About this Author
College chemistry, 1983
The 2002 Model
After 10 years of blogging. . .
Derek Lowe, an Arkansan by birth, got his BA from Hendrix College and his PhD in organic chemistry from Duke before spending time in Germany on a Humboldt Fellowship on his post-doc. He's worked for several major pharmaceutical companies since 1989 on drug discovery projects against schizophrenia, Alzheimer's, diabetes, osteoporosis and other diseases.
To contact Derek email him directly: firstname.lastname@example.org
December 5, 2012
It's a grim topic, but I see that there are worries that the Syrian government, or what's left of it, is being warned not to use its stockpiles of chemical weapons. Back in the early days of the blog, I did a series on the chemistry of these things, and they can be found by scrolling down to the bottom of this page.
As I said at the time, "I'm prepared to argue that against a competent and prepared opponent, the known chemical weapons are essentially useless. The historical record seems to bear this out. Look at the uses of mustard gas since World War I. Morocco in the 1920s, Ethiopian villages in the 1930s, Yemen in the 1960s - a motley assortment of atrocities against people who couldn't retaliate." The uses of nerve gas are a similarly horrible roll call, mainly (and infamously) in Northern Iraq, by the Saddam Hussein government against its Kurdish population. Let's hope that no one is going to add another entry to that list.
+ TrackBacks (0) | Category: Chem/Bio Warfare | Current Events
November 27, 2006
So, what actually happens, down at the molecular and cellular level, when a person is exposed to alpha radiation? If it’s coming from outside the body, not all that much. The outer layer of dead skin cells is enough to soak up most of the damage, and it’s not like alpha particles can make it that far through the air, anyway. This is good news for Londoners worried about exposure (I note that reports have at least three sites there showing traces of radioactivity). I strongly discourage anyone from standing around next to an alpha source, but there are a lot worse things that you can stand next to - a gamma or fast neutron source, for example, either of which will penetrate your tan and keep on going.
But inside the body, that’s a different story. Alexander Litvinenko was given polonium in his food or drink, and from there the stuff distributes fairly widely across many tissues. At lower radioactive doses, that pattern is probably a good thing. When you have a radionuclide that concentrates in a particular tissue, like iodine in the thyroid, a dose that would be bearable across the entire body can cause a lot of local damage when it piles up. At higher doses, though, the situation can flip around. People can survive with damaged thyroid glands, or after total bone marrow transplants or the like. But general tissue damage is much harder to deal with.
Polonium ends up concentrating in the kidneys, to the extent that it concentrates anywhere, and attempts have been made to minimize radiation damage there. But by then an awful lot of destruction has occurred elsewhere – the blood-forming tissues, the linings of the gastrointestinal tract and the blood vessels themselves, and others. Note that these are all fast-dividing cell populations.
Zooming in, the mechanisms for all that mayhem are complex, and they’re still not completely understood. The first thing you can imagine is the alpha particle smacking into something, which to a first approximation is exactly what happens. They don’t get far – less than 100 micrometers. But along the way they can bash into quite a few things, losing some energy each time, which shows up as flung-off electrons, various strengths of photons, and doubtless some good old kinetic bouncing around. Eventually, when the particle slows down enough, it drags off a couple of electrons in passing and settles down as a peaceful atom of helium. That leaves some positive charges to account for, though, since those electrons were otherwise employed before being press-ganged, and this ionization (along with that caused by those stray electrons along the way) is one of the major sources of cellular damage.
All this can take place either in the nucleus or out in the cytoplasm, with different effects. This sort of thing can damage the cell's outer membrane, for one thing, which can lead to trouble. In the nucleus, one of the more dramatic events is sudden double-strand DNA breakage. That's never a good thing, since the strands don't always get put back together correctly. A couple of years ago, a group from the Netherlands was able to come up with dramatic images of chromosome breakage along the tracks made by alpha particles in living cells.
Then there’s also the complication of the “bystander effect”. Untouched cells in the vicinity of one that has taken an ionizing radiation hit also show changes, which seem to be at least partly related to an inflammation response. This seems to happen mostly after damage to the nucleus.
All this focused destruction has long since drawn the attention of people who actually want to kill off cells, namely oncology researchers. Alpha sources conjugated to antibodies are a very big deal in cancer treatment, and a huge amount of work is going on in the area. The antibodies can, in theory, deliver the radiation source specifically to certain cell types, which soak up most of the exposure.
So there's a use for everything. But one of those uses, this time, was assassination. Alexander Litvinenko's killers knew exactly what they were doing, and exactly what would happen to him. I hope that they're eventually found and dealt with proportionately.
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August 29, 2006
There was a comment on the "Airplanes and Chemicals" post that brought up something I've been meaning to address. Says Steve, after describing an old TV show that gave rather too detailed a picture of nitroglycerin synthesis:
While I am first in line to defend freedom of speech and would balk at anyone trying to muzzle a scientist, I think as scientists we all have a personal and professional responsibility not to place metaphorical loaded guns into the hands of children, much less of certifiably crazy adults.
Exactly. I said something of the sort in the post itself, and I wanted to reiterate it. As a working organic chemist, I can yammer on for quite a while about explosive reagents, and while I've never (fortunately) had any need to make any of the classic explosives themselves, I know a fair amount about their synthesis and purification just through reading and general lab experience. But I'm not going to talk about them.
Now, I realize that over there on the right I have a whole category of alarming lab stories and another one of horrible reagents. But the first set of stories mostly concern common reagents and procedures made dangerous by the presence of fools, and won't be much help to someone actively seeking to do harm. And as for the second set, I've deliberately avoided some topics. I won't work with acetone peroxides, that's for sure, but I won't do a detailed blog post on them, either.
And this brings up another issue. Years ago, my wife had a somewhat paranoid co-worker who thought that his experiments were being sabotaged by someone else in the lab. That wasn't the case, but we got to talking about how easy it would be, if one were so minded, to completely screw up the work of a research lab. There are all sorts of ways to do it in an immediately noticeable fashion, but there are many that would be much harder to track down.
For a biologist, going in and switching the labels around on the cell cultures in the freezer would be a start. A little toxic additive or two in the growth media would slow things down, too, as would a few pellets of sodium hydroxide in various buffer solutions. For chemists, messing with the TFA that's used as an additive in the HPLC solvents would have everyone chasing their tails for a while, as would substituting the palladium catalysts with similarly colored iron or chromium compounds. Some methanol in the ethyl acetate bottle, to mess up all the TLCs? A little sulfur in the hydrogenation catalysts? Once you start thinking of these things, the ideas just tumble out.
It's the same with larger and more terrible issues. I, like (I'm sure) many other organic chemists, could sit down and think up all kinds of nasty stuff if I were so minded. I'm not, fortunately, but if I ever found myself on the rough end of a guerrilla war, I might be useful to have around. (Science fiction fans may recall a scientist character improvising chemical weapons in such a situation in Niven and Pournelle's potboiler disaster novel Lucifer's Hammer). The chemical weapons of World War I seem to have been an example of just this sort of thing, with university chemists basically clearing the shelves of all sorts of nasty lab reagents to toss them experimentally at the enemy.
No, it's easy, although weirdly depressing, to come up with interesting horrible ideas. (I'm reminded of how C. S. Lewis said he wrote from a demon's point of view in The Screwtape Letters). But it's not something I sit around doing, and I'm not going to share any of those thoughts I might have already. The world has enough horrible ideas as it stands.
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May 6, 2004
The Washington Post ran an article the other day on a home-grown ricin lab in Paris. It's disturbing reading, and it just goes to show how easy the stuff is to make. (I discussed ricin most recently here.)
Mind you, we don't know how good Menand Benchellali's ricin was, or what his batch-to-batch quality control was like, and that's because no one really knows how much of the damn stuff he made or where it all went. Here's hoping his lab technique was terrible, because his subsequent survival would then mean that the stuff wasn't very clean. Being careless around high-quality biotoxins does not make for a long-term career.
Some bloggers quote poems on Fridays. This brings a grim one to mind, unfortunately, which Kingsley Amis pointed out must be one of the only completely serious parodies in English. Starting off from Yeats's "Song of Wandering Aengus", which you should probably read first if you're not familiar with it, a 1974 IRA bombing inspired Roger Woddis to compose:
I went out to the city streets
Because a fire was in my head
And saw the people passing by
And wished the smallest of them dead,
And twisted by a bitter past,
And poisoned by a cold despair,
I found at last a resting place
And left my hatred ticking there.
When I was fleeing from the night
And sweating in my room again,
I heard the old futilities
Exploding like a cry of pain;
But horror, should it touch the heart,
Would freeze my hand upon the fuse,
And I must shed no tears for those
Who merely have a life to lose.
Though I am sick with murdering
Though killing is my native land,
I will find out where death has gone,
And kiss his lips and take his hand;
And hide among the withered grass,
And pluck, till love and life are done,
The shrivelled apples of the moon,
The cankered apples of the sun.
I hate to leave everyone for the weekend with thoughts like this, but others are spending their waking hours having far worse ones. Reader, are you a scientist yourself? Do you spend your days going wherever your curiosity takes you, reading what you want to and thinking what you want to think? Not to be crude about it, but it's people like Menand Benchellali, or it's us.
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April 6, 2004
This morning brings the news, via ABC, that the recently discovered bomb plot in London involved a quantity of osmium tetroxide. That's a surprise.
I know the reagent well, but it's not what anyone would call a common chemical, despite the news story above that calls it "easily obtained." It's quite odd that someone could accumulate a significant amount of it, and it's significant that anyone would have thought of it in the first place. It's found in small amounts in histology labs, particularly for staining in electron microscopy, but that's generally in very dilute solution. If these people had the pure stuff, well, someone's had some chemical education, and probably in my specialty, damn it all.
The reagent is used in organic synthesis for a specific (and not particularly common) reaction, the oxidation of carbon-carbon double bonds to diols. I've done that one myself once or twice. OsO4 comes in and turns the alkene into a matched pair of alcohols, one on each carbon, and it stops there. Other strong oxidizing reagents can't help themselves - they find the diol easier to attack than the double bond was, and go on to tear it up further. There was a recent paper in the literature on the mechanistic details, actually, going into just why the osmium reagent stops where it does.
Unfortunately, the alkenes it could attack are unsaturated fatty acids and such, as found in lipoproteins and cell membranes. Exposed tissue is vulnerable. Breathing a large amount of the vapor can kill a person through irritation of the lungs, but it's not as bad that way as the better-known agents like phosgene. A bigger problem is the cornea of the eyes, and the reagent is mostly feared for its ability to bring on temporary (and in some cases, permanent) blindness.
There's no doubt in my mind that any terrorist with the stuff was going for that effect. Could it have worked? Well, it's a solid at room temperature, but a hot day will melt it. The stuff sublimes easily; it has a high vapor pressure. Just being around the solid crystals is enough to get you overexposed to the vapors. I don't know how much of the reagent these people had, but I tend to think (again, contrary to the ABC story) that an explosion would have dispersed it to the point that it was just down to irritant levels. I wouldn't want to find out, though.
If they were planning to use it in a non-explosive gas attack, that's another matter. But the vapors are said to be very irritating, with a distinctive chlorine-like smell - which I cannot verify, thank God. It's not like no one would have noticed that there was some nasty chemical in the air. I think that they could have done some damage, certainly. But what disturbs me more than the reagent itself is the thinking behind it. . .
| Category: Chem/Bio Warfare | Current Events | Toxicology
February 3, 2004
Now that the suspected ricin in the Senate (and White House?) has been confirmed, I thought I'd repost a version of something I wrote about a year ago on my previous site, Lagniappe. (This was written after British authorities had rounded up several suspects in London who had some ricin of their own.) So what is the stuff, and what kind of threat is it?
Ricin's a protein from castor beans - yep, the same ones used to prepare castor oil. The parent plant is sometimes used as a warm-weather ornamental, and used to be an industrial crop. The leaves aren't a problem, but the beans contain up to 5% ricin, which is a rather high yield for a natural product. It's quite toxic, although there are certainly worse things out there. Botulinum toxin, for example, is a thousand times more potent, but you can't grow anerobic bacteria very well in your back yard (and they're not very ornamental, either.)
The purification methods for ricin are in the open literature, and aren't particularly challenging. I'm not going to go over them, though, in the interest of not making its isolation any easier than it already is - it's already probably one of the easiest toxins to isolate. For that matter, you can order various forms of it from biochemical supply houses. It's quite cheap, by the standards of protein natural products (which are usually priced rather steeply.)
And what does the stuff do? Briefly, it's a very potent inhibitor of protein synthesis, which it accomplishes by attacking one subunit of the ribosome (the central RNA-to-protein machinery of the cell.) Rather than just binding to ribosomes and gumming them up, ricin is actually an enzyme all by itself. It tears up a specific adenine base in the ribosomal RNA, which disables the whole thing, and then it moves on to the next ribosome. One ricin molecule can turn that reaction over thousands of times, and needless to say, a cell can't lose thousands of ribosomes and expect to survive.
Ricin's a reasonably large protein, and as a weapon it suffers from the defects of large proteins. The least dangerous way to be exposed to it is by eating it, since most of it gets digested, and much of the rest has trouble crossing from the gut into the bloodstream. In rodents, the worst way to be exposed is by inhalation. Oral dosing is about 4000 times less potent. The assumption is that if ricin were weaponized, it would be treated like anthrax spores and dispersed for maximum effect. The US and Britain carried out research that led to a prototype of a ricin bomb during World War II, just another one of many nasty weapons that actually didn't get used in that conflict. (It's hard to imagine the second World War being even worse than it was, but it had the potential.)
Needless to say, there's not a whole lot of public data on just how toxic ricin might be in that aerosol form, and its effects would certainly depend on particle size, static charge, and all the other variables we learned about during the anthrax scare. We sp have a single public data point about injected ricin, though: Georgi Markov, a Bulgarian exile who worked for Radio Free Europe. One day in 1978, he felt a sharp pain as a stranger poked him with the tip of an umbrella. He began to feel ill within a few hours, and three days later, he was dead. A small pellet containing ricin had been injected into the muscle of his leg, as it turns out, in one of the more exotic assassinations known to have been carried out by the KGB. The best guess is that about a half a milligram proved lethal.
Well, that sounds pretty bad - but consider that terrorists are unlikely to be able to give masses of people intramuscular injections. And if they want to use inhalation, which is certainly the way to cause real damage with the stuff, they're faced with manufacturing problems similar to the use of anthrax spores. It wouldn't be easy, fortunately.
Ricin's not particularly water-soluble, so dumping it into a reservoir would be a waste of time. And adulterating food would be almost useless. It takes a good handful of the beans themselves to kill an adult (and they have to be crunched up, too, because whole beans tend to pass, well, pretty much unchanged through the digestive tract.) A back-of-the-envelope calculation for the pure toxin suggests that it would take a gram or two to reliably kill someone by ingestion. That adds up to a few hundred casualties per pound of ricin, but only if you can get all your victims to eat enough of it. (And I've no idea how stable the protein is in hot food, but I'd have to think that it would be inactivated pretty quickly.)
The key to this latest ricin incident will be whether the stuff had been processed to the level of the anthrax attack material. If so, we have a potentially serious problem, but so far I don't see any sign that this is the case. Otherwise, this could well be the work of some disgruntled and/or deranged amateur. Those types I think we can deal with.
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January 8, 2003
I've had some interesting e-mail on the subject, which I thought I'd address here for the curious. One person mentioned the possibility of ricin dissolved in DMSO. I have to say that that's a nasty thought, because DMSO certainly does increase skin permeability. But I don't know how soluble a large peptide like this would be - even in DMSO, which is generally a solvent of last resort in chemistry. And even if you could get some of the protein in there, odds are excellent that it would denature, change its conformation as it went into solution. Most enzymes shift around so much going into solvents like DMSO that they lose their activity completely. Not all of them, though - but I would put ricin in the category of unlikely to survive the transition. It has an important disulfide bond that would probably be labile to oxidation on storage in DMSO as well.
Others have mentioned food adulteration. If my guesstimate of a gram or two for lethality is right, a big problem would be that the stuff would probably alter the taste of whatever you added it to. I certainly have no idea of what ricin tastes like - and I'm not about to find out, because sublethal doses are still pretty unpleasant. But it's unlikely to be unnoticable. The heat of cooking is an even better denaturant than any organic solvent, usually, but ricin is said to be unusually heat-stable. That's not saying much in protein chemistry, though - boiling water is considered insane heat in the protein world. It's not likely to be a useful agent in someone's french fries; you'll just have to count on the acrylamide.
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January 7, 2003
There's a report today that British authorities have rounded up several terrorist suspects in London - and that they had small quantities of ricin. So, what is the stuff, how bad is it, where did they get it, and what did they plan to do with it?
Ricin's a protein from castor beans - yep, the same ones used to prepare castor oil. The parent plant is sometimes used as a warm-weather ornamental, and used to be an industrial crop. The leaves aren't a problem, but the beans contain up to 5% ricin, which is a rather high yield for a natural product. It's quite toxic, although there are certainly worse things out there. Botulinum toxin, for example, is a thousand times more potent, but you can't grow anerobic bacteria very well in your back yard.
The purification methods for ricin are in the open literature, and aren't particularly challenging. It's probably one of the easiest toxins to isolate. For that matter, you can order various forms of it from biochemical supply houses. I looked at a few catalogs today, and it's quite cheap, by the standards of peptidic natural products (which are usually priced rather steeply.)
And what does the stuff do? Briefly, it's a very potent inhibitor of protein synthesis, which it accomplishes by attacking one subunit of the ribosome (the central RNA-to-protein machinery of the cell.) Rather than just binding to ribosomes and gumming them up, ricin is actually an enzyme all by itself. It tears up a specific adenine base in the ribosomal RNA, which disables the whole thing, and then it moves on to the next ribosome. One ricin molecule can turn over thousands of times, and needless to say, a cell can't lose thousands of ribosomes and expect to survive.
Ricin's a reasonably large protein, and it suffers from the defects of large proteins. The least dangerous way to be exposed to it is by eating it, since most of it gets digested, and much of the rest has trouble crossing from the gut into the bloodstream. In rodents, oral dosing is about 4000 times less potent than inhalation, which is the worst way to be exposed. The assumption is that if ricin were weaponized, it would be treated like anthrax spores and dispersed for maximum effect. The US and Britain carried out research that led to a prototype of a ricin bomb during World War II, just another one of many nasty weapons that actually didn't get used in that conflict.
Needless to say, there's not a whole lot of public data on just how toxic ricin might be in that form, and it would certainly depend on particle size, static charge, and all the other variables we learned about during the anthrax scare. We have a single public data point about injected ricin, though: Georgi Markov, a Bulgarian exile who worked for Radio Free Europe. One day in 1978, he felt a sharp pain as a stranger poked him with the tip of an umbrella. He began to feel ill within a few hours, and three days later, he was dead. A small pellet containing ricin had been injected into the muscle of his leg, as it turns out, in one of the more exotic assassinations known to have been carried out by the KGB. The best guess is that at most half a milligram proved lethal.
Which sounds pretty bad - but consider that terrorists are unlikely to be able to give masses of people intramuscular injections. And if they want to use inhalation, which is certainly the way to cause real damage with the stuff, they're faced with manufacturing problems similar to the use of anthrax spores.
It's not particularly water-soluble, so dumping it into a reservoir would be a waste of time. And adulterating food would be almost useless, although I've seen mentions of this possibility since the news story broke today. It takes a good handful of the beans themselves to kill an adult (and they have to be crunched up, too, because whole beans tend to pass unchanged through the digestive tract.) A back-of-the-envelope calculation for the pure toxin suggests that it would take a gram or two to reliably kill someone by ingestion. That adds up to a few hundred casualties per pound of ricin, but only if you can get all your victims to eat enough of it.
How worrisome is the news from London? It depends on how much ricin these people had, and what form it was in. I'm betting that it was straight precipitate from the beans, and not something ready to disperse for inhalation. In which case, the suspects were set up to commit retail murder. And not wholesale, fortunately.
(For as much detail as anyone could want, see this PDF, a book chapter written by two colonels from the Army's Medical Research Institute at Fort Detrick.)
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October 31, 2002
There's another report this morning of an arrest of a suspected Chechen terrorist, who was carrying what's described as 18 pounds of mercury in a champagne bottle. ""Such an amount of mercury would poison a very large number of people," said a spokesman for the Moscow police.
Would it? The amount is right - 18 pounds of mercury works out to about 600 mL, which would fit just fine into a bottle. But what could you do with it? Mercury, in its elemental form, is a very, very slow toxin indeed. You can even drink a shot of the stuff and pass it out of your body without getting killed. It won't improve you, that's for sure, but it won't kill you.
If you try that stunt, your body (or your intestinal bacteria) will take a very small amount of the metal up and convert it to organomercurial compounds, which are the real problem. Those are much more easily absorbed than the pure metal, and can really do some damage. (These are the forms of mercury found in fish, for example - it's not the free metal.) Mercury reacts with sulfur-containing proteins, among other things, and there are plenty of proteins that depend on sulfur for their structure and activity. You can't afford to lose 'em. Long-term exposure to mercury vapor (which the liquid metal is always producing, very slowly,) gives you the best (ie, worst) chance to absorb the element. That's how mercury's toxicity was first noticed, but this can take months or years to develop as the protein damage piles up.
Now, if this guy had been carrying a few pounds of something like dimethyl mercury, then things would be different. That's one of the simplest organomercurials, and it is extremely bad news indeed. Just a few years ago, a research chemist at Dartmouth was when a few drops of this compound fell onto her latex-gloved hand. It penetrated the glove, then her skin. She didn't notice a thing; nothing seemed amiss for several months. Then neurological symptoms rapidly began to show up, and she died within weeks.
That's about as bad as mercury compounds get, and it still takes time for it to kill you. This Chechen probably thought he was carrying a serious poison, but he was mostly hauling around a rather expensive barbell. Here's hoping he paid a lot of money for it.
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October 28, 2002
Since I did a multipart series on chemical warfare last month, I've had several e-mails asking for my take on the Russian gas used to break up the Chechen hostage situation. The information that I can get from wire-service reports doesn't make for a very coherent picture, but I imagine it's not very coherent in Moscow, either.
First off, I think we can rule out nerve gas itself, or some weaker form of same. None of the victims, as far as I've read, display signs of cholinergic poisoning. Any cholinesterase inhibitor strong enough to knock someone unconscious is strong enough to do a lot more to them, and I'm just not hearing about the symptoms you'd expect. For starters, there are effects on the salivary and sweat glands that are quite noticable. It wasn't nerve gas.
There's been speculation about an unusual agent known as BZ. This isn't one that I covered in my series of posts, since it's rarely (if ever) been used in the real world. BZ is a CNS agent, probably quinuclidinyl benzilate or a similar compound (the precise formula's never been made public.) It hits the muscarinic receptors, which are involved in nerve gas toxicity, and several others as well. It causes tremors, hallucinations, memory loss and various other odd symptoms. In fact, the lack of a predictable response is the main reason it's never been used much. I don't think that this was what was used in Moscow, although it can't be ruled out.
Whatever agent this was, its main effect seems to have been CNS depression. The loss of consciousness and vomiting reported would be typical of sedative overdoses or alcohol poisoning, for example. I've seen a report wondering if this was plain old chloroform, but I doubt it - the quantity of chloroform vapor needed to do what this did would have probably stripped the paint off the place, for one thing, since it condenses out to the liquid if it hits a cold surface. Sticking with that chemical class would lead you to a Freon of some sort, and I guess I can't rule that out, although it seems an odd thing to use. We're getting very close to medical anaesthetics like halothane, though.
Otherwise, I'd wonder about some sort of aerosol sedative, perhaps fentanyl or another compound that acts on opioid receptors. Getting that into an easily used form wouldn't be easy, but it's certainly not impossible. And it would fit with many of the symptoms that have been described.
What this tragic incident points out is that there's not such thing as the "knockout" gas beloved of thrillers and screenplays. Anything that can induce quick unconsciousness in a person can go on to kill them. No one's found a way around that problem, clearly.
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September 15, 2002
The previous posts have been a quick tour around the chemical weapons landscape. I have to say, it's a depressing place to visit, and I'll be glad to leave it. But I can't do that without some thoughts on what, in the end, the stuff is good for.
Well, killing people, obviously. Or threatening to kill them, more likely. That's leads to an old military issue: whether to make your fearsome weapons known or not. If other countries know that your state is armed to the teeth with nerve gas, this knowledge will probably serve as a deterrent should they think about attacking you. Of course, that means that anyone who does attack will be prepared for whatever you can throw at them (and, presumably, ready to respond in kind.) Perhaps you're better off hiding your worst stuff, so if you have to use it, it'll have the maximum effect. . .
This thinking can be seen in action in the First and Second World Wars. The German chlorine attacks in 1915 caught the Allies almost completely by surprise (despite a fair amount of intelligence beforehand, as is seemingly always the case with surprise attacks.) But the surprise didn't last long. Within ten days, Kitchener had directed that the British forces respond with chlorine of their own, and the race was on. As the chemistry (and the technology used to deliver it) evolved, so did protective gear and readiness. All in all, the gas warfare of WW I ended up as a reeking, corrosive stalemate.
World War II never went chemical, despite prewar expectations. This was in spite of a German technological advantage. As the last two posts outlined, they were alone in nerve gas technology, and they put significant resources behind developing it. Large stockpiles of ready-to-use nerve gas munitions were captured at the end of the war. Why weren't they fired?
For that matter, what about the World War I standbys, like mustard gas? Huge amounts of were ready on both sides, each ready to reply in kind if the other side used it. As an example, here's an account of the German raid on US military shipping at Bari, Italy in 1943. One of the ships destroyed was loaded with mustard gas, producing the only battlefield chemical casualties of the war. (Thanks to Stephen Den Beste for pointing this incident out to me.)
That knowledge, that both camps were stocked with mustard gas and protection against it, seems to be what kept it from ever being used. The experience of World War I strongly suggested that the situation would end up as status quo ante, albeit with everyone in protective gear and more destruction all around.
As for the Tabun, its initial use by German forces would surely have been effective, especially at first. No one was prepared for a chemical agent that lethal. But the fact of chemical warfare would have been immediately clear, even if the specific agent was new and unknown, and the retaliation would surely have been terrible. Recall that by the time the German military was desperate enough to use nerve gas, the Allies had increasingly established dominance in the skies, in huge bomber attacks. It's likely that these would have been used for chemical counterattacks, and the consequences of an RAF or 8th Air Force raid loaded with mustard gas would be terrible indeed.
At the same time, the German government wasn't completely sure that the Allies didn't have nerve gases of their own. Publications in the scientific literature on insecticide chemistry almost completely dried up during the war, a fact that was noted in Germany. They couldn't be certain that the US hadn't stumbled across the same discovery that Gerhard Schrader's group had. . .and if so, then those retaliatory bombers might even have been loaded with something like Tabun rather than mustard gas, with consequences that are difficult to imagine.
I'm prepared to argue that against a competent and prepared opponent, the known chemical weapons are essentially useless. The historical record seems to bear this out. Look at the uses of mustard gas since World War I. Morocco in the 1920s, Ethiopian villages in the 1930s, Yemen in the 1960s - a motley assortment of atrocities against people who couldn't retaliate.
The exception is the Iran-Iraq war, yet another way in which it reminded observers of World War I. Iraq surprised the Iranian forces with mustard gas (see this 1984 report from a Swedish arms-control group,) but eventually Iran was able to get its own chemical agents on line. Neither side ended up with much permanent advantage this way, although Iraq was able to compensate somewhat for its disadvantage in manpower. (By the way, the Iraqi government also lied constantly and inventively about its use of chemical agents. At one point they suggested that Iranian casualties must have somehow been exposed to mustard gas somewhere else.)
I see no reason to assume that the current chemical warfare situation with Iraq has changed. In a war with US and British forces, they would be facing the best-equipped and most technically competent militaries in the world, and they could not hope to tip any sort of balance by battlefield use of even large amounts of chemical weapons.
As the large PDF file I linked to yesterday makes clear, the quality of Iraqi agents during the war with Iran wasn't very high. They needed the stuff immediately and didn't want to invest the time and effort to purify things (by distillation, for example - there's another wonderful job for you.) Their nerve gases were typically contaminated with the hydrogen fluoride I spoke of, rendering them corrosive and unstable to long-term storage. One assumes that they've remedied this problem over the years, but this also means that Iraq may have even less supply of chemical agents than some have estimated.
So, if they're to be used at all, it would be against selected targets, and the only ones they'd be useful against are unprotected civilians. Iraq infamously ran field tests of various agents on its own Kurdish population in the late 1980s, and we can assume that they know what they're doing and how to do it. But what population of civilians could be attacked to Iraq's advantage? Certainly not those of the Arab states that are aiding the US military efforts (such as Qatar and Bahrain.) The only thing that makes any sort of (diseased) sense is an attack on Israel, similar to those in the (First) Gulf War.
That way, Saddam Hussein can make himself out to be the mighty warrior who gassed Israel, slaughtered the oppressor, took the battle to the common enemy of all Arabs. . .ah, you know the sort of thing. He might see it as the best way to try to split off any Arab or Moslem support and to ignite a full-scale Middle East conflict that would shuffle the deck. Of course, that appears to have been his calculation the first time around, and none of that came to pass. One would expect the Israelis to be even more prepared this time around
So much for the military uses of chemical weapons. I've alluded along the way to their uses in terrorism, which seem to me to be more worth worrying about. No one's expecting a chemical attack on a normal workday. If executed well, such an effort would, unfortunately, seem well worth a terrorist group's while.
I could go on for quite a while on that topic, but I don't think it's that great an idea. I can't talk about the problems involved without potentially giving someone a leg up on solving them. And I can't talk about what I'd be most worried about without giving someone a good starting point. The only thing, in good conscience, that I think I can do is end by quoting Wittgenstein: Wovon man nicht sprechen kann, darüber muß man schweigen. (Whereof one cannot speak, thereon must one remain silent.)
I'd like to thank all my visitors for sticking with me through these postings, which I hope have been worth the time to read. Pharmaceutical and science news will start again tomorrow. Here's hoping that we don't revisit this topic any time soon!
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September 14, 2002
A good short history of Tabun and other nerve agents, largely based on this book, can be found here. To summarize, in 1937 a report on Tabun made its way to the chemical warfare branch of the German military, and its value was recognized quickly. Gerhard Schrader's group was moved to new laboratory space and set to developing new agents in the same chemical class. Money and material was put on scaling up the synthesis of Tabun itself.
Now, that was no easy project to be assigned to. The biggest problem, of course, was the hideous toxicity of the product. The pilot plant had quite a containment system (double-walled enclosures with positive pressure and so on, very sophisticated for its time.) The workers wore rubber containment suits, which were rigorously cleaned and changed. People still got killed. The histories above give some examples - the one that sticks with me is the unfortunate who had two liters of Tabun suddenly pour down inside his rubber suit.
Even without the awful product, the chemistry by itself was pretty foul. To pick a major issue, it involved hot hydrofluoric acid. You really don't want HF around if you can help it. It attacks glass, for one thing, and goes after a number of metals. It leaves the really expensive ones untouched, though - if you read the old literature on the stuff, you find references to exotica like platinum dropping funnels and the like. The Germans had to use silver-lined reaction vessels in part of the plant; the sort of thing we'd use high-nickel alloys for today. On top of the corrosion problem, HF is also very toxic, and inflicts extremely dangerous time-delay burns. The idea of working in a process plant where hydrogen fluoride isn't the nastiest thing in the house gives me the shivers.
And just to top things off, the Tabun process also involves cyanide and produces HCN vapors, which have to be dealt with somehow. I spent a paragraph the other day talking about how HCN wasn't a very useful war gas (which it isn't,) but being cooped up in a factory with it is another matter entirely. All in all, this is a one-damn-thing-after-another process that no one would scale up under normal circumstances.
The route worked, though, although it took a couple of years to get it going reliably enough to where it wouldn't kill everyone in the vicinity. By the end of the war, Germany had produced 12,000 tons of Tabun, a figure to give anyone pause. (We'll talk about why they never used it in the next post.) Meanwhile, Schrader's group continued to work in the area, producing Sarin (or GB) in 1938 and Soman (GD) in 1944. While Tabun has largely disappeared (except for nations just getting into the nerve gas synthesis business,) Soman and Sarin are still very much with us. The chemical routes were just as nasty, though - they still hadn't found a way around the fluorine reagents, and Sarin has a fluorine group directly bonded to the phosphorus. At least the cyanide part was gone. Still, production of Sarin by the end of the war was merely a few tons, and Tabun still has the reputation, despite all the nasty steps, of being the easiest nerve agent to synthesize in bulk.
In the 1950s, post-war research led to the discovery of several other effective compounds, including VX, which still sets the standard. These were discovered in several countries, more or less simultaneously. VX has a structure reminiscent of the others, but where the fluorines (or cyano) groups are on the phosphorus, there's an aminoalkane linked through a sulfur atom. The Soviets stockpiled their own, very similar compound with almost identical properties. VX's structure wasn't publicly disclosed until the early 1970s, but as it turns out, a 1960s German patent had made its way into the various open databases which (to everyone's embarassment and surprise) had VX in it. The inventor was. . .Gerhard Schrader, still at the phosphorus chemistry after thirty years, and obviously a man with very good lab technique to have survived that long.
Improvements were made over the years to the syntheses of all these compounds, but I'm not going to go into the details. It's an interesting set of process chemistry problems, but you have to be conversant in that sort of thing to get the most out of the discussion, and I assume that a majority of my readers aren't. There are many discussions in the open literature. For example, see this large PDF file entitled "Technical Aspects of Chemical Weapon Proliferation," which has a vast amount of detail.
No matter what the route, anyone outside of a serious industrial setting who wants to try this chemistry runs a mortal risk. I've worked with some really toxic stuff in my years in the lab, but I wouldn't touch any of the nerve agents with a platinum pole. 10 milligrams of VX on the skin is the approximate lethal dose - is my lab technique really that good? Well, I think so. . .but is that the phrase that I want them to put on my tombstone?
No one knows if there's been much subsequent R&D in this area, but I doubt it. Chemical weapons have the reputation of being living fossils compared to how other weaponry has developed. A Russian report from the early 1990s spoke of a completely new chemical class of lethal agents, which is certainly possible - but why bother? The phosphorus-based ones are about as bad as it's possible to get. (An overview of their comparative properties with some similar historical background is here, and the link I provided yesterday goes into great detail, too.)
Of the agents that have been used in the real world, Sarin's the most volatile, and does a lot of its work by inhalation (it's likely that if Schrader's lab had made that one first that they all would have died.) Meanwhile, VX is more persistant, rather like mustard gas, and works mainly by contact. Both can be formulated so that the last chemical step in the syntheses takes place in the shell or bomb, after it's been fired or dropped. To the best of my knowledge, there has been no hostile use of these "binary" weapons, except for an alarmingly crude dump-and-seal technique tried by the Iraqis during the war with Iran.
So how does one deal with these things? In the way of organic chemistry, the same reactivity that allows these compounds to inactivate cholinesterase also gives you a handle to break them down. All these reactive groups attached to phosphorus can be hydrolyzed by things like sodium hydroxide or bleach, or reacted with a nucleophile like ammonia. The resulting phosphoric acids or phosphoramides are basically harmelss. (VX's hydrolysis product, though, is unusually toxic. Fortunately, it doesn't penetrate the skin.)
That's all very well for decontaminating a concrete wall, but what about decontaminating yourself? The fast action of the nerve agents makes speed the main consideration. Even potentially lethal exposures can be compensated for if treated quickly enough. There are two therapeutic approaches, which are generally used simultaneously: Oxime compounds can actually react with the cholinesterase-bound form of the nerve agent, knocking it out of the active site in the process and regenerating the enzyme. Meanwhile, out in the synapse, a cholinergic antagonist can block the receptors and keep the signaling at the neurons from getting out of hand.
One antagonist that's usually provided for this purpose is atropine, which under normal conditions is quite poisonous itself (since blocking acetylcholine signaling for no reason is arguably just as bad as overloading it.) Really heroic doses of the stuff can be used in nerve gas poisoning cases, though. An important part of any chemical-warfare supply kit is a supply of these antidotes, ready to inject. There's a picture of a standard apparatus in another of the links from yesterday's posting .
Finally, giving a reversible inhibitor of acetylcholinesterase can protect against nerve gas before any exposure. That seems rather odd at first, but the idea is that the inhibitor ties up a certain proportion of your enzyme (but not enough to cause trouble.) The reversible chemical equilibrium causes it to gradually be freed up, even after nerve gas exposure, and this gives you a reserve of active enzyme coming on line that hasn't been hit by the irreversible nerve agent. Used properly, this can be enough to prevent much of the damage. Here's a military manual on chemical agents that goes into more detail on treatments for exposure to all of them.
In the next post, which I hope will be tomorrow, I'll try to wrap things up with a strategic discussion - no, I'm not turning into Den Beste (he fills that role just fine!) - but now that I've talked about the history and properties of these things, it's time to see what's been done with them, and what might still be waiting.
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September 13, 2002
Descending past mere irritants and past disfiguring killers, we arrive at the bottom of the pit. These are compounds that are to humans what a spray-can of insecticide is to flies.
I mean that literally. Back in the 1930s, a group at IG Farben in Germany was searching for new classes of compounds to kill insect pests. After trying out several classes of organofluorines, Gerhard Schrader's lab made a phosphoramide fluorine derivative in 1935. That was a pretty potent compound, and a whole new area of research opened up.
Two days before Christmas of 1936, Schrader used the fluorine intermediate to make the first compound of the type we know as nerve gas. This was what's now called Tabun or GA, and it was the one of the most potent insecticides the lab had produced. After the Christmas holidays, he and his lab assistant were continuing their work when they noticed that they were getting short of breath, and that their vision was dimming. They evacuated the lab, which was a good call - a few minutes more would surely have killed both of them.
Those side effects are among the earliest signs of nerve gas poisoning, no matter what the agent. That's because they all work by the same mechanism. Some of the compounds are easier to make than others, some are more potent (so you don't have to make as much,) and some are more stable (so you can keep them in storage until you feel the need to commit mass murder.) But all of them do the same thing: irreversibly inhibit esterase enzymes.
A little-known fact is how broad-spectrum that activity is, and how little that matters. There are probably dozens of enzymes that a nerve agent shuts down in vivo, and this wholesale disruption would probably cause death in hours or days. Those pathways never get the chance, though, because the enzyme that counts is acetylcholinesterase.
Here's why: a number of different compounds are used in the nervous signaling for neuron-to-neuron crosstalk, but real workhorse is a small one called acetylcholine. It's made in the neuron, stored in vesicles up near the cell surface, and released to float across the synapse. Once it makes it across, it binds to one or more members of two families of proteins (muscarinic receptors and nicotinic receptors.) That docking sets off further signaling inside the receiving neuron. Fellow medicinal chemists and biologists know this as a prime example of a G-protein coupled receptor mechanism; it's a theme that shows up in many other signaling pathways.
The thing is, a signal across the synapse isn't a continuous current. It's a pulse across a gap, and when the signal has been received, the synapse has to be cleared. That's the job of the acetylcholinesterase enzyme. It's extremely efficient at breaking down acetylcholine, insuring that the signaling pathway doesn't stay switched on.
And nerve agents are extremely efficient at deactivating the enzyme. One molecule of nerve gas, if it makes it to the enzyme, will shut it down. When you consider that each enzyme molecule would otherwise turn over thousands upon thousands of acetylcholines - well, things get out of hand very quickly. The acetylcholine piles up in the synapse, causing all the receptors on the receiving neuron to get switched to an unnatural full-on overload. The entire nervous system goes down within minutes (at best) under these conditions - no interpretable signals to the muscles can get through at all. The limbs, the heart, the lungs all shut down or spasm uncontrollably.
Schrader and his assistant felt what they did because those organs were the first to be affected by the Tabun vapors, which were absorbed by the moist tissues of the eyes and taken up through their lungs. Their intercostal muscles were being partially inactivated (shortness of breath,) and the blast of acetylcholine signaling switched on the M1 muscarinic receptors in their pupillary muscles, causing them to contract. [Note added later - the shortness of breath was more likely due to bronchial effects, or the beginning of effects on the diaphragm muscle. The effects on the eyes are complex, probably involving both m1 and m3 receptors.] Further exposure starts to affect other muscle groups, and you get a mixture of muscarinic and nicotinergic symptoms. The only people who can tell you how this feels live in Japan (thanks to Aum Shinrikyo) and in northern Iraq (thanks to Saddam Hussein.) I should warn you, the New Yorker article that link goes to is very difficult to take. It's vital reading for an understanding of chemical warfare in Iraq, but it'll give you bad dreams.
Another thing that isn't widely known is that cholinesterase inhibition actually has positive medical uses. It's one of the few therapies now available for Alzheimer's disease, for example. The idea, which is admittedly a crude one, is to crank up the volume of the brains' acetylcholine signaling to compensate for the damage of AD. It works, a little, for a while. Of course, the sorts of drugs you use for this therapy need to be a bit less. . .efficacious than nerve gas. Ideally, they're weak, reversible inhibitors of the enzyme (as opposed to butt-kicking irreversible ones,) and they should tend to concentrate in the brain while getting cleared from the rest of the body.
The dose makes the poison, indeed. We'll return to Gerhard Schrader in the next article, after he learned to treat his compounds with more respect.
[Post edited after inital version - cleaned up some pharmacology and added links.]
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September 12, 2002
We'll cover three World War I compounds, saving the latter-day nerve agents for a separate posting. 1915 was a terrible year, one among many, because it saw the advent of militarized chlorine, followed shortly by phosgene. Those two (though technically obsolete) are still in play, because their manufacture is so low-tech. Mustard gas (bis(chloroethyl)sulfide,) which is really a liquid for the most part, was also famously effective. I'm not going to talk much about the arsenical agents like Lewisite - they're nasty, but of less relevence, I believe, to modern warfare or terrorism.
Some of the other things from that era, ones that you'd think would be quite destructive, turned out to be useless. Gaseous hydrogen cyanide is a notable example, and illustrates some of the complications. For one thing, HCN is too light - the vapor disperses rapidly, instead of hugging the ground like phosgene. It's also a little-appreciated fact that HCN isn't really that toxic below a certain threshold. I've smelled the stuff myself in the lab - by accident, I should make clear. (Its aroma is distinctive, but not as bitter-almondy as advertised, at least to me.) People can survive just fine around low concentrations of cyanide gas, although I'm not endorsing it as a lifestyle choice. Achieving lethal concentrations of it in the field just isn't very practical. Not that it wasn't tried.
The three agents from the first paragraph, though, suffer from no such limitations. Chlorine and phosgene are heavier than air, and accumulate in low places (such as a World War I trench) if there isn't a strong wind. They're both reasonably persistent as well. Mustard gas is very persistent indeed, to the point that it couldn't be used against positions that attacking troops were going to occupy any time soon. All three have effectively no minimum concentration below which they stop doing some sort of harm. Very low exposure to any of them certainly isn't fatal, and you can even get away with no lasting damage, but it's still unwelcome.
While not the most effective chemical warfare agents (we'll get to those next week,) these things are all easily purchased or made in quantity. No doubt they have some appeal for terrorists, and as such they're worth looking at in a bit more detail.
Chlorine is a basic industrial chemical, prepared in immense quantities by electrolysis of brine. This is the chlor-alkali process, a classic of chemical engineering which has been refined but never superseded. This technique means that wherever they make chlorine, they make sodium hydroxide, too, and generally they go on to make sodium hypochlorite bleach for you, too.
There's been tremendous back-and-forth about chlorine use and production in Iraq, since it's also used to purify drinking water supplies. While Saddam Hussein certainly would have no qualms about using it, it's still not the most effective war gas by a long shot (we'll be getting to those in the next post.) I believe that the more likely use of chlorine would be as part of a low-tech terrorist operation involving its transport through a population center.
Its effects can be completely mitigated by reasonable protective gear, but that's just what ordinary people won't have. It has severe effects on the lungs, which is how it kills. One thing that keeps it from being more destructive is that it has a powerful smell, even at low concentrations. No one gets exposed to chlorine without realizing it and trying to get away.
Phosgene is worse. It also causes severe lung damage, but it's harder to detect. There's certainly a distinct phosgene odor (sort of an acrid rotting-vegetation smell, supposedly not so bad a low concentrations.) But that means the gas can be present at dangerous levels (especially over time) without being particularly noticeable or offensive. And if you don't know what the smell is (and what it means) you can be badly injured without realizing the danger. The majority of chemical fatalities in World War I came from phosgene.
On a personal note, perhaps the single longest day I've spent in my chemical career came some years ago, after I thought I might have been exposed to some phosgene one morning. I didn't really notice the distinct smell, but here was also plenty of HCl vapor present, and I worried that it had masked the phosgene. Surely, I thought, I'd notice some immediate effects if I'd been exposed. . .so I went and did some reading, and that's when I really started to get the cold sweats. The symptoms of even a fatal exposure to phosgene can be, initially. . .nothing. Only with time does it hydrolyze inside the epithelial cells of your lung tissue, causing increasing and irreversible damage. I spent a rather jumpy day, checking my breathing while trying to correct for the unusual general shortness of breath I was feeling.
Phosgene is also a large-scale article of commerce. It's synthesized from carbon monoxide and chlorine, using various catalysts. Not something that you would make in your basement, but if you're a country with a thermoplastics industry, you make phosgene or you deal with someone who does. As far as I know, it's not usually shipped around or stored in large quantities, which makes it less of a civilian terrorist threat. If you have an industrial phosgene synthesis, you generally make it on-site as needed.
Finally, we have mustard gas (something of a misnomer, as I've mentioned.) It didn't cause as many fatalities on the battlefield, but its insidious nature made it an effective weapon. It's not immediately irritating to the eyes or lungs, and it can be tremendously harmful at levels well below those that can be smelled. It's persistent, and penetrates ordinary clothing very well. A few hours after exposure is when the trouble begins. It attacks the lungs (although with a different sort of action than phosgene) and causes terrible burns to exposed tissue - all of this long after you have the chance to do much of anything about it. That's the main reason for its military effectiveness, since full body coverage is needed rather than just eye/lung protection. As a weapon of terror, this might be the worst of the three, if the people involved were to disperse it well enough.
Fortunately, it's also the hardest to get. There's no industrial application for the compound, and no legitimate reason to produce it in any quantity. However, its immediate precursor compound, thiodiglycol, is used industrially, although in quantities that don't come anywhere near chlorine or phosgene. It shows up as a component in inks and dyes, mostly, which means that an unsavory government could claim that a particular factory was making ball-point pen ink or the like. Synthesizing the mustard itself from the precursor wouldn't be much of a feat for any decently equipped lab. You might not get the cleanest product in the world, but it would be bad enough.
Trying it in a garage (or a cave!) though, would be another matter entirely. We've now crossed over from the list of "things you can buy" (or "things you can hijack a truckload of") into the territory of "things you have to make." And even a one-step synthesis like mustard gas, if it's to be done on any harmful scale, needs some equipment that you're not going to have in your kitchen - that is, if you're not going to gas yourself in the process. None of the problems is insurmountable, unfortunately, but they do raise the bar.
I mentioned the problem of dispersal. I don't want to gloss over it, but I don't want to give anyone a road map, either. The use of chemical agents in World War I, for example, evolved from opening cylinders and letting the wind blow the stuff across no-man's-land (in early 1915) to various types of sophisticated gas artillery shells. That was a direct result of experience - the wind could blow the gas all over the map, or right back at you, while shells could be targeted where you needed them.
As we'll see later in the discussion of nerve gas, the Aum cult in Japan found that even highly toxic compounds aren't as effective as they could be when poorly delivered. We can assume that Iraq has a real supply of chemical munitions (more on this later on, too,) while less infrastructure-rich terrorists probably don't (unless they buy them off of the Iraqis or any of the many other governments that are holding on to this stuff.) If they're going to use chemical agents on their own, though, they'll have to figure out a way to do so effectively. And that is, fortunately, not trivial. Beyond that I will speculate no more in public.
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I don't often deal with politics and world events on this site (much less than I thought I might when I started it.) There are usually plenty of other worthy writers out there who are saying just what I would, so I've settled on science (and the business of science) as my ecological niche in the Blogosphere. But these days, current events may be crossing paths again with chemistry, so I thought I'd use my scientific background to cover a topic that I fervently hope will end up being of no interest at all: chemical warfare.
There's a reasonable chance that an invasion of Iraq would trigger use of Saddam Hussein's remaining chemical weapons stores (either against US troops, or on a missile lobbed into Israel, as in the Gulf War.) The Iraqis themselves have credited their chemical warfare capacity with giving them an edge against the much larger Iranian forces in the 1980s, and Hussein has (infamously) used what appears to have been the nerve agent VX against his own Kurdish population.
On the home front, there are terrorist possibilities as well, both with industrial chemicals as well as with more specific war gases. I'll take on the subject in several postings over the next few days (with my more traditional blog material showing up in between, as time permits.)
To begin with, it's important to realize that chemical munitions, nasty as they are, do not have the same destructive potential as atomic or nuclear explosives. As readers will see, releasing a van full of (say) benzyl bromide would be a tremendous irritant. A vanload of mustard gas would be far worse than that. A similar quantity of nerve gas would, of course, be an atrocity.
But keep in mind that a fission (or worse, a fusion) weapon could be contained in the same van, and would be many orders of magnitude more terrible in every way. Fortunately, they're also many orders of magnitude harder to acquire. Much depends on keeping that difficulty as high as possible.
Chemical weapons are, then, more likely to actually be encountered, and they're plenty bad enough. The ideal chemical agent would be totally incapacitating or lethal, hard to detect, extremely potent, and easy to deliver and disperse. Since the advent of modern chemical warfare in the First World War, those qualities have largely led to the use of toxic gases or their corresponding liquids. The delivery problems of solid agents have kept them from being as fully developed.
Different compounds meet these criteria to different extents. A much wider variety of agents were tried out during the First World War than is generally realized, almost 40 different compounds. (See this excerpt from a 1926 US government report for a comprehensive list and a lot more detail than I have space to go into.) That list was a real surprise, personally, since I realized that I have a number of these things in my lab. I have to say, I'd never thought about loading them up and throwing them at someone - which is probably the same thought many chemists had during the war. Several of the things on the list are still relevant to today's situation.
Others aren't. Many substances from that era are little more than irritating tear gases. I've been exposed to some of them myself in my chemical career, most memorably a face full of benzyl bromide fumes in graduate school. It wasn't truly incapacitating - I still had plenty of capacity to lurch around the lab toward the eye wash fountain, cursing and banging into things. Such compounds would be of little use against anyone properly equipped, and would do little lasting harm even to unprepared civilians.
Some of the other World War I irritants were had a delayed onset, designed to make later gas-mask wearing very uncomfortable. By which time, the plan was, more lethal agents would be in the area, exposing troops who otherwise would have been better protected. This sort of thing is still a potential military problem, but there's still no point in enemy use of such compounds against civilians who won't have masks to start with.
No, for both battlefield use and in terrorism, the lethal agents are the ones to worry about. I'll be covering these in some detail over the next few posts - how they're obtained, how likely they are to be encountered, and how they're dealt with.
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