Chemical weapons were first developed for use during World War I,1 but their actual use in war has been limited. Their development was met with a worldwide public outcry that they were inhumane and should be banned, and in April 1997 the Chemical Weapons Convention was signed. This treaty “prohibits the development, production, acquisition, stockpiling, retention or use of chemical weapons, as well as the transfer, directly or indirectly, of chemical weapons.”2 It now includes 145 signatories.
While most countries’ military establishments have abandoned chemical weapons (at least officially), such weapons have become items of great interest to terrorist groups like al Qaeda, Aum Shinrikyo and even some domestic groups.3 Chemical agents have been called “the poor man’s atomic bomb” because of their ease of acquisition, production and potential use.4 The Aum Shinrikyo religious cult’s 1995 nerve gas attack on the Tokyo subway system, using sarin, highlighted the destructive and chaotic power of these agents. The rush-hour attack killed 12 people, injured many others and sent more than 5,000 people to hospitals (though most were just worried they’d been exposed).5 Fortunately, the sarin preparation used was relatively weak, and the number of actual victims was comparatively small. However, the chaos that gripped the city demonstrated what could happen in a large chemical-weapon attack. Documents confiscated from Taliban and al Qaeda camps show that these groups also have procedures for making chemical weapons and have planned attacks using them in England and other locations.6
What Are Chemical Weapons?
Chemical weapons utilize chemical agents, compounds designed to kill or injure beyond reasonable functional recovery.7 Chemical warfare/terrorism weapons fall into four general classes based on their effects on the victim: Nerve agents, choking agents, blood agents and blister agents (see Table 1).
Nerve Agents—Nerve agents are the most likely candidates for use in a terrorist attack.1 Nerve agents, or nerve gases, are all similar in their chemical structure and mechanism of action. Nerve agents are organo-phosphate compounds, all of which have a phosphate group (PO4) in which one or more of the oxygen atoms has been replaced with another element like carbon, fluorine or sulfur. Organophosphate toxicity is due to the inhibition of acetylcholinesterase at cholinergic junctions of the nervous system.8 When the nerve agent enters a cell in the nervous system, it reacts with the enzyme acetylcholinesterase (also called RBC cholinesterase) and blocks its action. Acetylcholine is a neurotransmitter essential for the transmission of nerve impulses to muscles and organs. After an impulse is received, the acetylcholine must be destroyed and recycled in order for the muscle or organ to relax and the cycle to begin again. Acetylcholinesterase normally performs this function, but it cannot act when blocked by the nerve agent.9
Initially the blockage is reversible, but within a short time after exposure, the enzyme’s active site becomes phosphorylated and the block becomes irreversible, a process known as aging. Thus, acetylcholine continues to build up, and nerve impulses continue to be received by the muscles because the enzyme cannot hydrolyze the nerve agent due to the missing carbon-to-oxygen bond. Acetylcholine cannot bind to the enzyme because its binding site is blocked.8,9 Buildup of acetylcholine at the nerve endings mimics hyperactivity of the parasympathetic nervous system. This leads to a variety of clinical signs and symptoms including excess salivation, lacrimation, abdominal pain, vomiting and diarrhea. Effects are also seen at the parasympathetic neuroeffector junctions, sites of muscarinic activity, resulting in increased bronchial secretions and bronchoconstriction. At the neuromuscular junctions and autonomic ganglia (nicotinic activity sites) and also at certain synapses in the central nervous system, effects include weakness of voluntary muscles, irregular and violent contractions of involuntary muscles, twitching, paralysis and respiratory arrest.8,9