“Peace on earth!” was said. We sing it,
And pay a million priests to bring it.
After two thousand years of mass
We’ve got as far as poison gas.
Thomas Hardy, Christmas: 1924
Two millennia before Hardy penned these bitter words, Spartan allies during the Peloponnesian War captured an Athenian-held fort by piping smoke from lighted coals, sulfur, and pitch into the fort through a hollowed-out beam.
This might be the first documented use of poison gas in war, a stratagem which came to the fore in the nineteenth century. In 1812, the British Admiralty had decided that the use of burning ships loaded with sulfur before marine landings in France would be against the rules of warfare, but such scruples would be long forgotten in only 100 years.
In 1854, as Europe languished in the grip of the Crimean War, Sir Lyon Playfair suggested the use of shells filled with cacodyl cyanide against the Russians to break the siege of Sebastopol. The War Office called this “as inhumane and as bad as poisoning the enemy’s water supply,” suggesting they had not read their Pausanias. Playfair answered that it was considered legitimate to spray the enemy with molten metal that produced the “most frightful modes of death,” and so he found the response incomprehensible. Perceptively, he commented that “no doubt in time chemistry will be used to lessen the sufferings of combatants.”
Poison in war was an acceptable stratagem in ancient times. Pausanias tells how Solon defeated the people of Cirrha by diverting a river that flowed through a canal into the besieged town. When the people of Cirrha still held out, drinking rain and well water, Solon had hellebore roots thrown into the stream, and then allowed the waters to flow again. The Cir-rheans all drank deep of the water; the sentries were struck down by diarrhea, and left the walls, allowing the town to be taken.
In 1864, a proposal for the Union army to use chlorine shells against the Confederacy was also rejected, but the idea was clearly alive and well. The 1874 Brussels Convention tried to preempt the inevitable by banning the use of poisons in war, while the Hague Conventions of 1899 and 1907 only offered a weak and vaguely worded resolution against the use of chemicals on the battlefield. Time was slipping away while the diplomats fiddled, and science was advancing as World War I approached.
Of course, much of the science had been in place for a long while. Phosgene and chlorine, two of the most deadly gases, had been around for more than a century when war broke out in 1914. Scheele had first prepared chlorine in 1774, and it was named in 1810 by Humphry Davy, who proved it to be an element. Two years later, his little-known brother John discovered phosgene or carbonyl chloride, COCl2, when he exposed carbon monoxide and chlorine to sunlight while they were contained in a glass vessel. John Davy described it as “producing a rapid flow of tears and occasioning painful sensations.”
By 1914, even more chemical weapons were available. In Paris, gendarmes had been using unpleasant gases to control rioters for a number of years, and it seems the first chemical shots in the war were actually French antiriot agents lobbed into German lines, although it is more usual to accuse the Germans of being the first to use poisonous gases to kill. History may not always be written by the victors, but they do tend to get the major blame-allocation rights.
Poison gas, in the strict sense, was first used on a battlefield in April 1915. The German plans of moving across the country fast and outmaneuvering their enemy had become bogged down in trenches, barbed wire, and mud. Infantry sat in their trenches while the artillery behind them lobbed high-explosive shells into the enemy’s trenches. Once the enemy was sufficiently softened up (they hoped), machine-gun fodder would be sent forward to a point where they could be mown down by the surviving defenders.
In spite of all the snide comments made about military intelligence, field commanders had no problem working out that a barrage from the other side indicated an impending attack, so reinforcements would be readied and the frontline troops would shelter in bunkers, ready to emerge and man the machine guns once the barrage stopped and the enemy advanced.
It was a total stalemate, and it was likely to go on until there was one soldier left standing. The lack of progress came down to access to resources: the Allies could milk their overseas colonies of both fuel for what was increasingly a mechanized war and nitrogen compounds for explosives. Given time, they should have been able to wear Germany down. Germany’s biggest challenge was maintaining the supply of explosives, and this need had been met largely by one man, Fritz Haber.
Nitrogen is available for free—it makes up about 80 percent of the atmosphere—but the stuff in the atmosphere is almost inert, and almost useless for fertilizing plants or making useful compounds. Nitrates were needed to fertilize crops, and guano supplies in Chile were running out. This was the situation confronted by Sir William Crookes in a presidential address to the British Association in 1898. More wheat was needed, he said: “The world’s demand for wheat—the leading bread-stuff—increases in a crescendo ratio, year by year.”
Haber took up the challenge, and developed a method of forcing nitrogen to react with hydrogen to make ammonia, the first key step in synthesizing nitrates. Haber’s method proved to be highly successful—the first plant opened in 1913, and even now the Haber process is still used in 600 plants, which generate a world total of more than 100 million tons of ammonia each year.
It is brutal chemistry, combining the gases at a temperature of 400–500°C and a pressure of 20 atmospheres or more in the presence of an iron catalyst. Curiously, the ammonia is a poison to us, but the catalyst is said by chemists to be “poisoned” by oxygen. There is just no way we can escape poisons, it seems, but a third of the world depends on Haber process products for its continued survival.
As the war in the trenches lost momentum, Haber’s plant quickly became crucial to the German war effort. Perhaps Haber can be accused of contributing to the stalemate because his process maintained the supply of ammonia needed to make nitrates and nitric acid for the German munitions industry.
Apparently Haber commented to Gustav Krupp von Bohlen und Handbach that, after the first few months in the trenches, each side had become better at defense than offense. A new weapon was needed, he said, to break the murderous stalemate of trench warfare. Echoing Lyon Playfair, Haber actually saw the use of gas as humanitarian, because the gas immobilized, rather than killed, its victims. There has to be some doubt about the German claim that gas warfare was only inspired by the stalemate, and certainly the victorious Allies would later counterclaim that the Germans had planned their gas attacks long before the war began. For whatever reason, on April 22, 1915, the Germans launched their third attempt to break through and take Calais. They were tired of mounting mass attacks and getting slaughtered under machine-gun and rifle fire. For the first few days, the nature of the gas was unknown, and it was referred to only as “asphyxiating gases.” We know now it was 500 tons of chlorine, released from 200,000 cylinders, and the Allies’ bewilderment seems a little strange. Any worker from St. Helens or Widnes could have told them what it was: the Germans were attacking them with Roger.
The gas was identified in the first reports as “contrary to the rules of The Hague Convention,” a rising cloud of greenish-gray iridescent vapor. The Germans, said reports, were prepared to work within the gas, as though this somehow made it more reprehensible. Men dressed in what looked like diving suits could be seen handling the cylinders, with hoses directed at the French lines. About 800 Allied defenders were killed, while a further 15,000 were forced to flee.
According to the New York Tribune, the German troops following up “held inspirators in their mouths to protect them from the fumes”:
This new form of attack needs for success a favorable wind. Twice in the day that followed the Germans tried trench vapor on the Canadians.... In both cases the wind was not favorable, and the Canadians managed to stick through it. The noxious, explosive bombs were, however, used continually against the Canadian forces and caused some losses.
New York Tribune, 1915
Victor LeFebure recorded General Sir John French’s original, horrified reaction:
Following a heavy bombardment, the enemy attacked the French Division at about 5 p.m., using asphyxiating gases for the first time. Aircraft reported that at about 5 p. m. thick yellow smoke had been seen issuing from the German trenches between Langemarck and Bixschoote. What follows almost defies description. The effect of these poisonous gases was so virulent as to render the whole of the line held by the French Division mentioned above practically incapable of any action at all. It was at first impossible for any one to realise what had actually happened. The smoke and fumes hid everything from sight, and hundreds of men were thrown into a comatose or dying condition, and within an hour the whole position had to be abandoned, together with about fifty guns. I wish particularly to repudiate any idea of attaching the least blame to the French Division for this unfortunate incident.
Victor LeFebure, The Riddle of the Rhine, 1923
Still, the Germans failed to break through, and the Allied troops were given temporary cotton masks, which they had to soak in their own urine. The urine broke down to release ammonia (itself a poison under the right conditions), which neutralized the chlorine. In July 1915, they got their first “efficient” gas masks and respirators, although Robert Graves was rather scathing about their prophylactic qualities:
This, the first respirator issued in France, was a gauze-pad filled with chemically treated cotton waste, for tying across the mouth and nose. Reputedly it could not keep out the German gas, which had been used at Ypres against the Canadian Division; but we never put it to the test. A week or two later came the ‘smoke-helmet’, a greasy grey-felt bag with a talc window to look through, and no mouthpiece, certainly ineffective against gas. The talc was always cracking, and visible leaks showed at the stitches joining it to the helmet.
Robert Graves, Goodbye to All That, 1929
For all that, the Allies had been discussing the possible use of poison gas since at least 1812, and despite depicting the vile Hun as a baby-bayoneting monster, the Allies seem not to have anticipated that someone else might have had the same idea. General French complained on June 15, 1915, that “All the scientific resources of Germany have apparently been brought into play to produce a gas of so virulent and poisonous a nature that any human being brought into contact with it is first paralyzed and then meets with a lingering and agonising death.”
By September 25, the British were ready to retaliate, but their first trial failed when the wind blew the chlorine back on their own advancing troops. Soon after, gas began to be delivered in shells, and the cumbersome arrangements of gas tanks and hoses could be disposed of.
The problem with chlorine as a weapon was that the victims started coughing as soon as the gas arrived, making it hard for them to inhale a lot of it. The coughing reflex also prompted troops to don their gas masks. Phosgene, a compound of chlorine and carbon monoxide, was brought into play in December 1915 and proved more effective. It was often used along with chlorine in a mix called “white star.” Phosgene causes at most a minor irritation of the lungs and throat, and there is no respiratory reflex, no coughing to protect the victim, so the gas can move deep into the lungs, where hydrogen chloride is released and causes congestion and fluid buildup. The odor threshold for the gas is 1.5 milligrams per cubic meter, and it irritates the mucous membranes at 4 mg/m3. The lethal concentration/exposure measure (LCt50) of phosgene is about 3200 mg min/m3. At low levels, then, it will affect the victims slowly, and, because it smells like new-mown hay, it has every chance of getting past a soldier’s sensory defenses.
The French tried a different tack, firing off a total of 4,000 tons of cyanide, as 0.5- or 1-kilogram payloads, apparently without killing a single German, as the gas dispersed too fast to have an effect. Even so, tabloid scaremongers still bleat about terrorists developing “the capability to make cyanide,” without considering the challenge of transporting the cyanide and then releasing it effectively. Cyanide gas must be relegated to the role of effective suicide tool and potential indoor killer; it is of little value in the open.
Oddly enough, a few Germans did die of cyanide poisoning during World War I, but only after using the gas to destroy vermin. In Essen, some Krupp workmen’s barracks were treated with cyanide gas and improperly aired. Five of the workmen who entered the barracks became comatose but revived, while another ten died from the fumes. In another case, 100 soldiers put deloused clothes on too soon after they had been treated with cyanide and presumably absorbed the poison through their skin: ten lost consciousness, but in the end, none died.
By 1917, however, gas warfare had taken a nasty new turn with mustard gas being brought into the war on both sides. Dichloroethyl sulfide gets its common name because it smells a bit like mustard, though its effects are rather less appetizing. Mustard gas causes irritation, and then turns the lungs solid. Fewer than 5 percent of casualties who were treated died of mustard, but they were typically convalescent for 6 weeks.
By the end of the war, Britain had 2,000 dead and 125,000 incapacitated and hospitalized by mustard, proving its effectiveness against an enemy’s war effort. Like chlorine, mustard was first used at Ypres, but on July 12, 1917, it was delivered by artillery shells, and one attack caused 20,000 casualties.
Mustard is a persistent liquid, so it made anything a soldier touched a potential enemy weapon. Most importantly, there was a latent period of several hours, so there was no immediate sign that the victim had been exposed. Horses were still used for transport in 1917, and they also needed protection from sulfur mustard, while men had to wear hot and bulky protective suits.
The substance was first made in the early 1800s, and is sometimes referred to as Yprite or HS, short for Hun stoffe. More recently, it was used by Mussolini’s army in what was then Abyssinia, mainly to interdict areas, and by Iraq against Iranian troops and, later, against its own Kurdish citizens. British forces used it near Baghdad in about 1920, when liberated Mesopotamians decided they were insufficiently liberated. Britain is also said to have used mustard in Russia in about 1920, and in Afghanistan soon after World War I, while the Spanish used gas against the Riff tribes in Morocco. The Japanese used it in China before World War II was declared.
No one could doubt the power of poison gas as a weapon after World War I. In America, General Pershing wrote, “The effect is so deadly to the unprepared that we can never afford to neglect the question.” Yet during the late 1920s and 1930s, while the world’s nations were developing new and better armaments, there seems to have been remarkably little work on new poison gases except in Germany, where they arose out of insecticide development.
By 1936, Gerhard Schrader and his colleagues had identified chemical agents that blocked cholinesterase, causing loss of control over respiration and other functions and leading to asphyxiation. The first was tabun (dimethylphosphoramido-cyanidate) and the second was sarin (isopropylmethylphosphoro-fluoridate), named after its developers, Schrader, Ambros, Rüdiger, and van der Linde. Sarin is similar to tabun, but even more toxic—it was the gas used in Tokyo in 1995 by Aum Shinrikyo.
These agents were weaponized and stored, so by the end of 1944 Germany had a stockpile of 12,000 tons of tabun. No one really knows why they weren’t used—possibly it came down to fear of retaliation, but Britain had nothing more deadly than a new version of mustard gas. One interesting theory is that Hitler, himself a mustard gas victim in World War I, may have been against the weapons—his senior staff would also have been junior officers in World War I and so equally exposed and inclined to be opposed to the use of gas.
All the same, the British expected gas attacks to come, and the fourth edition of A Catechism of Air Raid Precautions, published in 1939, lists ten gases, classified as: persistent and non-persistent; choking (phosgene and chlorine); and tear, nose, and blister (mustard and Lewisite—developed by Dr. Wilford Lee Lewis, perhaps the only human to have a poison named after him, if you discount sarin’s inventors). Citizens were expected to read, mark, and inwardly digest that Lewisite is chloro-vinyl-dichloro-arsine; that one of the tear gases, SK, was named for South Kensington, where it was first developed; and that BBC had nothing to do with the British national broadcaster but was in fact bromo benzyl cyanide. If the citizens were going to die of noxious gases, they would die educated.
The details show a strange matter-of-factness. Americans knew Lewisite as Dew of Death. The catechism tells us that it smells pungently of geraniums, although the purer the gas, the less pungent the odor. It says that phosgene smells of musty (rather than new-mown) hay and causes coughing for a few minutes, but that the coughing then goes away for some hours before returning.
One question in the catechism asks why it is necessary to put on and take off protective clothing by numbers. The answer:
For the same reason that Lewis gunners were taught to deal with stoppages by numbers, i.e., because the process must be done accurately and thoroughly, and usually will need to be done in conditions of hurry and perhaps some excitement. It is found by experience that the best preparation for such hurried work is constant practice under drill conditions, so that in an emergency the act is done rapidly, automatically and properly. The purpose of discipline is efficiency in action. A badly-put-on kit is dangerous by reason of the false confidence it engenders, and the unsuspected risks it exposes one to.
A Catechism of Air Raid Precautions, 1939
The handy, pocket-sized booklet lists instructions for decontamination and gas-proofing windows with putty and sticky tape; stuffing chimneys and sealing doorways; formulas for converting floor area to breathing-time in a sealed room; and drill procedures, decontamination depot design, and much more, all in 140 pages. The Home Office also produced pocket books on gas and gas defenses, as early as 1937.
This chapter was first sketched out in a time of war, a time when the excitable media were rattling on about stockpiles of cyanide shells and bioterrorists using cyanide in public spaces. In 1937, people seem to have been a little better informed:
In closed spaces [hydrocyanic acid] is extremely toxic; in the open, however, the dispersion of the gas is so rapid that relatively low concentrations result that are not lethal. This fact explains the failure of hydrocyanic acid gas shells in the last war in the open field, where they caused but few casualties.
Home Office, Medical Treatment of Gas Casualties, 1937
In 2000 it came out that members of the chemistry department at Cambridge University tested nerve gases and other chemical warfare agents on themselves during secret World War II experiments. Nature quoted chemist Fred Pattison, who went blind for ten days when his dosage was too high. “I thought I was permanently blinded,” he recalled. Pattison said everyone accepted the risks at the time, because they saw their work as part of the war effort and as something of national importance. One of the chemists involved in the Cambridge experiments said he shuddered to think what an ethics committee would say today about the research. But as another said, “It was war time. Everyone was taking risks. You were not offering yourself as sacrifice, but it took away the boredom of the war years in Cambridge.”
Perhaps there was more to it than that, because this sort of risk-taking seems to be something of a Cambridge tradition. J. S. Haldane rushed off to France for the postmortem of a victim of the first gas attack in World War I, a young Canadian officer killed by chlorine. On his return, his attic became a sort of gas chamber, where he and his son, J. B. S. Haldane, tested assorted toxic gases and gas masks of their own design. Haldane senior’s lungs were permanently damaged, but the household carried on blithely. His daughter Naomi (later the writer Naomi Mitchison) and their lodger Aldous Huxley shredded stockings, vests, Naomi’s knitted cap, and Aldous’s scarf to provide the absorbent filling for the prototype respirators.
In a letter to his father in June 1915, Huxley recounted how he “walked into some nitric acid, which one of Dr. Haldane’s assistants had put outside the lab and left in the pathway. It squirted over my foot and leg,” and while he did not notice it at the time, some 45 minutes later he suspected a fly bite and, later still, found a brilliant yellow stain on his heel and blisters. So it wasn’t just the Haldanes who bore the risks in their house. Huxley did report a small advantage a week later: the limp secured him a seat on a bus, he said.
Poison would be used in World War II in two main ways: in the gas chambers of the Nazi death camps, where cyanide and carbon monoxide took human lives; and in the form of DDT, which saved lives. There were, however, some deaths from mustard gas. In 1943, German aircraft bombed the John Harvey, a cargo ship moored in Bari Harbor, Italy. This ship carried 2,000 American 100-pound mustard bombs, and the resulting gas cloud caused 600 military casualties plus an unknown number of civilian casualties. There was reportedly a 14 percent fatality rate, mostly sailors who dived into the mustard-contaminated waters. They swallowed some and absorbed more through the skin, but they were the only combatants to die of recognized war poisons during the conflict.
Zyklon B, originally a pesticide, was the major poison killer of World War II, used by the Nazis to kill millions of Jews and other “undesirables.” There were a number of variants of Zyklon, but it was basically hydrocyanic acid on a carrier substance. As we have seen, this is ineffective in open spaces, but in the death chambers of the camps, it was very effective indeed, though it would have taken victims several terror-filled minutes to die.
The only seeming streak of humanity in the entire operation was the removal of the smell agent from the Zyklon B, which served to warn those using it to fumigate for pests of a leak. It appears, however, that this was an economy rather than an attempt to ease the victims’ pain. At Treblinka, a simpler method was used. Two engines from captured Soviet tanks were rigged up so that carbon monoxide poured into the death chamber, taking from 30 to 40 minutes to kill the unfortunates herded inside.
There are those who have denied that the horrors of the Holocaust happened, but contemporary evidence and reports from people who entered the camps during the war cannot be denied. There was simply no time to fabricate the evidence, though some still insist that the deaths in the camps were caused by typhus. It is true that typhus carried off many in the camps, but poison did for many more.
Oddly, typhus was the target of the third but less lethal use of poison in World War II, which, like the John Harvey incident, happened in Italy in 1943. A typhus outbreak among refugees in Naples led to 1.3 million people being dusted at the rate of 10 pounds to 150 people with a white powder that destroyed the lice that spread typhus. The lice were stopped in their tracks, no humans were harmed, and the powder was greeted as nothing less than miraculous. Winston Churchill said in September 1944, “The excellent DDT powder, which has been fully experimented with and found to yield astonishing results, will henceforth be used on a great scale by the British forces in Burma and by the American and Australian forces in the Pacific and India in all theatres.”
DDT is dichlorodiphenyltrichloroethane, which may be more easily read as dichloro-diphenyl-trichloro-ethane (real chemists don’t use hyphens, but I find it easier to understand that way). It was first made in 1874, but it was only in 1939 that Swiss chemist Paul Müller recognized its insecticidal properties. The toxic dose of DDT in humans is known to be greater than 10 milligrams per kilogram of body weight, and no human fatalities have ever been recorded. In one study, human volunteers took 35 milligrams per day for a year, with no demonstrable toxicity. Nobody knows to this day how it affects insects, but it probably acts on their motor nerve fibers or the motor cortex, changing the transport of sodium and potassium ions, the key process that makes up a nerve impulse.
Müller was awarded the 1948 Nobel Prize for Medicine or Physiology for his discovery of DDT, but before long the environmental damage that DDT causes started to become apparent. DDT is chemically stable, insoluble in water, soluble in fat, and some of it breaks down to DDE, dichlorodiphenyldichloroethylene. The real problem is in the fat solubility, because when one animal eats another, it retains its meal’s DDT and DDE.
The facts and figures are alarming. In one area of California, plankton had 4 parts per million of DDT, while bass in the same area had 138 ppm, and grebes feeding on the bass had 1500 ppm. For some reason, toxic concentrations affect birds and fish, especially in egg production. Human mothers exposed to 0.0005 mg/kg/day produced milk with 0.08 ppm DDT, so the infants were exposed to 0.0112 mg/kg/day/—a magnification of more than twenty-fold.
This has led to a murderous overreaction, with green groups demanding a total ban on DDT, but DDT is used in more than one way. Most DDT is used in wild and uncontrolled agricultural spraying, and this should be stopped as soon as possible. A far smaller amount is used in malaria spraying to kill mosquitoes, and so long as there is no other way to control malaria, this may need to be continued, even though it is undesirable. On the other hand, there is a minor application that loses almost no DDT to the environment: DDT-impregnated pads for mosquitoes to rest and die on.
When the DDT pads are used, if the dead mosquitoes are eaten by scavengers, some of the DDT will enter the food chain, but it is a very small amount compared with the amount spread all over the place by spraying, and it is essential that these pads continue to be made and used, perhaps with more creative management of the distribution and disposal of the pads—such as getting funding for a pad replacement scheme, where old pads are handed in and replaced with new ones. The problem is not DDT; the problem is the way it has been used.
When the POPs (Persistent Organic Pollutants) Treaty was being argued in 2000, Roger Bates of Africa Fighting Malaria, a loose coalition of DDT supporters in South Africa, said banning DDT now would be like “crossing a street with heavy traffic to avoid a crack in the pavement.” His group gained support from the World Health Organization, and in the end the treaty required registration of DDT use but did not ban it. This left the way open for Western aid organizations to bring pressure to bear on countries still using DDT, poisoning good science. Any such ban will almost certainly rule out DDT-soaked pads as well.
DDT may have been used successfully to save human life during World War II, but the same cannot be said of the other environmental poisons of the twentieth century—a list that includes PCBs, dioxins, furans, aldrin, dieldrin, endrin, chlor-dane, hexachlorobenzene, mirex, toxaphene, and heptachlor.
Two of these stand out as needing special discussion: the PCBs and the dioxins. Polychlorinated biphenyls (PCBs) are chlorinated aromatic hydrocarbons that were used in capacitors, transformers, plastics, and in other ways for half a century. There are more than 200 combinations, and most are made as mixtures. Generally, the more chlorine it contains, the more toxic the PCB will be. PCBs are everywhere, even in (or on) Arctic ice. For the most part, PCBs are bioaccumulated in seafoods, although there was a Japanese case where Yusho, or rice oil disease, was caused by rice oil contaminated with PCBs. More than 50 percent of the women affected gave birth to children with abnormalities, suggesting the PCBs may be fetotoxic. Recent studies suggest that at least part of PCBs’ toxicity may be due to dibenzofurans, relatives of the dioxins.
Dioxins are truly terrible. The devastation caused by Agent Orange may in fact be due largely to dioxin impurities that were not eliminated during the production of its main components, 2,4-D and 2,4,5-T. American forces used Agent Orange in Indochina during the Vietnam War, mainly to clear the jungle and deny cover to Viet Cong soldiers. This poisoned the trees, broke down the natural regeneration cycle of the rain forest, and triggered major ecological devastation, as well as leaving residues that affected not only the Vietnamese and the American forces on the ground but also the children born long after the war to all those touched by the sprays or by spillages.
In 1966, the United States argued that the Geneva Protocol of 1925, which banned poison gas and germ warfare, did not cover the use of riot control agents or defoliants, and this justified their continued use of the defoliants. In fairness, the prevalent scientific view at that time was that 2,4-D and 2,4,5-T were mere plant hormones and harmless to humans. How wrong we were!
Any dioxin poisoning in Vietnam was accidental and unintended, but it would probably help to clarify just what a dioxin is. Strictly, they are chlorinated dibenzodioxins, two benzene rings linked by two oxygen atoms and able to add up to eight chlorines. As more chlorines are added, there are more and more possible ways of arranging the atoms, up to four chlorines, and then the numbers fall away again. There are two monochloro or octachloro, ten di or hepta, 14 tri and penta, and 22 tetrachloro dibenzodioxins, one of which, referred to as 2,3,7,8 TCDD, is perhaps the nastiest.
Dioxins were shown to be hazardous to at least some mammals in the early 1970s, when many horses in Times Beach, Missouri, were poisoned because dioxin-contaminated oil was used to settle the dust in an exercise yard. Then, in 1976, somewhere between 2 and 7 kilograms of 2,3,7,8 TCDD escaped from a chemical plant in Seveso, Italy. This was when toxicologists discovered an interesting fact they could never have learned from experiments: humans are less affected than most other mammals by 2,3,7,8 TCDD.
After the escape at Seveso, rabbits, chickens, and wild birds died first, then larger animals, but no humans. Some women in the first trimester of pregnancy had terminations, but many did not, and there seems to be no evidence of any more abnormalities in the resultant children than you would expect to find in a random sample.
Biological and chemical weapons excite the righteous wrath of the world’s media, and we read time and time again of suspected terrorists with stocks of suspicious white powder, the favorite terror agent since the 2001 anthrax cases in the United States, where weaponized anthrax spores were sent through the mail to a number of outlets. The spores had been mixed with bentonite, and while U.S. law enforcement agents believe they know who was responsible, nobody has been charged, and the media’s initial reaction was that this was a typical Iraqi practice.
Such a claim conveniently overlooked the fact that bentonite is a clay mineral that can be bought by the barrel or even the container-load in Texas and Oklahoma, where it is mainly used to seal off old wells and stop surface water from contaminating the water table. Bentonite is also used in some medicines and in kitty-litter—it is not hard to obtain. Second, the strain of anthrax used was the Ames strain, a virulent form commonly found in American biowarfare labs and which also originated in Texas, but that is neither here nor there. Meanwhile, the white powder, which has assumed mythic importance, is not particularly Iraqi at all: it is merely a carrier that is effective in carrying anthrax spores up into the air, where they may be breathed in.
Anthrax occurs in many places around the world, and workers in a number of industries are likely to be inoculated already against the disease, which can, in any case, be counteracted with the antibiotic Cipro. A committed terrorist would have no problem preparing the anthrax white powder, even without a high-quality laboratory, but it is unlikely any anthrax attack would ever rate among the world’s great poisonings. Like the French cyanide shells, it would be one of the great poison flops instead.
The same applies to ricin, botulinum toxin, cyanide, and most of the other potential terror poisons as well, if they are sprayed. To be effective, poisons have to be limited to random attacks, a few here and a few there, to raise public fears, just as the U.S. anthrax attacks caused alarm and panic in many places, but killed very few. Mass murder brings terror, but random murder is more terrifying.
The Aum Shinrikyo sarin attack in the Tokyo subway in 1995 killed 12, but 1,000 more were affected. The 2003 invasion of Iraq, supposedly over chemical and biological weapons, saw none used by the Iraqis. It appears the world’s armies are wary of using poison gas in open warfare, though it seems to be more acceptable to use gas against those unlikely to retaliate in kind. When Saddam Hussein’s forces used gas against Kurds in northern Iraq, survivors who took refuge in Turkey were not examined for six weeks, but doctors found evidence of a vesicant like mustard gas and, from the survivors’ descriptions, concluded that a nerve agent was also used. Later, traces of mustard gas were found at some of the villages.
Gases and nerve toxins can have devastating effects, but the days of genocide through poison are now gone, for the single reason that it would be impossible to cover up such an event. A far more insidious and secret poisoner may be bacteria.
In their 2000 book Plague Wars, Tom Mangold and Jeff Goldberg claim that, during the apartheid era, the South African government’s agents may have killed as many as 200 of its opponents with food and drink laced with bacteria. Somebody knew what they were doing, because bacteria and small animals have been poisoning large animals and humans far longer than humans have been using poison.