Nerve agents are the most popular kind of chemical weapon
available today, and the most (potentially) deadly. Odorless, colorless, tasteless, and quick, they are the evildoer
's wet dream
in death technology. Their usability as weapons of terror has been hyped way up by the media, as they all have to be spread out pretty well to kill many people. While this is easy for militaries
to accomplish with shells and specialized hardware, the terrorist must use overpowered high explosives
style airplane spraying. As the Aum Shinrikyo
group in Japan
has shown us, it's not that easy to kill people with nerve agents no matter how much of them you possess.
How do they work?
Nerves trigger muscles to contract by releasing acetylcholine into the neuromuscular synapse. Acetylcholinesterase, on the receiving side of the synapse, breaks down the acetylcholine and lets the muscle relax. When a muscle is consciously held tense for a period of time, it's actually different nerves firing to different sub-muscular groups to keep the tension, rather than the all of the muscle being stimulated at once.
Nerve agents work by interrupting the acetylcholine cycle, specifically by blocking the action of acytlcholinesterase. Thus, muscle contraction are overstimulated and it isn't possible to relax the muscle. When breathed, this first effects the muscles of the lungs, but they are dense and take a long time to be completely shut down. In the mean time, the nerve agent spreads throughout the body as the victim breaths, cramping up the much less resilient arms, legs, etc. Death occurs when the agent has either completely infiltrated the diaphragm and the victim can no longer breathe, or has reached the heart and stopped it cold.
Interestingly, nerve agents have fairly little effect on the organ we immediately think of when we talk about neurons, the brain. Agents are always gigantic phosphoric molecules, and the blood-brain barrier is excellent at keeping large molecules out. For this reason it should be noted that persistent paranoid rumors of an agent that "will kill dead you before you notice there's anything wrong" are completely bogus. Even if the agent was so concentrated that your lungs stopped immediately upon exposure, you would be conscious of being unable to breathe or move until your brain ran out of oxygen.
How can their action be stopped?
Most importantly, if you want to stop the agent from killing somebody you have to act fast. That means having the anti-toxins ready to use when an attack occurs, and getting them to the victims immediately after the rescue personnel are themselves protected. If the situation is war-time rather than terrorism, this means having every second or fourth soldier carry enough antidote for himself and a few others. In the US, every soldier is issued antidotes if nerve agent use is suspected. Auto-injectors are often used, which are syringes or pressure injections that are self contained and fire at the press of a button. With luck, the victims will realize they're under attack before they loose too much muscle control to trigger the applicator.
Of the two antidotes used today, oximes like HI-6 are the safest and most effective for treatment. These chemicals also interact with anticholinesterase, by reactivating it after the nerve agent has shut it down. VX and sarin are both extremely well treated by oximes, while the aging process caused by soman renders them ineffective, except for HI-6 in some cases. Oximes are even chunkier than the nerve agents, and can't penetrate the blood-brain barrier at all, so they do not stop damage there. While oximes do stop further damage from occurring, it should be noted that any damage that's already been done is permanent.
Atropine is the other antidote, and has been used for nerve agent treatment almost as long as there have been nerve agents. Unfortunately, instead of neutralizing the damage as the oximes do, it merely stops the symptoms. Atropine works by attaching to the acetylcholine receptors and inhibiting them from reacting to actual acetylcholine. Thus, it stops all of the extra acetylcholine floating around in the synapse from overstimulating the receptor. In any situation other than nerve agent exposure the atropine itself would be poisonous, since it stops neurons from communicating with their receptors. Atropine and the oximes have a synergistic effect, making each others' effects more powerful when they are used at the same time.
The other approach to limiting nerve agent toxicity is to give a preventive agent before the attacks happen, but when they are being expected. Pyridostigmine is one of them, it inhibits acetylcholinesterase like the nerve agents do, but by a much lower amount. When the enzymes are inhibited with pyridostigmine they are continuously activated and released from activity, so nerve agents have a hard time finding enzymes to attack. Diazepam (aka everybody's best friend Valium) is also effective, as it relaxes tensed muscles and can stop brain damage due to heavy exposure. Both of these should be administered at least thirty minutes before the attack, and are effective for about eight hours after administration. Pyridostigmine given after exposure will aggravate the nerve agent damage, but diazepam will only help the other antidotes.
What kinds are there?
There are two classifications of nerve agent, the G agents and the V agents. G agents are more volatile (that is, they will evaporate into the air) than V agents, but also much weaker. V agents are oily and often insoluble in water, and are powerful enough to kill by absorption through the skin. They are known as persistent nerve agents, as they don't evaporate can be sprayed on territory and equipment to make it permanently unusable. G agents tend to be much easier to manufacture.
- Tabun - Tabun was the first nerve agent to be discovered, by Dr. Gerhard Schrader of I.G. Farben in Germany. At the beginning of the thirties I.G. Farben had discovered that organic phosphorus compounds could be deadly, but no further research was done. By 1934 they needed a new pesticide, and tabun was one of the candidates. Upon testing they found out how effective the compound really was, and turned it over to the military as required by German law. Between 1942 and 1945 the German military produced around 12,000 tons of tabun for the war, and that isn't counting the tabun which was deployed.
Today, tabun is known as GA. It is relatively easy to manufacture, and many developing powers produce it as their first nerve agent. Since it takes so much of it to be deadly (three times as high a concentration as for sarin or soman) it isn't really considered an option by more modern countries.
- Sarin - Sarin was discovered by Schrader's team in 1938, who by that time had become employed solely to work on nerve agents. It was named and put into production because of its extreme volatility -- it evaporates into the air faster than water. Sarin is now known as GB. For more information, see shale's great writeup under sarin.
- Soman - Soman was discovered last of the G agents, in 1944. It's an interesting nerve agent because after it reacts with acetylcholinesterase the enzyme goes through a further "aging" process after which it cannot be reactivated. If this aging occurs, no treatment is possible. For this reason, soman is the most difficult to treat nerve agent, HI-6 has only marginal effect and atropine has none at all. Today, soman is called GD.
- VX - VX is the only V agent that has become popular, but they all have roughly the same description. It was, again, first developed as a pesticide, this time by an American team. Military production began in 1961, but wasn't published on or publicized until 1972. It's an order of magnitude more powerful than the G agents, and can thus kill with only a few milligrams exposed to the skin. Notably, it was the nerve gas featured in the movie The Rock.
VX is persistent, and will stay on equipment and land for a few weeks killing anything that touches it. It is oily and has the remarkable feature of being soluble in cold water and insoluble in warm. Hypochlorite ions from chlorine bleach are great at neutralizing VX (and the rest of the nerve agents, really), bleach is even called for in the military decontamination procedure. VX responds well to treatment.
What do they feel like? - This is fiction, but all major symptoms are represented.
It's a nice day, by any measure of the phrase; the sky has perfect fluffy clouds, and the temperature is seventy-three degrees in the shade. You've just left the store in the clean part of downtown, and have a paper sack of new and colorful clothes to wear to Robin's party tomorrow night. You've already walked half way back to your car, and life is good.
For a split-second you are in shadow, a flash of darkness far enough out on the edges of your perception to nearly be ignored. You raise your eyebrows momentarily and look up towards the sky. A block away already you see it, a slow moving little prop-plane like your uncle used to have. It was what caused the flash of shadow, and while it seems to be flying awfully low, you don't give it a second thought as you keep going. Your thoughts are better occupied with how glad you'll be to see all of your friends.
Suddenly, for no reason at all, your mouth fills with saliva like you'd just sat down before the tastiest stir-fry ever woked. Swallowing doesn't help much, it just keeps coming out, to the point where the flow is makes you cough a little. Coughing doesn't feel right at all, your chest has become almost painfully tight, bringing up a memory of the pneumonia you had in eighth grade like deja-vu. What's more, you can't see very well either; everything close to you has gone blurry and trying to focus on it gives instant, sickening headache pain. This combined with the saliva that's now drooling hopelessly out of your mouth makes you realize that you have to get to the hospital NOW, so you break for your car.
Funny, it seems like the deeper you breath as you run, the harder the act itself becomes. The muscles in both arms burn like hell, and when you look down at them you see that you've reflexively dropped your shopping bag and curled them up against yourself. Without warning your legs simply stop working, and begin cramping in acyclic seizures, every charlie-horse you've ever had rolled into one and tied with a razor wire bow. The world shifts into slow motion bullet time as you fall, and you see that everyone else in the world is already collapsed or prone on the sidewalk. You feel your lungs stop, just as your legs did, and as the blackness fades in you realize that shit this surreal only happens in dreams, so you must just be dreaming.
As it turned out, you weren't.