Oh what can ail thee, knight-at-arms,
Alone and palely loitering?
The sedge has withered from the lake,
And no birds sing.
John Keats, La Belle Dame sans Merci, manuscript version, 1819
After gaining her verdict of “Not Proven,” Madeleine Smith moved to London and married Pre-Raphaelite artist and designer George Wardle. She was welcomed into those circles, and when George Bernard Shaw met Lena Wardle later, he found her to be a pleasant woman, not at all sinister, he said. She and Wardle had two children but separated after 28 years of marriage. She went to America a few years later and eventually married again and lived in New York, where she died in 1928.
This is not quite as surprising as it might first appear. Poison—real as well as figurative—seems to feature quite a lot in the arts, a notion that would surprise very few who have ever been involved even peripherally with art critics or arts administrators. Madeleine probably met Elizabeth Siddal among the Pre-Raphaelites, at least fleetingly, but she would have known many others in her husband’s circle of acquaintances who worked with poisons every day. Many of those she knew were, in all probability, at least slightly poisoned by their materials and their studios.
Painters generally use mineral-based pigments for the same reason that Schweinfurter green was so popular. Vegetable dyes fade within only a few years, while minerals are usually much more stable. They might weather and break down in the field, but those bound up in oil on canvas are well able to survive in the shelter of the average home or art gallery. There is just one small catch: as a general rule, colored inorganic compounds are toxic, and artists must risk being poisoned to create great and lasting art.
One of these poisonous colors was minium, but its contents changed over time. The ancient Romans obtained their minium from Spain. The name came from the Basques, who used this word for red mercury sulfide. Others called it cinnabar, a Persian name that came into Latin via the Greeks. Minium came into the English language later, but by then the name was attached to red lead, Pb3O4, a useful color when red letters were required to mark something special—a rubric, from the Latin for “red.” The verb for doing this sort of illustration was miniate, and the result was a miniature. Of course, the same practice also gave us “red letter days.”
Chromium compounds, including lead chromate, yielded oranges, yellows, and some greens; cadmium compounds covered the reds and additional yellows; white lead, otherwise known as lead oxide, gave a nice matte white surface; while vermilion is just cinnabar by another name. Naples yellow contained lead and antimony, and so the list progresses, a spectrum of heavy metals. (Some mineral pigments are less stable than others, however. The white lead base has proved a problem in some old masters, because it slowly combines with atmospheric pollutants that contain sulfur, changing to black lead sulfide.)
Unscrupulous apothecaries might mix brick dust with vermilion, and so turn a handy profit, or they might sell azurite as the far more precious ultramarine, so the early artists needed to be passable alchemists, buying and grinding minerals to fine powders, making sure they were the right minerals, and concocting systems to carry them and hold them on a canvas. Even today, some chemistry is needed: for example, Prussian blue breaks down in alkali, which means it cannot be used in an acrylic paint. With all the dust that was blowing about in their studios, it is hardly surprising that painter’s colic, colica pictorum to the Latin-favoring doctors, was known as far back as the eighteenth century. In 1767, Benjamin Franklin mentions having seen a list of tradespeople suffering from colic in Paris:
I had the Curiosity to examine that List, and found that all the Patients were of Trades that some way or other use or work in Lead; such as Plumbers, Glasiers, Painters, etc. excepting only two kinds, Stonecutters and Soldiers. These I could not reconcile to my Notion that Lead was the Cause of that Disorder. But on my mentioning this Difficulty to a Physician of that Hospital, he inform’d me that the Stonecutters are continually using melted Lead to fix the Ends of Iron Balustrades in Stone; and that the Soldiers had been employ’d by Painters as Labourers in Grinding of Colours.
Benjamin Franklin, letter to Benjamin Vaughan, 1786
As recently as 1962, the brilliant (if slightly mixed-up) Brazilian artist Candido Portinari died of lead poisoning from the lead-based yellows and whites he used. In 1948, he had used an arsenic-based paint and ended up in hospital. This is not why I call him mixed-up, though—Portinari was an atheist who painted saints, a communist who painted the official portrait of a dictator, and an excellent artist to boot.
These days, artists are generally more aware of the poisons that surround them. There is evidence that such an awareness has been around for a while, but it was not enough to safeguard Raphaelle Peale, an important American still-life painter of the early nineteenth century. Peale’s father owned a natural history museum where Raphaelle was the taxidermist. His father believed Raphaelle’s physical and emotional problems were caused by gout and drink, but a combination of arsenic and mercury poisoning seems more likely. Yet Raphaelle was well aware of the dangers of the arsenic that was used to protect the stuffed birds from pests, and posted signs in the museum reading, “Do not touch the birds, they are covered with arsnic [sic] Poison.” He lived from 1774 to 1825, which was not excessively bad in those days, but not outstanding, either.
The dangers of working with lead were well-known as far back as Roman times. The Roman writer Vitruvius mentions them, and it is significant that the patron god of metalsmiths was Vulcan. Like their patron, Roman metalsmiths were often lame, pallid, and wizened, but it was lead that made them so, not a kick from one of Vulcan’s parents (there are conflicting versions on whether it was Jupiter or Juno who lamed Vulcan). This would also explain why lead was the metal associated with Saturn in Roman mythology. The association was with both the god and the planet, and so we sometimes come across references to “saturnine poisoning,” which is just lead poisoning with social-climbing tendencies.
While the Romans agreed that lead was dangerous, they seemed to think small doses did no harm. The slaves who mined the lead might die—not those who ingested it through their food and wine. This may have been selective blindness, a bit like the attitude of Victorian industrialists to the plight of their poisoned workers, but neither case can be excused.
Hippocrates described a case of lead poisoning in 300 BC, and Dioscorides left us a detailed account of lead poisoning and the paralysis it caused. In it, he mentions lead fumes, and refers to molybdania, probably litharge (lead monoxide) and minium, red lead oxide. By the nineteenth century, lead was taking on an altogether more sinister role, at least in the industrial nations. Artists and philanthropists such as Robert Sherard and H. G. Wells spoke out about the evils of lead, even as everybody else tried to ignore them.
Sherard was a journalist and social campaigner who wrote for Pearson’s Magazine and later published his work as The White Slaves of England, where he looked at some of the degrading trades that English workers were subjected to. We do not have the space to describe the plights of the nailmakers, slipper-makers, tailors, woolcombers, and chainmakers, but let us spend some time with the alkali workers and the white-lead workers, for here we will see a clear and dreadful picture of what it was like to work with poison.
Sherard got very seriously up the noses of the industrialists who believed it was their social and moral duty to make obscene profits. Like today’s economic rationalists, they believed all social ills could be remedied if a few people became vastly wealthy. As they spent their money, everybody would benefit from their largesse trickling down the economic chain. The only flaw in their master plan was that for them to become very rich in the first place, a lot of people needed to stay very poor, very diseased, or very dead. People like Robert Sherard were determined to expose them for what they were. He was unwelcome—in fact, in The White Slaves, Sherard shares some of the viler attacks made on him for “scurrilous dickturpinism,” libel, and worse. The factory owners were unlikely to give such a troublemaker easy access to their workers, and a foreman told Sherard there had been too much written about them.
The lead works are carefully guarded. High walls surround them like prisons, whilst each entrance is watched by yard policemen. The things that are done here are not for the public eye. A stranger could more easily obtain permission to visit the Tsar’s palace of Gatschina than a laissez-passer for most of the factories in Newcastle where white-lead is made.
Robert Sherard, The White Slaves of England, 1897
Nonetheless, Sherard managed. On one occasion, he interviewed the doctor who looked after the factory workers. The doctor had no doubt about the effects of lead:
For checking a too rapid growth of the population, indeed, nothing better could be devised than the employment of women in the white-lead factories, for the lead woman—according to Doctor Oliver’s long experience—almost invariably miscarries, while if the children are born, very few of them live.
Robert Sherard, The White Slaves of England, 1897
The dangers of lead for pregnant women and their babies are borne out by evidence from Italy, gathered in 1930. In Milan, where miscarriage rates were around 4 to 4.5 percent for the whole population, the wives of printers showed a miscarriage rate of 14 percent, and women printers an appalling 24 percent. In 1930, the average death rate for the first year of life was 150 per 1,000; for the babies of women associated with printing, it was 320 per 1,000. A few years earlier, in Japan, a researcher had found that male lead workers in storage battery plants had 24.7 percent sterile marriages (against 14.8 percent for a non-lead group), with 8.2 percent of pregnancies ending early or in stillbirth, against 0.2 percent in a control group.
Sherard describes how workers would be examined for signs of plumbism, lead poisoning, and ordered away from work if the telltale signs presented.
. . . there are certain signs which unmistakably betray lead-poisoning, and the most important and sure of these is the appearance of a blue line on the gums. This blue line, by the way, may be noticed in about 75 per cent of lead-workers. It is due ... to the action of sulphuretted hydrogen upon lead circulating in the blood, and has been noticed well-marked in girls who have only worked one week at the trade.
Robert Sherard, The White Slaves of England, 1897
Those laid off would do the reverse of malingering to get back to work, even applying to another works under a false name, because their own name would be on the blacklists circulated by the factory owners. Given the choice between a quick death by starvation and a slow death by poisoning, most opted for the poison.
One woman, Sherard said, told him that dangerous as the lead work was, it was either that or go on the streets, “and we prefer anything to dishonour.” But powerful as his arguments were, he was mostly preaching to the converted, to those already aware of the evils their society imposed on its weaker victims. It needed a popular writer of fiction, such as H. G. Wells, to reach a wider audience. In his powerful The New Machiavelli, Wells described lead palsy in such terms that the housewives of Britain began to demand “fritted ware,” rather than the traditional pots and crocks. To make a fritted glaze, the lead is added before fusing and forms largely insoluble lead silicate and lead borosili-cate. The risks to both the makers of the crockery and its users were considerably lessened.
Wells’s finely honed prose exposed the factory owners and their attitudes to the public’s gaze. This was not the dickturpinism that Sherard was accused of—this was dickensism, pure and simple. Take Richard Remington, for example, a future politician, who is learning about the real world from his uncle, who owns a pottery where plumbism was rife.
‘None of your gas,’ he said, ‘all this. It’s real, every bit of it. Hard cash and hard glaze.’
‘Yes,’ I said, with memories of a carelessly read pamphlet in my mind, and without any satirical intention, ‘I suppose you MUST use lead in your glazes?’
Whereupon I found I had tapped the ruling grievance of my uncle’s life. He hated leadless glazes more than he hated anything, except the benevolent people who had organised the agitation for their use. ‘Leadless glazes ain’t only fit for buns,’ he said. ‘Let me tell you, my boy—’
He began in a voice of bland persuasiveness that presently warmed to anger, to explain the whole matter. I hadn’t the rights of the matter at all. Firstly, there was practically no such thing as lead poisoning. Secondly, not everyone was liable to lead poisoning, and it would be quite easy to pick out the susceptible types—as soon as they had it—and put them to other work. Thirdly, the evil effects of lead poisoning were much exaggerated. Fourthly, and this was in a particularly confidential undertone, many of the people liked to get lead poisoning, especially the women, because it caused abortion. I might not believe it, but he knew it for a fact. Fifthly, the work-people simply would not learn the gravity of the danger, and would eat with unwashed hands, and incur all sorts of risks, so that as my uncle put it: ‘the fools deserve what they get.’ Sixthly, he and several associated firms had organised a simple and generous insurance scheme against lead-poisoning risks. Seventhly, he never wearied in rational (as distinguished from excessive, futile and expensive) precautions against the disease. Eighthly, in the ill-equipped shops of his minor competitors lead poisoning was a frequent and virulent evil, and people had generalised from these exceptional cases. The small shops, he hazarded, looking out of the cracked and dirty window at distant chimneys, might be advantageously closed.
H. G. Wells, The New Machiavelli, 1911
Wells slips in a reference to a “sickly-looking girl with a sallow face, who dragged her limbs and peered at us dimly with painful eyes. She stood back, as partly blinded people will do, to allow us to pass, although there was plenty of room for us,” obviously assuming his readers would know that lead poisoning can lead to blindness. The damage was to the nerves, and a British study in 1910 showed 7.7 percent of women potters with lead poisoning went blind, while 10.2 percent had some significant loss of vision, and 14 percent a slighter loss.
White lead used to be made by the Old Dutch process, where strips of lead metal are buried in spent tanbark (or horse dung) and doused with acetic acid. Lead acetate forms, and as the tanbark ferments it produces carbon dioxide, which converts the acetate to the carbonate. It was not until the 1940s that British Australian Lead Manufacturers (now Dulux) developed a safer way of making white lead, by exposing finely divided lead in rotating barrels with acetic acid and horse dung and tanbark, but in the bad old days the workers needed to remove the strips of lead from their acidic mulch by hand and scrape off the white lead crystals.
The chemistry is fairly straightforward. The horse dung and tanbark fermented, producing heat that evaporated the acetic acid, which reacted with the lead to make lead acetate. The fermentation also produced carbon dioxide, which reacted with the lead acetate to make white lead.
Those who jumped from the frying pan of England’s factories into the fire of World War I experienced their own curious form of poisoning: recruits from lead pottery areas suffered a typical lead colic as a result of an exhausting military drill. The lead stored in their bodies had been released by stress and made them ill. After the war, it would be noted that the stress of infection or alcoholism could trigger acute lead poisoning in exposed workers, and cases of acute lead colic commonly appeared on Mondays after weekend excesses, but this was wartime, and normal exertions were damaging soldiers who needed to be fit enough to go over the top, and take their dose of ballistic lead—but here they were, complaining of colic! If it was going to affect the war effort, Something Had To Be Done.
By 1916, the use of lead in potteries had finally become the subject of official concern. Four classes of glaze were established as standards. A “leadless” glaze contained less than 1 percent lead (calculated as metallic lead); the next class had less than 2 percent soluble lead monoxide; the next less than 5 percent soluble lead monoxide; and the last group gave no account of their lead content and solubility (and presumably included those with more than 5 percent lead).
In 1916, Sir William Tilden reported with some pride that the British government was purchasing only leadless glaze, or glaze in which all of the glaze lead was “mainly in the insoluble condition,” that is, fritted ware. This specification applied to telegraph insulators, glazed bricks and tiles, and sanitary and domestic ware, and it had a marked effect in driving manufacturers to meet the required standards.
After the war, however, a new problem had to be overcome: swords had to become ploughshares once more, as battleships were laid off and cut up during 1921. Between their gray paint and the steel, there was a protective coat of red lead, but if the steel had been protected at sea, the workers in the breaking yards were not. This red lead episode was over before the red lead’s cumulative effects were sufficient to energize official intervention, but lead would play its part in a brand-new era of motor transport. In 1921, the same year the battleships were disappearing, Thomas Midgeley, Charles Kettering, and Thomas Boyd found that adding tetraethyl lead (TEL) to motor fuel reduced engine knock. The Ethyl Corporation was soon formed as a GM subsidiary, and the automotive industry took off, especially in the United States.
More roads, wider roads, better roads opened up, only to be filled with more and more vehicles, all spewing out the lead that had been added to their fuel. Market gardens near highways grew lead-spattered lettuce, people living near roads breathed fine particles of lead—it was everywhere. By 1924, the first warning sign appeared when Midgeley himself fell ill from working with TEL, but it was not sufficient to ring alarm bells.
By 1925, health checks on garage workers who manually added the TEL to fuel showed that the exposed workers were adversely affected, but chauffeurs and other garage workers seemed to be unaffected. It was agreed that the gasoline should be supplied already blended, and that the containers should carry warning signs, indicating that their contents were unsafe for cleansing and dangerous if spilled on the skin.
In 1926, a Surgeon General’s inquiry was rushed through in seven months. It reported that there were no good reasons to ban the use of TEL, provided there were proper regulations, and it would be almost 50 years before lead levels would be grudgingly reduced, microgram by microgram.
Robert Sherard identified other poisons too, such as chlorine. Spring, he wrote, never came to Widnes or St. Helens, the centers of the alkali trade, because the foul belching gases killed every tree and blade of grass for miles around. Farmers complained so often of their crops being ruined by fumes that the factory owners found it cheaper to buy up the affected land than to pay for the damage. Trees cannot live in this wasteland, Sherard said, “but men must and do.”
Surprisingly, the evidence against chlorine was hard to find. Dr. O’Keefe, who treated the St. Helens workers for over 30 years, told Sherard the alkali trade was an unhealthy one, even though the statistics failed to show it. “The chemical yard only kills a man three parts out of four, leaving the workhouse to do the rest.” The good doctor conceded that sulphuretted hydrogen was “a terribly poisonous gas, and but one of several which in these alkali works shorten life.”
He tried to look on the bright side. “There is this, however, to be said in its favour, that if it poisons men, it poisons microbes also, and its effect is to minimise contagion by fever. We have but three patients at present in the fever hospital.” Dr. O’Keefe did, however, note that few men got above 60 years of age. It is difficult to see a bright side in conditions such as these:
Roger is their best joke, as Roger is their worst enemy. Roger is the chlorine gas, which, pumped on to slaked lime, transforms this into bleaching powder. Roger is a green gas, and is so poisonous that the men (packers) who pack the bleaching powder after the process into the barrels in which it is exported work with goggles on their eyes and twenty thicknesses of flannel over their mouths, these muzzles being tightly secured by stout cords. They can pack but a few minutes at a time. A ‘feed’ of this gas kills its man in an hour.
For all that, Roger is the butt, not the bogey. True, that at the cry ‘Roger is coming! Clear lads!’ so frequently heard in the works, a wild sauve qui peut of panic-stricken men may be seen scurrying before a green, perceptible, and palpable fog borne on the wind, but all the same, once the danger is past, Roger evokes smiles.
Robert Sherard, The White Slaves of England, 1897
To be able to joke about “Roger” makes it clear that these men had little else to laugh about, but they retained a clear vision and black humor about what was being done to them. One of the men explained to Sherard how easy it was for the factory owners to manipulate the statistics. “It’s like this. You get gas. We run to the office for the brandy bottle and say, ‘So-and-so’s got gas.’ Brandy is served out. You go home and die. Doctor says you died of faint, and the proof is that brandy was needed to revive you.”
We will return to chlorine when we examine its use as a calculated weapon of war. It was the same gas, just with a different motivation. For now, however, let us close with one of Sherard’s finest lines:
In Wiston Workhouse is a legless man, with whom an armless man keeps company. They were both alkali workers.
Robert Sherard, The White Slaves of England, 1897
One of the saddest and most unnecessary forms of profit-hungry poisoning was the condition commonly known as “phossy jaw.” It was seen first in the manufacture of Congreve matches—matches named after the famous Congreve incendiary rockets and packed with white phosphorus. These fire-starters were also called Lucifers, though Lucifer was originally the name of a potassium chlorate device with no phosphorus.
There was a long gap between the first reported case of phossy jaw, that of Marie Jankovitz in Vienna in 1838, and the eventual phasing out of the white phosphorus matches in 1906. The first London case was recorded in 1846, and Boston’s first case was recorded at about the same time. Cases were reported regularly thereafter, but not one of them need ever have happened, if a small invention of 1824, a clever use of catalysis, had taken off:
Amongst the ingenious novelties of the present day is a machine . . . for the purpose of producing instantaneous light; which appears to be more simple, and less liable to be put out of order, than the Volta lamp, and other machines of a similar kind. It has lately been discovered that a stream of hydrogen gas, passing over finely-granulated platinum, inflames it. The whole contrivance, therefore, consists in retaining a quantity of hydrogen gas over water; which is perpetually produced by a mixture of a small quantity of zinc and sulphuric acid, and which, being suffered to escape by a small stop-cock, passes over a little scoop, containing the platinum, which it instantly inflames. From this a candle or lamp may be ignited . . . it forms an elegant little ornament—of small expense, and easily kept in order; and, once charged, will last many months.
The Gentleman’s Magazine, September 1824, p. 259
Matches, however, were cheap, as were workers, and platinum was expensive—and to ignite the hydrogen, nothing else would really do. So matches needed to be made, but the phosphorus problem could have been dealt with as soon as it surfaced, if anybody had cared. By 1845, the safer red allotrope had been identified, and by 1855, a Swedish researcher had developed a match based on this safer form.
By 1898, phosphorus sesquisulfide, P4S3, was being used for matches in France, and finally, in 1906, the Berne Convention banned the use of white phosphorus. Only the United States failed to sign this convention, citing constitutional grounds, but in 1913 the U.S. Congress imposed a punitive tax, through the Esch Law, on white phosphorus matches and so eradicated them by making them as expensive as phosphorus sesquisulfide matches.
We should not be excessively harsh on the manufacturers. After all, phossy jaw killed relatively few. It started usually with a headache and was an extremely painful condition. There was a foul fetid discharge from the jaw and sufferers had such “garlic breath” that they were shunned by their fellows. It caused a raging thirst, led to grotesque disfigurement, and was a chronic condition. It might not have killed many, but most of its sufferers might have welcomed death.
Phossy jaw was called “the disease,” “the flute,” or “the compo,” from the composition paste used to make match heads. Each year, composition paste in Britain absorbed 60 tons of phosphorus, and the workers absorbed an unknown amount of this mass of poison. More importantly, individual factories varied widely in their ventilation and in the mortality rates of their workers. We must assume that there was either a different morality in those days of stern Victorian scrupulous church-going, or that the factory owners were remarkably myopic.
In 1862, Britain’s Privy Council commissioned a report on match factories that recommended better ventilation and hygiene and separate rooms for workers to eat in, but this was not enforceable by law, and its recommendations were largely ignored. There could be little doubt phosphorus was a poison: the lethal dose of white phosphorus for an adult is about the same as in a box of matches.
In Britain phosphorus was used to murder family, friends, enemies, and potential postmortem benefactors until 1963, the year in which Rodine (a paste of bran and molasses containing 2 percent phosphorus, and the most common phosphorus poison) was banned under the Animals (Cruel Poisons) Regulations. It was none too soon, whether for animals or humans.
Mercury poisoning is also hard to miss, and mercurialism was known to the Romans as a disease of slaves, because only slaves were used in the Spanish mercury mine of Almaden. The emperor Justinian considered a sentence to work there tantamount to a sentence of death, and so unpleasant was the death that Plutarch criticized a mine owner who used slaves in mercury mining who were not convicted criminals.
The subject was raised again in the 1500s, when Andrea Mattioli described mercurialism, and another Italian, Giovanni Scopoli, described the condition at Idria in 1761. By then, some had been trying to counter mercurialism for just under a century: in 1665, a short working day had been instituted for Friulian mercury miners, who had to work just six hours a day. This was the first known law to enforce industrial hygiene anywhere in the world. It took over 200 years for this initiative to be finally adopted at Idria, in 1897.
Most people know mercurialism as a disease of hatters, though the connection is a curious one, known long before Tenniel drew his famous Mad Hatter for Lewis Carroll. Hatters used the mercury in the felting process, to make the fur fibers stick together to form felt.
There is a pretty legend that Saint Clement, later the patron saint of hatters, was on a pilgrimage to Jerusalem. He is said to have lined his sandals with camel hair to ease his feet and, over time, the combination of heat, sweat, and pressure formed a sheet of felt, which was transferred to the head as hatting. This may be news to the makers of Kyrgyz yurts and Mongolian gers, both traditional felt tents.
I doubt that Saint Clement’s method would have been used to make hats, given the combined odors of camel and human sweat that would have impregnated the felt, but we do know that even before 1685 hatters in Paris were using mercuric nitrate in a process they called carroting, because it gave an orange color to the fibers. The process was a trade secret within the hatters’ guild, because the key to persuading the fibers to hook up to each other is to roughen them. This makes the fibers limp and twisted, so as they are cut and blown onto a cone-shaped form and then pressed down with a hot wet cloth, they stick to each other.
The mercuric nitrate solution is still known in France as le secret, and the process of felting with mercuric nitrate le secretage. After the revocation of the Edict of Nantes, in 1685, thousands of Protestants, Huguenot hatters among them, were forced out of Paris, many of them taking refuge in England. The use of the solution persisted across Europe into the early twentieth century, and even later in Russia, but there is now a nonmercurial method of felting, and, with luck, mercury has been phased out everywhere.
In the days when mercury vacuum pumps were used to exhaust the air from lightbulbs, spillages were common and mercurialism was rife in the lightbulb industry. Mercuric fulminate was used to set off explosions in guns and rockets, while calomel (HgCl) was used in tracer bullets. Both caused quite a few problems for munitions workers in World War II, although nothing near as nasty as those experienced by an unfortunate Allied airman who was struck by a phosphorus tracer bullet. The missile dissolved in his body and poisoned him.
Most metals used in industry have their own special quirks. Antimony is used in alloys, including the lead in storage batteries, paint, glass, pottery, varnish, and tartar emetic—a poison that provokes vomiting and so sometimes negates other poisons. Large amounts of arsenic are used each year, not only as a poison in herbicides but also as animal feed additives.
Poisonous substances sometimes only act as poisons when they are applied in the right way. If a child bites on a thermometer and swallows the mercury, no great harm will be done by the metal (the glass may be more of a worry), as it will pass straight through and out of the body. On the other hand, the same amount of mercury in the form of mercury salts would be absorbed far more effectively and be far more dangerous. If the same amount of mercury went down the throat each day, there would be a progressive buildup. Surprisingly, the contents of the thermometer are far more dangerous if they are spilled and go into a carpet or floor cracks, as this will establish a low but dangerous level of mercury vapor in the air. About the only thing that would make the situation worse would be to try and clean the spill up with a vacuum cleaner.
About this time, the thoughtful reader with dental fillings may be wondering about dental amalgam. For about a week after getting a silver amalgam, the patient has raised mercury levels in the urine, but it is always within safe levels and falls away. In simple terms, the amalgam is a potential threat to dentists and their assistants if it is used carelessly, but not to patients. This has led to three court cases seeking damages from the American Dental Association being thrown out in 2003 as having no merit.
In one of the cases, a New York Supreme Court judge dismissed two of the suits against the American Dental Association because the complaints showed no “cognizable cause of action.” The ADA hailed this, not surprisingly, as “a victory for dentistry and science over superstition and hearsay.”
One of the most deadly of poisons, in terms of the number of its victims, is an alkaloid that is legally sold all over the world without any permit being required. Charles Lamb knew it for what it was:
Stinking’st of the stinking kind,
Filth of the mouth and fog of the mind,
Africa, that brags her foyson,
Breeds no such prodigious poison,
Henbane, nightshade, both together,
Hemlock, aconite—nay, rather,
Plant divine, of rarest virtue;
Blisters on the tongue would hurt you.
Charles Lamb, “A Farewell to Tobacco,” 1811
There can be few lethal substances as easily purchased as nicotine, and few poisons that bring in as much revenue to governments, though sometimes this may be a poor bargain: in 1993, China’s tax revenue from tobacco was estimated at 41 billion yuan, while the estimated costs of smoking illness and death totaled 65 billion yuan. This, of course, is an underestimate, because the true costs of today’s smoking will only show up in two or three decades.
In 1995, a quarter of all deaths in the United States and 14 percent of the deaths in Europe were smoking-related, but, in theory, the effects should be far higher. A single cigarette contains sufficient nicotine to kill a person if it were extracted and injected, yet no smoker dies of acute nicotine poisoning, because of the way it is taken in and filtered by the lungs. Direct skin contact is a different matter.
In one nineteenth-century case, a smuggler covered his skin with tobacco leaves in order to defraud the revenue. The leaves were moistened by his perspiration and he developed all the symptoms of acute nicotine poisoning. Even today, itinerant farm workers in North Carolina develop a form of acute nicotine poisoning, green tobacco sickness, each year.
The modern condition typically occurs after pickers are exposed to wet tobacco leaves, either early in the morning or after rain. Being an alkaloid, the nicotine in the leaves is rapidly absorbed through the skin. As an industrial disease, the condition was first recorded in 1970, and is exacerbated during the harvest by a process called priming, when workers break off the ripe leaves and hold them under their arms as they move down the rows. As the day progresses, say researchers, the workers’ shirts and skin grow stiff with sticky—and poisonous—tobacco juice.
The region known medically as the axilla, described quaintly in one research study as “the area under the shoulder joint” and known in more robust circles as the armpit, absorbs more chemicals than other skin areas. It might be worth publicizing this condition more widely, both to alert workers to the problem and also to alert smokers to just what it is they are putting in their mouths, and where it has been.
So long as there is enough of a poison, it can kill, even a poison that is a natural part of the atmosphere. Take carbon dioxide, for example. In August 1986, Lake Nyos in Cameroon became unstable for some reason. There was an eruption of carbon dioxide gas from deep in the lake, and once an upwelling had started, it was like a bottle of champagne blowing its top. Enough carbon dioxide poured down into the valleys below the lake to smother 1,700 people.
The geophysics behind this sort of eruption is remarkable. The lake is in a volcanic area, and it is about 200 meters deep, with an unremarkable upper 50 meters of ordinary water over a CO2-rich lower level, where the gas is concentrated but remains dissolved because of the greater water pressure. In the depths of the lake, this saturated water is quite stable, but bring some up to a higher level and a few gas bubbles can start to form. As these rise, some more of the saturated water is carried up and more bubbles form.
As the new bubbles rush to the surface, they push water in front of them, and water rises behind, until the trickle of bubbles turns into a torrent, a huge fountain of gas and gas-soaked water, roaring to the surface, splashing high into the air, and releasing its load of heavy gas, where it forms a spreading blanket that can smother life. The carbon dioxide soon reaches the rock wall that holds the lake in place, and plunges over, an invisible and deadly torrent of gas, sweeping down into the valley below.
After its outburst, the lake settles again. Over time, more and more carbon dioxide would seep into the water from soda springs fed by volcanic fissures deep in the lake, until the whole bottom area was unstable, and the slightest swirl enough to form a few stray bubbles and send the geyser up, creating another murderous cloud capable of killing all before it. But no more. In February 2001, a 14.5 cm diameter polyethylene pipe was sunk into the lake, to a depth of about 7 meters from the bottom. This is now being used to bleed off the gas, hopefully keeping it below the unstable point, and plans are in place to add extra pipes.
These pipes will, I hope, be in action soon, as the lake is held in place by a natural dam of loosely packed volcanic rock and waterfalls run over the edge in the wet season. This wall is heavily eroded, and the top 40 meters could fail at any time. This would certainly trigger a catastrophic degassing—as well as flash floods in populated parts of Nigeria, 150 km from the lake.
Tests in 2003 showed the carbon dioxide levels were falling slowly, and a report in Science indicated that nearby Lake Monoun was also to be “bled,” and engineers were trying to work out if Lake Kivu, between Rwanda and the Democratic Republic of the Congo, could also be drained of its gases—Kivu contains large amounts of flammable methane as well.
Carbon dioxide might be a suffocating agent rather than a poison, but the end result is the same.
Carbon monoxide (CO) is a true poison, and a highly effective one because it is colorless, odorless, tasteless, and non-irritating, so it sneaks up on its victims. Unlike oxygen and carbon dioxide, the CO molecule takes hold of our hemoglobin molecules and will not let go. The stability of the resulting carboxyhemoglobin unit means that no oxygen is carried to the cells. Within a few minutes, our brains are so starved of oxygen that we become brain-dead before we die. Carboxyhemoglobin makes the skin and internal organs go bright red. The absence of this coloration has trapped many a murderer who thought that smoke and flames would cover up the evidence of their crime. A dead body, planted at a fire scene, will not have the bright red blood of a genuine fire victim who has been asphyxiated.
Inhaling CO from car exhausts is a common method for suicide in Australia. Accidental deaths are common in the United States, which uses more fuel-burning heaters. This is not a new problem. A 1935 study in Philadelphia revealed 95 cases of coronary thrombosis during autumn and winter, and only 14 in spring and summer—the difference was attributed to the increased use of CO-producing fuels and poor ventilation in the cold months.
Traffic also generates huge amounts of CO, and toll collectors can be at risk, as can ordinary pedestrians. In 1962, during an oil importation crisis, the only traffic in London was diesel-powered. Diesel produces very little CO, and the measured levels fell almost to zero, except in smokers, who get sublethal doses of the poison from the partial combustion of their tobacco.
CO’s effects must have been known before people realized that it was formed when carbon-based fuels burn in low oxygen supplies. While a wood fire dies down comparatively fast, a coal fire is slower, and may exhaust the available oxygen, explaining this reference:
It was then believed that sea or pit-coal was poisonous when burnt in dwellings, and that it was especially injurious to the human complexion. All sorts of diseases were attributed to its use, and at one time it was even penal to burn it. The Londoners only began to reconcile themselves to the use of coal when the wood within reach of the metropolis had been nearly all burnt up, and no other fuel was to be had.
Samuel Smiles, Industrial Biography, 1863
Sea coal was so called because it was carried to London from the mines in the north by ships; while plain “coal” in that period was charcoal. The preponderance of coal fires, however, contributed to London’s smog problem, yet another mass killer in its time. The Great Smog of London in December 1952 is credited with killing 4,000 people and led directly to the Clean Air Act that stopped the pea-soupers that had made life so easy for villains like Jack the Ripper.
Toxic gases can harm by mischance, with no ill will involved, but there are those who feel that Union Carbide was taking advantage of the ignorance of those living around the site when they built their factory in Bhopal, India. These unfortunates would become the victims of one of the worst chemical leaks in recent years. The factory made carbaryl, a general-use pesticide, but the actual leak was of an intermediate product, methyliso-cyanate. Little was known of its toxicity, which did not help in the treatment. As we know now, it is a toxic and corrosive gas, and in December 1984 a large amount of it, probably 30 or 40 tons, escaped into the atmosphere. The poison leaked for three hours before it was shut off, which points to remarkably sloppy management. The number of dead will never be known, but an Indian court’s estimates were of 3,000 dead, 30,000 with permanent injuries, 20,000 with temporary injuries, and 150,000 with minor injuries. Other estimates list 7,000 deaths at the time, rising over two decades to a toll of 20,000, with 100,000 victims left chronically ill. As of this writing, the site is still contaminated and toxic materials have leached into the water supply, poisoning drinking water for local residents.
Not only in the United States but around the world, Love Canal is synonymous with “toxic waste dump disaster.” There have been other cases in other countries, but few have had the ramifications of Love Canal, which was used as a dump between 1942 and 1952 for 22,000 tons of chemicals that, in the lab, would require labeling as hazards. Mercaptans, phenols, chlorobenzenes, and other nasties were dumped at this site, close to the Niagara River in the city of Niagara Falls, New York.
The Love Canal was a clay-lined hole in the ground that seemed ideally suited for dumping waste, but trouble came after 1953, when development of the 16-acre landfill and its surroundings added a school and 200 homes, which meant digging, and breaching the seals on the toxic waste below. During the 1960s, people noticed unpleasant smells, and toxic chemicals were found in nearby waterways. In response to public outcry over this and other hazardous waste emergencies, Congress passed the Superfund law in 1980. The idea was that polluting companies would be forced to clean up their own sites, but the law also provided for a general fund to be created from targeted industry taxes.
By 2004, some $400 million later, Love Canal was off the Superfund list, with a 40-acre site sealed and capped, and with controls in place to trap any leaching. The toxins will remain until they are released by some future ice age, but by then humans will probably be long gone, and other species will reap our harvest. In the interim, the area has been declared safe, and houses that once had to be evacuated are able to be sold again.
Across America, only about 1,300 of the worst locations are officially listed as Superfund sites, and about 900 of these are regarded as close to fixed. That said, there are probably still 100,000 sites, large and small, across the U.S., where some sort of remediation is required. Many of these will be dealt with through bioremediation, where German fungi consume asbestos, weeds clear lead from soil in Hartford, Connecticut, bacteria in a Wisconsin mine take zinc out of solution, tailored bacteria being developed in Baltimore tear apart noxious PCBs, and brake ferns in Florida strip arsenic from contaminated ground. In others, well, we just don’t know what will happen.
All in all, toxic waste dumps don’t sound like something you would want near human habitation—yet every city has one, somewhere, and people have to live with them. In 2000, the Sydney Olympics were held on the remains of a toxic waste dump, and while it was no great secret, nobody really cared, because even before Sydney was awarded the Olympics in 1993 plans had been under way to solve the problem. The polluted soil would not be carted away to create a hazard somewhere else: it was bulldozed up into large mounds.
You might be forgiven for asking, “But how would this solve anything?” It works like this. Water seeps down through such hills, leaching out the poisons they contain. So the next step is to put in a drainage system that catches this seepage and returns it to the mound. Then each hill is completely covered in plastic, to stop excess water penetrating the polluted levels, and the plastic is covered in a thick layer of clean soil. The pollutants are thus stabilized and contained, for the present, but at some time in the future, when bioremediation is available, tough microbes will be sent in to shred the poisonous molecules, one by one. Poisoning can be undone, but only at a cost far greater than the profit some slick operator made by dumping the waste in the first place, for which we all pay.
Then again, organisms are sometimes excellent at protecting themselves against poison, using all sorts of biochemical tricks. Evolution sees prey developing ever better poisons, so as to discourage predators. As a rule, the more toxic something is, the more likely it is to survive and breed. This in turn means predators must also evolve, because only those consumers able to withstand or deflect the poisons survive.
Arsenic is the fourteenth most common element in the Earth’s crust, and many organisms, including humans, need a defense against arsenic. Accordingly they have developed the detoxifying trick of biomethylation, that is, adding one or more methyl groups (CH3) to heavy metals and making the metal easier to excrete. In the last half century, we have learned that, in addition to arsenic, selenium, mercury, tin, lead, bismuth, and antimony are also methylated under natural conditions. While this may help an organism to get rid of them, most of these methyl adducts are very toxic when they are disposed of—as we saw in chapter 6, methylation of the arsenic in Schweinfurter green may have killed Napoleon. And it was most certainly the methylation of mercury that did the harm at Minamata, and made the name of a bay a synonym for mercury poisoning.
At Minamata, in Japan, a paper mill released methylated mercury salts that got into the human food chain and harmed many, but even natural background mercury can be a problem. In the 1960s, Hydro Québec built a number of new dams to generate hydroelectricity, as did other Canadian provinces. Not long after, the local Indians began to show signs of mercury poisoning. These were people who typically ate a lot of fish, so the fish in the dams were tested and found to be overloaded with mercury. This puzzled the authorities, because these dams were in pristine wilderness, not downstream from factories spewing toxic effluent. Only four years after a new dam had filled, most of the fish in it were at or above the Canadian safe limit for mercury (0.5 parts per million), but explaining where it had come from involved some clever geology and physics.
Since the last Ice Age, Canada has acted as a mercury sink, a place where traces of mercury, vaporized in warmer places, settled out, like the condensation of water on a cold bottle. The mercury found its way into the soil and plants, mainly as relatively harmless inorganic salts. When the lakes created by the dams filled, large amounts of mercury went into solution quickly. In the deeper waters, the dead vegetation on the flooded ground made conditions oxygen-free and perfect for mercury methylation, driven by anaerobic microbes, to occur. Once the methyl mercury was in the water, it was concentrated up the food chain, until pike showed levels well in excess of the safety limit, and people eating the pike started to be affected.
The solution was to empty the lakes and refill them, flushing away the mercury, which was, after all, limited. When the lakes refilled, the lake waters returned to safe levels, and so did the fish, but the damage was done so far as people were concerned, because they were well and truly poisoned.
Whatever poison you care to nominate, there is always something worse, and it may be hiding in something as innocuous as a motor vehicle’s airbags. These contain sodium azide, NaN3, and each vehicle contains around 250 grams of the white, salt-like material. To inflate the bag, an electrical heater breaks the sodium azide down to sodium metal and nitrogen gas, but if the sodium azide comes in contact with water, hydrazoic acid, HN3, is released.
In the ground, low concentrations of sodium azide—as little as 200ppm—can sterilize the soil. In a worst-case scenario, the contents of an average car would produce enough hydrazoic acid to put 5,000 people in a coma, and while it should never come to that, it might. Sooner or later, a car fitted with airbags will go into a wet crusher, or some sodium azide will be spilled into a waterway. In 1996, a truck carrying 50 44-gallon drums of sodium azide overturned and burst into flames 50 miles south of Salt Lake City, Utah. A huge plume of toxic vapors went up, forcing the evacuation of 2,000 people from the small town of Mona, Utah. The same plume in a city would be a much more serious problem. Sodium azide is a disaster waiting to happen.
Around the world, stores of poison are waiting to wreak havoc as people go about their daily business of making a profit. In 1995, 3 million cubic meters of waste water containing cyanide and copper spilled into the Essequibo River from a dam at a mine in Guyana, South America. In 1998, heavy metal pollution from a Spanish mine damaged wildlife in the Guadiamar River and the Doñana National Park. The 1990s also saw cyanide spills in Latvia and Kyrgyzstan, but these were nothing compared with a spill on the night of January 30, 2000, at Baia Mare in Romania.
Cyanide is commonly used to separate gold from tailings left at old mines, but the cyanide sludge is typically left in a dam—and dams fail. The Baia Mare dam did just that, and around 100 million liters of waste water poured northward down the Somes River into Hungary and the Tisza River. The Somes and Tisza were scoured of all life by the torrent of heavy metal–and cyanide-laden water as it started its three-week journey of 1,000 kilometers—a journey that would take it down the Danube all the way to the Black Sea, and leave in its wake a trail of dead fish and less visible but more deadly disruption to the entire ecosystem. Plankton, invertebrates, the 400 protected otters on the Tisza, and the local eagles—all will be affected for years to come.
Cyanide levels in the Tisza River were measured at 12 milligrams per liter, 100 times the level for a “very polluted river,” and well above the European Union’s safe level for drinking water of 0.05 milligrams per liter. Copper levels were reported at 36 times the “very polluted” level. Over time, the rivers have begun to recover, but Hungarian scientists warn that it is only a matter of time before such a disaster happens again. Most of the water in Hungary’s rivers originates in other former Soviet-bloc countries, and their banks are lined with old mines, chemical factories, and worse.
In August 2002, it looked as though they were about to be proven horribly right, as 100-year floods rolled through Europe for the second time in a decade. We have been poisoning our atmosphere in a gentle way with carbon dioxide for hundreds of years, despite Swedish chemist Svante Arrhenius’s warnings in the 1890s that this would lead to global warming. Some said that it was still open to doubt, that maybe the thermometers were wrong. But by 2002, few could question that global warming was real, that our climate was changing.
Suddenly, people began to think of what sat on the river banks—all the great rivers of Europe were being flooded with dioxins, mercury, arsenic, lead, and bacteria from sewage, and they in turn were flooding the great cities of Europe. The owners of the Spolana chemical plant at Neratovice, north of Prague, went into overdrive, denying that any of their stored unpleasantness could have or had ended up in the River Elbe, but environmentalists were less sure. Unfortunately, the environmentalists were right, and tons of hazardous chemicals were washed into the mines and released into the air. The effects are still being measured today.
In the nineteenth century, and even into the twentieth, the new industrialists could get away with wholesale pollution; they could dump waste into rivers in an out-of-sight, out-of-mind approach. Dye makers, paper mills, slaughterhouses, foundries—factories of all sorts just pumped the waste into the nearest river through underwater pipes to allow the current to dilute the waste and disappear it. People took this in their stride; but in the 1960s, when people finally began to question the status quo in almost all walks of life, Rachel Carson published Silent Spring. Industrialists have been forced, over the past 40 years, to modify their existing practices and initiate new drives toward bio-mimicry rather than biocide.
Once it took many years for a new poison and its risks to be identified, but now, if anything, we are too quick to label something as evil and toxic. There is a middle ground to be found, somewhere between allowing the profit-hungry to destroy this earth and letting the media-hungry destroy our lives and our joy in life. The question, though, is whether that middle ground encompasses the official use of poison.