not to be so non-lethal after all.

Any ideas?

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Source 1: http://chppm-www.apgea.army.mil/dts/docs/detbz.pdf

Toxic Properties of 3-Quinuclidinyl Benzilate

The chemical BZ, also known as "agent buzz" was produced at Pine Bluff Arsenal between 1962 and 1965. It was dropped from the chemical arsenal because its effects on enemy front-linetroops would be varied and unpredictable. BZ is usually disseminated as an aerosol with the primary route of entry into the body through the respiratory system; the secondary route is through the digestive tract. BZ blocks the action of acetylcholine in both the peripheral and central nervous systems. As such, it lessens the degree and extent of the transmission of impulses from one nerve fiber to another through their connecting synaptic junctions. It stimulates the action of noradrenaline (norepinephrine) in the brain, much as do amphetamines and cocaine. Thus, is may induce vivid hallucinations as it sedates the victim. Toxic delirium is very common.

Overexposure Effects

BZ is a very potent psychoactive chemical affecting the central nervous system as well as the organs of circulation, digestion, salivation, sweating, and vision. Its pharmacological action is similar to that of other anticholinergic drugs (e.g., atropine, scopolamine, etc.), but longer lasting. Acute exposure produces increased heart and respiratory rates; mydriasis; mouth, skin, and lip dryness; cycloplegia; high temperature; ataxia; flushing of face and neck; hallucinations; stupor; forgetfulness; and confusion. The initial symptoms after to 4 hours of exposure include: dizziness, mouth dryness, and increased heart rate; secondary symptoms, after 3-5 hours of exposure, include: restlessness, involuntary muscular movements, rear vision impairment, and total incapacitation; final symptoms, after 6-10 hours of exposure are psychotropic in nature. After 3-4 days, full recovery from BZ intoxication is expected.

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Source 2: http://www.emedicine.com/emerg/topic912.htm

Background:

The chemical warfare agent 3-quinuclidinyl benzilate (also known as QNB or BZ) is an anticholinergic agent that affects both the peripheral and central nervous systems (CNS). It is one of the most potent anticholinergic psychomimetics known, with only small doses necessary to produce incapacitation. It is classified as a hallucinogenic chemical warfare agent. QNB usually is disseminated as an aerosol, and the primary route of absorption is through the respiratory system. Absorption also can occur through the skin or gastrointestinal tract. It is odorless. QNB's pharmacologic activity is similar to other anticholinergic drugs (eg, atropine) but with a much longer duration of action.

Pathophysiology:

QNB acts by competitively inhibiting muscarinic receptors. Muscarinic receptors primarily are associated with the parasympathetic nervous system, which innervates numerous organ systems, including the eye, heart, respiratory system, skin, gastrointestinal tract, and bladder. Sweat glands, innervated by the sympathetic nervous system, also are modulated by muscarinic receptors. The ICt50 (concentration in air of QNB necessary to incapacitate 50% of exposed and unprotected individuals through inhalation during a set time) has been reported to be 100 mgmin/m3. Effects of QNB by any route of exposure are slow in onset and long in duration. The onset of action is approximately 1 hour, with peak effects occurring 8 hours postexposure. Symptoms gradually subside over 2-4 days. Most of the QNB that enters the body is excreted by the kidneys, making urine the choice for detection.

Mortality/Morbidity:

The LCt50 of QNB is reportedly 200,000 mgmin/m3. This means, for example, that 50% of an unprotected group would die following inhalation of air that contained 200,000 mg of QNB per cubic meter for 1 minute. By comparison, the highly toxic compound hydrogen cyanide has an LCt50 of 5000 mgmin/m3. The LD50 (lethal dose to 50% of an exposed population) for BZ is estimated to be similar to that of atropine, which is approximately 100 mg. Other factors also are important, such as the exposed patient's preexisting health status and the time from exposure to medical care.

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