Magazine article Drug Topics

Chemical and Biological Agents of War: Concept, Cause, Care

Magazine article Drug Topics

Chemical and Biological Agents of War: Concept, Cause, Care

Article excerpt

Use of chemical and biological weapons for terrorism became a key concern of the U.S. Army in the 1990s. In 1994, a Japanese religious cult, Aum Shinrikyo, reportedly released a nerve agent in a residential area of Japan, killing seven and injuring 500. A second attack in 1995 spread Sarin through a crowded Tokyo subway. This attack killed 12 and necessitated medical attention for 5,500 civilians.

Chemical and biological terrorism was not limited to foreign countries. The first conviction under the Biological Weapons Anti-Terrorism Act of 1989 occurred in 1995 when a U.S. citizen was sentenced to 33 months in prison for possession of 0.7 gm of ricin toxin (Ricinus communis), a highly potent and easily produced plant toxin. The same year, a nonprofit organization shipped plague bacteria, Yersinia pesos, to an alleged white supremacist group.

Highly toxic industrial chemicals also pose a potential risk to our community. The disaster in Bhopal, India, in 1984, when an estimated 8,000 persons died and another 30,000 were injured from breathing methylisocyanate and chlorine vapors released in an industrial accident, is but one example of the devastating effects of poisonous gases.

In 1996, the U.S. Congress passed a new antiterrorism training bill to prepare the United States for future chemical and biological terrorism incidents. As health professionals, pharmacists have an obligation to become knowledgeable in this area.

Chemical terrorism- Cheap, easy, devastating

The growth of the chemical and pharmaceutical industries has inadvertently given terrorist groups access to chemicals. Compounds contaning such chemicals as chlorine, phosgene, and cyanide are commonplace, and theft of such materials has been reported. Chemical agents of war or terrorism are classified by the nature of their use, their persistency in the field, and their physiological action. Toxic chemical agents are capable of producing incapacitation, serious injury, and death.

The neurotransmitters used in the human body are: acetylcholine (Ach), adrenaline (norepinephrine), gammaminobutyric acid (GABA), and dopamine (DM). Acetylcholine is the neurotransmitter to skeletal muscle. Excess Ach, a condition caused by nerve agents, causes stimulation of the muscles and other structures innervated by these fibers.

Nerve agents such as tabun (GA), satin (GB), roman (GD), and VX inhibit acetylcholinesterase (AchE) enzyme throughout the body, notably in the nervous system. This causes hyperactivation of cholinergic pathways, causing convulsive seizures and respiratory failure. The blockage of a normal biochemical reaction stops the hydrolysis of Ach. This classic explanation of nerve agent poisoning holds that the intoxicating effects are due to the excess endogenous Ach. A common analogy would be an electrical motor that has short-circuited or changed polarity.

These nerve agents are classified as organophosphorus compounds. The agents in the "G" series were given that code letter because they originated in Germany. The chemical agent VX (the "V" stands for venomous) was discovered in England in the 1950s and possesses low volatility, allowing for safer handling.

The carbamates comprise another cholinesterase-inhibiting class. These, unlike the organophosphorus class, have some beneficial medical applications. Among the carbamates is physostigmine, which has been used in medicine for more than a century. Neostigmine (Prostigmin), developed in the early 1930s, and pyridostigmine bromide (Mestonin) have been used for decades for the management of myasthenia gravis. This class of cholinesterase inhibitors has been used as a pretreatment or antidote-enhancing substance against certain nerve agents.

Pyridostigmine bromide is known as PB or NAPP (nerve agent pyridostigmine pretreatment). Since both of these classes of AchE inhibitors attach to the esteratic site on AchE, a second binding compound cannot attach to that site if it is already occupied by a molecule. …

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