“I’ve had 19 straight whiskies. I believe that’s the record.”
Dylan Thomas’s reputed last words, 1953
We talk happily of “intoxication” and “toxicology,” usually without making the link between the words, even if we have heard of “alcohol poisoning.” Alcohol is a poison, though one we have learned to deal with. We turn an enzyme called alcohol dehydrogenase on it, a protein that rips the alcohol molecule apart, taking away its poisonous power.
We can break down alcohol because bacteria in our intestines have been producing small quantities of alcohol over a very long time. On average, each day your stomach is delivered the alcoholic equivalent of half a pint of beer, and as this small dose seeps into your bloodstream, the enzymes attack it and render it powerless, stopping your otherwise inevitable internal pickling (and mine as well, for you are not alone in this). It is only a slow production of alcohol, though, which is probably just as well or the government would want to slap a tax on it. This bodily process explains why we can intoxicate ourselves with falling-down juice and still be conscious enough the next day to wish we were dead.
We have a secondary defense against alcohol; the ability to eject the contents of our stomachs when we need to get rid of something disagreeable. It’s an ability we share with our canine companions but one which we humans seem able to wear down with experience. Hardened drinkers such as the late Dylan Thomas can withstand the increase in acetaldehyde produced as the enzymes in their liver break down their overload of ethanol. In the end, the alcohol will kill them without being summarily thrown up and out.
People jokingly refer to alcohol as a poison, but in reality there is enough ethanol in a liter of spirits to kill most adults. Not everyone has the same form of the alcohol dehydrogenase enzyme. Native Americans commonly have a less efficient form of the enzyme, leaving them more susceptible to the intoxicating effects of liquor than others—the stereotypical “drunken Indian” of mid-twentieth-century cowboy movies was as much a victim of his genes as he was of the rotgut, or those who sold it.
More commonly, though, the usage is figurative. In The Tenant of Wildfell Hall, for example, Lord Lowborough declares he will give up alcohol: “‘It’s rank poison,’ said he, grasping the bottle by the neck, ‘and I forswear it.’” Some alcohols are more poisonous than others. Take Ginger Jake, for example, a popular substitute for liquor during Prohibition in the United States. This was an alcoholic extract of Jamaica ginger, and legally listed in the U.S. Pharmacopoeia as a cure for assorted ailments. It tasted so horrible that the authorities thought it would surely be safe enough to sell, but the poor bought it anyhow to satisfy their need for a buzz. Sadly, in 1930 one batch was accidentally adulterated with poisonous tri-orthocresyl phosphate. As many as 50,000 people were affected, their symptoms beginning with cramps and sore calf muscles but developing into a form of leg paralysis known and celebrated in song as Jake Leg.
Alcohol can sometimes make another substance even more dangerous. Some otherwise harmless fungi are toxic when ingested with alcohol—Morchella and Coprinus are two of them. Later we will look at some of the problems caused by various foreign substances in rum, beer, wine, and cider, but let us first consider other toxic beverages.
Benjamin Thompson is best known to physicists for his studies on the conversion of mechanical energy to heat, observed during the boring of cannon barrels, but this unusual polymath was never slow to label something a poison. An American self-made scientist and probable English spy who ended up as the German Count Rumford, Thompson denounced beer as a poison that was debilitating the German workers. He believed they would be better off drinking coffee, but he knew something had to be done about people spoiling the coffee by boiling it, so he invented the percolator. He might have been in favor of coffee, but he had severe reservations about tea:
When tea is mixed with a sufficient quantity of sugar and good cream; when it is taken with a large quantity of bread and butter, or with toast and boiled eggs; and above all, when it is not drank too hot, it is certainly less unwholesome; but a simple infusion of this drug, drank boiling hot, as the Poor usually take it, is certainly a poison which, though it is sometimes slow in its operation, never fails to produce very fatal effects, even in the strongest constitution, where the free use of it is continued for a considerable length of time.
Benjamin Thompson, Count Rumford,
Of Food and Particularly of Feeding the Poor, 1796
Thompson also offered a “Receipt for making brown soup.” Note the use of rye in the recipe, and his warning about copper poisoning, both of which we shall come across later.
Take a small piece of butter and put it over the fire in a clean frying-pan made of iron (not copper, for that metal used for this purpose would be poisonous);—put to it a few spoonfuls of wheat or rye meal; stir the whole about briskly with a broad wooden spoon, or rather knife, with a broad and thin edge, till the butter has disappeared, and the meal is uniformly of a deep brown colour; great care being taken, by stirring it continually, to prevent the meal from being burned to the pan.
Benjamin Thompson, Count Rumford,
Of Food and Particularly of Feeding the Poor, 1796
If G. K. Chesterton is to be relied on, it was the grocers, the people responsible for selling goods such as tea in bulk, who were the greatest poisoners, because of the adulterations they committed on the food they sold.
He sells us sands of Araby
As sugar for cash down;
He sweeps his shop and sells the dust
The purest salt in town,
He crams with cans of poisoned meat
The subjects of the King,
And when they die by thousands
Why, he laughs like anything.
G. K. Chesterton, “Song Against Grocers,” 1914
As early as 1612, the grocers themselves were complaining of others doing the same thing. The Master and Wardens of the Grocers’ Company of London were enraged about cheap foreign competition. They complained that “a filthy and unwholesome baggage composition was being brought into this realm as Tryacle of Genoa, made only of the rotten garble and refuse outcast of all kinds of spices and drugs, hand overhead with a little filthy molasses and tarre to work it up withal.” (Remember this “Tryacle” or treacle, because we will return to it in the next chapter.)
Take tea, for example: it was normal to find sulfate of iron in tea and beer; and ferric ferrocyanide, calcium sulfate, and turmeric would as like as not be lurking in Chinese tea. Spent tea leaves were sometimes refurbished, the appearance of the leaves being improved by a process called facing. This involved the agitation of the used leaves with soapstone and Prussian blue. Some of these substances might not strictly be poisons, but they weren’t exactly good for you either.
In December 1859, six people in Clifton, with no obvious connection to each other, suffered from the usual symptoms of poisoning by arsenic. Investigations revealed the source to be Bath buns. A local confectioner had used, or so he believed, chrome yellow (lead chromate), to give his buns a rich yellow color and make them more attractive, but the druggist had supplied him with orpiment or arsenic sulfide instead.
Lead chromate would not be a desirable additive from today’s perspective, but at least it was not absorbed, which was probably just as well, since it was commonly added to both mustard and snuff. Red lead was also added to snuff, and was responsible for Gloucester cheese’s nice red hue.
In truth, almost everybody was adulterating food, slipping “extras” into food and drink, or passing the extras off as food and drink. In one case, early in the twentieth century, an alleged cider was claimed to be prepared from concentrated apple juice. On analysis, the “cider” turned out to be sugar, fruit essence, and aniline dye, with not even a trace of apple juice.
The Black Book: An Exposition of Abuses in Church and State was published in London in 1832, and Michael Gilbert quotes the following alarming report:
We had a singular instance of this in the case of Mr. Abbott, brewer and magistrate, of Canterbury. This man had for a long time been selling, according to Lord Brougham’s statement, rank poison in the beverage of the people. It appears he had been selling a beverage resembling beer, manufactured from beer-grounds, distillers’ spent wash, quassia, opium, guinea pepper, vitriol, and other deleterious and poisonous ingredients. The officers of Excise having examined this worthy magistrate’s premises, found 12 lbs. of prepared powder, and 14 lbs. of vitriol or copperas; in boxes; which, if full, would have contained 56 lbs.
The Black Book, 1832
Sadly, Mr. Abbott was well-connected, and a fine of £9,000 was reduced to a mere £500. His friend, the Dean of Canterbury, pointed out that this was a matter that affected only ale-drinkers, clearly seeing this as an extenuating circumstance.
It seems almost everything was being colored in some fashion to make it more attractive to customers. Vegetable dyes were often used, but vegetables themselves might be colored with copper salts. Confectionery might include a range of chrome yellow, Prussian blue, copper, and arsenic compounds. Butter was colored with aniline dye, and today you can hear how devious dairy interests prevented margarine makers from coloring their product to look like butter—given the likely dyes, the butter makers probably saved the margarine eaters, even as they poisoned the butter munchers. Yellow was always a problem, particularly in yellow- and orange-colored sweets.
Aniline was also involved in a 1981 case in Spain, which has engaged conspiracy theorists for over 20 years. The official (and quite possibly correct) version is that cheap rapeseed oil containing denaturants was being sold for cooking, that it poisoned some 20,000 people and killed about 300. The figures may have been slightly inflated, as there was compensation money to be had if you claimed your illness or a relative’s death was caused by the toxic oil. There is some good circumstantial evidence for blaming the oil, but there are also quite a few oddities that make it possible to argue that the oil had nothing to do with it at all.
Rapeseed oil (canola oil to some) had been allowed into Spain for industrial uses, but it was required by law to be denatured by the addition of aniline to stop it from being used in place of olive oil. Some shady operators refined the oil and sold it from stalls in markets as cooking oil. The authorities claimed that aniline poisoned the consumers. Objectors, however, claim that there is no animal model for aniline poisoning, and the symptoms have not been reliably reproduced.
Medical and toxicological studies require a suspected disease-causing organism or toxin to be present in all reported cases, and it must be shown to have caused the disease. With a poison, it is usual to test the suspected toxin on animals, rather than humans, but no animal studies with the dubious rapeseed oil produced the same effects. Until you get that direct evidence, it is usual to keep an open mind, but, as we shall see, this was a most unusual case.
There may have been hereditary differences, or the aniline could have been interacting with something else in the victims’ diet—but it might have been something else. Most of the objectors believe the real cause was organophosphorus pesticide residues. It was easier, say the objectors, to blame the operators of small market stalls, leaving vegetable growers in the clear.
A Guardian article by Bob Woffinden claimed in 2001 that more than 1,000 died, and alleged scientific fraud on a grand scale. His case was a circumstantial one, and the logic is flawed in places, but he seems to have identified some interesting discrepancies in the official version—and quite a few unexplained smoking guns. The account below follows Woffinden’s outline.
The first diagnosis in the outbreak came when six members of the Garcia family were admitted to two hospitals in Madrid in early May of 1981, all apparently with atypical pneumonia. Dr. Muro y Fernandez-Cavada, the director of the Hospital del Rey, rejected the pneumonia diagnosis, arguing that pneumonia in so many family members did not make sense. Then, as more cases came in, all from the same area, he began to suspect food poisoning. Given the locations of the patients’ homes he suspected the cause was some food marketed through alternative routes, not the usual retail outlets.
This was a clever piece of epidemiological reasoning, and Muro and his colleagues came quickly to suspect the unlabeled bottles of cheap oil that they found on sale in the markets. They obtained samples from the homes of victims, and sent them for analysis. It was at this time that administrative paralysis began to set in. Dr. Angel Peralta, at La Paz hospital, suggested publicly that organophosphate poisoning was a likely cause. The next morning, he received a call from the health ministry, during which he was ordered not to say any more about the epidemic, and certainly not to mention organophosphates.
There is a remarkably distinctive smell emitted by fearful bureaucrats. It is acrid, rank, and seems to cling to the clothing and the hair. Acting like a pheromone, it drives senior management to form small defensive herds from which to scream homicidally at middle management that they must not tell junior staff who can fix the problem what is going on because everything, including what has just been reported on the radio, is secret.
Anybody who has been subjected to administrative paralysis would recognize what had happened to Angel Peralta: he had threatened some bureaucrat’s promotion chances. So of course he was warned off. When Dr. Muro announced, the very next day, that the outbreaks were market-associated, sterner action was needed and Dr. Muro was relieved of his duties as hospital director, a dead giveaway that administrative paralysis has been overtaken by administrative paranoia. Terrified administrators are, by their cultivated inaction, among the most poisonous objects known.
Almost a month later, the Spanish government declared that the contaminated oils were to blame, yet just the day before this announcement Muro and his colleagues obtained their analysts’ results. The oils may have been other than what they claimed to be, but they had different constituents, and therefore could not be the cause of the condition. The real cause was more likely something else, bought in the same markets.
To Woffinden, the real truth seems to be revealed in the pattern of hospital admissions, which peaked at the end of May, ten days before the oil was first officially blamed, and a month before the oil was withdrawn. In addition, the aniline-laced oil had been available for some time before the poisonings started, so what was the trigger? Enter Enrique Martinez de Genique, Secretary of State for Consumer Affairs. Like others, he drew up maps, and realized the same oil had been sold also in Catalonia, yet no cases of toxic oil syndrome had arisen there. In short, the oil could not be to blame, he said. Bad move. The first secret of success in a bureaucracy is not to rock the boat. Señor Martinez was sacked.
A husband-and-wife team of epidemiologists, Javier Martinez Ruiz and Maria Clavera Ortiz, had also mapped the disease distribution and noticed the Catalonian anomaly. They had been appointed to a commission of inquiry, they spoke out, they were sacked. Then, to make sure, the commission of inquiry was closed down.
All of this was circumstantial. What was needed was one case of toxic oil syndrome in a person who had been nowhere near the allegedly toxic oil. Woffinden cites two such cases: one, a woman whose oil came from the olive groves of her Andalusian relatives, the other a lawyer whose husband was certain they had only ever used reputable oils. The lawyer’s symptoms were identical to those of the main group of victims, but when it was realized her symptoms had developed 18 months before the main outbreak, she was removed from the list of victims.
Muro and his colleagues went to the markets, talked to stallholders and truck drivers, and concluded that the problems arose from tomatoes grown in Almeria, in the southeast of Spain. This is a dry area but, thanks to plastic tunnels and underground water and chemicals, remarkably productive. If the culprit was indeed organophosphorus poisoning, a reasonable case can be made for this as the source, but Muro died in 1985 and contaminated oil still gets the blame.
I generally prefer not to share the trail with conspiracy theorists and investigative journalists, because they draw bows too long for me, but Woffinden would appear to have outlined a case that is yet to be answered. Either way, members of the public were poisoned by something, but it appears the real poison here was a political fear of being found out, with a synergistic helping of administrative paranoia. If, as Woffinden avers and I suspect, the truth has been hidden, the poisoning could happen again.
There is a delightful case (for students of the matter, not the participants at the time) that was revisited in the Pharmaceutical Journal in 2001. Ian Jones describes the case of Humbug Billy, who accidentally poisoned some children in Bradford, England, in 1858. This character, more formally known as William Hardaker, operated from a stall in the Green Market in central Bradford, and he bought his candies ready-made from one Joseph Neale. They were humbugs, lozenges containing peppermint oil in, theoretically, a base of sugar and gum.
Despite the fact that the price of sugar had been falling steadily throughout the nineteenth century, it was still too high for the cannier confectioners, who eked it out with a filler known as “daft.” This was usually plaster of paris, powdered limestone, or gypsum, none of them particularly harmful. In this case, problems arose when a lodger of Neale’s, James Archer, made the five-mile trip to buy some daft. In the absence of the druggist, Charles Hodgson, Archer was served by his assistant Goddard, who gave him twelve pounds of arsenious trioxide by mistake.
In those days, there was no control over how arsenic was sold, as long as the sale was recorded, so the poison was held in the same stockroom as innocuous stuff like daft. This is how such errors occurred. Knowing no better, Neale used the arsenic to make up a fresh supply of candies, and when the sweets looked different, presumably because of the arsenic, he sold them at a discount to Humbug Billy.
Humbug Billy himself must have had a few doubts about the odd-looking sweets, as he tried one and was promptly sick, but a bargain is only a bargain if you sell what you buy, so he still sold them. The result was that he made perhaps 200 people severely ill, and killed 20. The death toll could have been much higher, but once the police realized the deaths were not due to cholera—as was first thought—they were able to trace the source fairly quickly. Goddard, Hodgson, and Neale were charged with manslaughter but were later discharged, and Humbug Billy, who should have known better, given his own illness, wasn’t even charged. Even when the pharmacists are taking care, poisoning and contamination can happen, but when people cheat, poisoning and death can happen and cover-ups are likely.
The price of sugar again featured in a case in Manchester, England, at the end of 1900, when local beer was found to contain arsenic. Tests later established that glucose had been used in the brewing. Sulfuric acid had been used to convert sucrose, normal sugar, to glucose, but the acid was prepared from iron pyrites rather than pure sulfur and this mineral was the source of the arsenic. The brewers would not have bothered if the price of sucrose hadn’t fallen so far that it was now an economical raw material. In short, a worldwide overproduction of sugar led to some 6,000 people being made ill and 70 dying in that single incident.
A consumption of six pints of beer a night was not uncommon, and that would have delivered 45 milligrams (mg) of arsenic. The lethal dose for an adult is typically estimated at about 200 mg, or a week’s drinking. After that incident, beer was tested more often, and chemist Sir William Tilden reports that in 1911–12, 1,046 samples of English beer were tested for arsenic. Only 18 of these exceeded the specified level of 1/100 of a grain of arsenious oxide per pound in solids, or per gallon in liquids. In these cases, Tilden believed that the arsenic came from the fuel used to dry the malt in the kiln.
In ancient Rome, soured wine was sweetened with lead acetate, and lead could still be found in drinks as late as the nineteenth century. In 1745, Thomas Cadwalader wrote his Essay on the West-India Dry-Gripes, an account of chronic lead poisoning from rum distilled through lead pipes. In 1767, Sir George Baker reported that Devonshire colic was due to the lead lining of the cider apparatus, but the time was not ripe for any centralized control of food, and the wicked grocers could continue to have their way. Taylor mentions deaths from lead contamination of Worcestershire cider as late as 1864.
A little earlier, in 1850, sugar refiners had proposed treating raw sugar with a salt of lead as part of the process of removing impurities from the juice of the crushed sugar cane. This use of lead was known in Egypt around AD 1000. The presence of lead could be detected by exposing suspect sugar near a privy. If the sugar was leaded, the lead salts would react with hydrogen sulfide to produce black lead sulfide (the same chemical reaction that powers lead-based hair dyes). The proportion of lead contained in sugar refined by this process varied from one-twentieth to one-tenth of a grain in a pound. The commissioners of Inland Revenue, considering that even this small quantity might affect the public health, referred the consideration of the question to three men: Pereira, Carpenter, and our old friend, Professor Taylor.
They concluded that even this small degree of contamination, in such a universal article of food as sugar, was objectionable, and that the use of lead should be prohibited as firmly as possible. In any case, it was not so much the quantity of lead taken that determined the symptoms of lead poisoning, said Taylor. Rather, it was its continued ingestion.
Taylor offered up this cheery tale of lead acetate contamination in bread as a salutary lesson:
. . . about thirty pounds of this substance were mixed at a miller’s with eighty sacks of flour, and the whole was made into bread by the bakers and supplied as usual to their customers. It seems that no fewer than 500 persons were attacked with symptoms of poisoning after partaking of this bread. In a few days they complained of a sense of constriction in the throat. . . . The mental faculties were undisturbed. Not one of the cases proved fatal, but among the more aggravated, there was great prostration. . . .
Lancet, May 1849
It seems the lead acetate was unevenly distributed in the bread, so we can’t be sure how much was consumed, but at least some of those affected must have been lucky. Still, lead was in more foods than people realized. Taylor mentions that pork was sometimes salted in leaden vessels, leaving a residue of lead in the meat. He also mentions that people were still adding litharge (lead monoxide) to sour wine, to give it a sweeter taste. In fact, this must have been fairly common.
Other common sources of lead in the Victorian era were vinegar, which might contain as much as 2 percent lead (along with small amounts of arsenic, copper, and sulfuric acid), and tobacco that had been packed in “patent tin foil,” in reality tin-coated lead sheeting that would leave a small amount of lead carbonate. Not all of the human lead dose came from food, because the lead industry has always been profitable and poisonous, as we will see in chapter 7. Water, too, would have been contaminated from traveling through lead pipes, but the lead would only have been an additional contaminant.
Once it is absorbed, 97 percent of the lead is taken up by the red blood cells, where it has a half-life in the body of two or three weeks. Some of it ends up in the liver or the kidneys, and some is taken up in hydroxyapatite, a mineral found in bones and teeth. That absorption means we can assess past exposure by X-rays of skeletons and teeth, while urine and blood analysis will reveal current exposures in the living.
We can also assess the lead loads experienced by humans of the past, when we come upon their remains. These days, the normal lead levels for the USA are in the range 0.15 to 0.7 micrograms per milliliter, with an average of 0.3 micrograms per milliliter. The threshold for toxicity is just 0.8 micrograms per liter, but biochemical effects happen at lower levels than this. In the past, many people operated at much higher levels.
Clean water sources will become increasingly important, and scarce, throughout the first half of the twenty-first century. In some parts of the world, unchecked population expansion will compel people to use more groundwater, and this may come at a price if more water is being drawn from the aquifer than is added, but there are other traps as well.
In Bangladesh, for example, overpopulation has resulted in grossly polluted surface water, leading to frequent bouts of dysentery and worse. Shallow wells tend to carry the same unpleasant loads as surface water: enter the World Bank and tube well technology. This method has several variations, but each of them results in a small-diameter tube dropping down into clean and unpolluted water. The water was, undoubtedly, clean in the germ-free sense and it was readily available, but it resulted in many Bangladeshis drinking water that well and truly exceeded the World Health Organization (WHO) guidelines for dissolved arsenic.
By the time this became apparent, in the early 1990s, some people had been drinking arsenical water for as long as twenty years. So why hadn’t anybody noticed? The short answer is that arsenic builds up in the system and the victims sicken slowly, with none of the sudden symptoms of classical poisoning you would see with a massive dose of rat poison. This buildup of arsenic caused slow, equally lethal damage to selected organs of the body, and a variety of cancers, but the level of medical support in rural Bangladesh was insufficient to detect the pattern.
The problem would have been picked up sooner in the developed world, where all deaths are looked at closely, as are certain sorts of disease. The results are plotted on graphs and examined closely by epidemiologists, to see if any patterns can be detected. This luxury is not available in the underdeveloped world, and the telltale pattern did not show up. To make matters more difficult, only tube wells drawing water from a depth of 65 to 200 feet carry heavy loads of arsenic and, even then, the dosage can vary markedly. As the water table rises and falls, the dosage may change again. In short, there was no smoking gun, no clear pattern to show up in the records in the far-off capital city, just dispersed illness and slow death from causes apparently unrelated to poison.
The poisoner in this case is nature, though plenty would like to blame the World Bank. The World Bank is a favorite target of activists, because so many of its plans are big plans, said to be unsuited to the developing world. On the subcontinent, the bank is not highly regarded, as Australian poet Mark O’Connor told me in 2003:
After lunch we drove out through the Prosopis thornbush to the Barefoot College, a famous grassroots movement that spreads practical technology in rural India. They told me firmly that they avoid troubling poor people with too much “paper-learning,” and they find the World Bank reports extremely useful—for turning into papier maché dolls for village children!
According to activists, tube well water was referred to at first as devil’s water, which they took to indicate some traditional knowledge of deep water being dangerous. There is no real evidence for this assumption, and it seems equally likely that it was so called only because it came from a considerable depth. The activists also say that when the problem was detected, cover-ups were attempted at first, and this does seem to have been the case.
You can cover up a one-off mistake but not an ongoing poisoning. An estimated 87 percent of Bangladeshis now have access to a tube well within 500 feet of their homes, and there may be as many as 10 or 11 million tube wells. A bad mistake has been made, which now has to be fixed. The mistake was a reasonable one, as the previous water sources were fecally contaminated surface pools, and about a quarter of a million children were dying each year from water-borne disease.
Groundwater had been used in the past, but it was taken from shallow “dug wells” that took only recent rainwater as it sank down, water lying in sediments leached clean of arsenic. Deeper down, the arsenic still has to be flushed out of the 65- to 200-foot sediments. Below 200 feet, the sediments are ancient, flushed, and largely safe. If there is extensive pumping from the lower levels, however, arsenical water will sink down to replace what has been pumped out. Cases of previously “clean” wells showing higher levels of arsenic are now being reported.
The most urgent needs to remedy the problem are: developing some sort of indicator paper that will reliably test water for arsenic content; developing some simple and robust means of clearing most of the arsenic from the water (clearing all of it would be better, but the chemistry means this is unlikely); and instigating a massive drive to sink more deep wells that will draw safe water. There is also a need for consensus on the reason why the water from 65 to 200 feet contains so much arsenic: it is probably a matter of air getting into the soil and releasing the arsenic, but it may also have something to do with fertilizers and organic matter added to the soil.
So where does the arsenic come from? Geologically, Bangladesh is a broad swathe of sediment, and groundwater drifts slowly through it on its way to the sea. Some of the sediment is old, some of it is recent: the older sediment has had most of the arsenic taken out, while any arsenic in surface sediments has long since interacted with air in times of drought, or with organic matter, and turned into soluble arsenic that has leached away.
The piece that is still to be fitted into the puzzle is establishing the actual cause of the release at this time. There is quite a lot of arsenic in the Earth’s crust, often found as arsenopyrite in iron pyrite rocks. This is the form in which it is present beneath West Bengal. One widely held theory is that as groundwater is pumped out and the water table is lowered, air infiltrates the sediments, oxidizing the arsenic sulfides and releasing the previously insoluble arsenic in soluble forms. The concentrations are still low, but after an outbreak in Taiwan, the WHO revised its maximum limit for arsenic in drinking water from 50 milligrams per liter to 10 milligrams. To find the Environmental Protection Agency’s (EPA) current maximum level for arsenic (and other contaminants) in the United States, go on the Web to www.epa.gov and search under “water.”
There are ways in which contaminated water can be treated to bring it within the strict WHO guidelines. For example, carrying and storing water for about three hours in a plastic jerry can that contains a small packet of iron filings will generally remove most of the arsenic, and the packet of filings can be used for 100 days before it has to be replaced. Trials of this method in Nepal gave disappointing results, however, probably because of low sulfate levels in the water. In such cases the addition of small amounts of gypsum (hydrogenated calcium sulfate) may be needed. In laboratory tests, the presence of a sulfate in the water enhanced arsenic removal, while a phosphate suppressed it.
Nature’s additives were sometimes augmented and the unpleasant items in your drink put there deliberately. The most common example of this was sailors shanghaied onto ships. Charles Dickens introduces us to such practices as “hocusing”:
“Nothin’ at all, Sir,” replied his attendant. “The night afore the last day o’ the last election here, the opposite party bribed the barmaid at the Town Arms, to hocus the brandy-and-water of fourteen unpolled electors as was a-stoppin’ in the house.”
“What do you mean by ‘hocusing’ brandy-and-water?” inquired Mr. Pickwick.
“Puttin’ laud’num in it,” replied Sam. “Blessed if she didn’t send ’em all to sleep till twelve hours arter the election was over. They took one man up to the booth, in a truck, fast asleep, by way of experiment, but it was no go—they wouldn’t poll him; so they brought him back, and put him to bed again.”
“Strange practices, these,” said Mr. Pickwick; half speaking to himself and half addressing Sam.
Charles Dickens, Pickwick Papers, 1837
The practice of using knockout drops, Mickey Finns, or whatever, is by no means a new one, and laudanum was not the only poison available. In India, says Taylor, the seed of the datura was commonly used, though once in a while the poisoner ended up caught in his own trap:
Bassawur Singh, a professional Indian poisoner, ate some of the poisoned food to lull suspicion. In due course, his victims fell insensible, and he robbed them, but after they came around and reported the theft to police, the thief was found about a mile away, quite insensible—and he never came around. All the stolen property was recovered, along with a supply of seeds.
Alfred Taylor, Principles and Practice of Medical Jurisprudence, 3rd edition, 1883
There are two species, he tells us, Datura stramonium and Datura alba, and he explains that the bitter taste was often hidden by serving the drug in a curry “or in some other highly-flavored article of food.” The Thugs of India, he notes, commonly use the seeds of D. alba.
Another drug used in England for hocusing was a decoction of the levant nut, Cocculus indicus. This was also sold mixed with grain as “Barber’s poisoned wheat,” but there was another cunning use of the poison, extracted from the plant’s berries. Porter, ale, and beer sometimes owed their intoxicating properties to this extract, a practice of which Professor Taylor clearly did not approve:
The fraud is perpetrated by a low class of publicans. They reduce the strength of the beer by water and salt, then give to it an intoxicating property by means of this poisonous extract. A medical man consulted the author some years since in reference to the similarity of cerebral symptoms suffered by several of his patients in a district in London. It was ascertained that they were supplied with porter by retail from the same [public] house.
Alfred Taylor, Principles and Practice of Medical Jurisprudence, 3rd edition, 1883
In short, some people were getting a different poison, picrotoxin, rather than ethanol in their beer, producing symptoms similar to those of drunkenness, but far more cheaply, and free of any excise. Those poisoned want to sleep, yet at the same time they are beset by wakefulness and a heavy lethargic stupor. They retain a consciousness of passing events, but feel a complete loss of voluntary power, according to Taylor. Slipping foreign material into food was something of an art in the nineteenth century, but almost everywhere you turned then, you were beset by poisons.
Anamirta cocculus (paniculata)
Strange foods have always posed a problem for travelers, where there was no precedent, no standard way of dealing with them. When he was visiting Australia in 1770, Joseph Banks noted how the crew had been so long at sea “with but a scanty supply of fresh provisions that we had long usd to eat every thing we could lay our hands upon, fish, flesh or vegetable which only was not poisonous.” Later, he recorded his experiences with seeds of a cycad, which he believed would be safe to eat, going on the evidence of them being eaten regularly by the locals:
By the hulls of these which we found plentifully near the Indian fires we were assurd that these people eat them, and some of our gentlemen tried to do the same, but were deterrd from a second experiment by a hearty fit of vomiting and purging which was the consequence of the first. The hogs however who were still shorter of provision than we were eat them heartily and we concluded their constitutions [were] stronger than ours, till after about a week they were all taken extreemly ill of indigestions; two died and the rest were savd with difficulty.
Joseph Banks, Journal, 1770
Banks was unaware of the proper methods for preparing the seeds. He learned better when he called at Prince’s Island (Pulau Panaitan), on the way to Sumatra:
Their food was nearly the same as the Batavian Indians, adding only to it the nuts of the Palm calld Cycas circinalis with which on the Coast of New Holland some of our people were made ill and some of our hogs Poisond outright. Their method of preparing them to get out their deleterious qualities they told me were first to cut the nuts into thin slices and dry them in the sun, then to steep them in fresh water for three months, afterwards pressing the water from them and drying them in the sun once more; they however were so far from being a delicious food that they never usd them but in times of scarcity when they mixt the preparation with their rice.
Joseph Banks, Journal, 1770
Rule number 1, then, is to assume that the food may need some preparation; rule number 2, to assume the locals know what to do; and rule number 3, to make sure you find out what they do. Ludwig Leichhardt, the Australian explorer, described the preparation of Cycas in these terms:
I also observed that seeds of Cycas were cut into very thin slices, about the size of a shilling, and these were spread out carefully on the ground to dry, after which (as I saw in another camp a few days later), it seemed that the dry slices are put for several days in water, and, after a good soaking, are closely tied up in tea-tree bark to undergo a peculiar process of fermentation.
Ludwig Leichhardt, Journal of an Overland Expedition in Australia, 1846
Leichhardt would try foods found in the crops of parrots he shot, assuming that what was safe for them might be safe for him. With some birds, this could be a little risky, given that cassowaries in northern Australia eat the blue fruits of the cassowary plum, Cerbera floribunda, with impunity because the poisonous seeds pass through with no harm to seed or bird. An examination of a dead cassowary’s crop might easily suggest, falsely, that the seeds were harmless.
Around 2,000 plant species contain the cyanogenic glycosides found in Cycas, so when the plant cells are crushed, wilted, or frozen, enzymes are released that hydrolyze the glycosides to cyanide. Examples include sorghum, corn, some of the clovers, and, in particular, cassava. The glycoside in cassava is called lina-marin. If untreated cassava is eaten, this will cause a disease known in rural Nigeria as konzo. Over time, people there have learned to leave cassava to soak for some days to allow the lina-marin to be broken down, either by enzymes in the cassava or by lactobacteria.
Konzo causes irreversible paralysis of the legs. The name means “tired legs,” because of the ways the knees are drawn together. Typically a person with konzo walks leaning over backward, but some of the worst-affected children can only crawl. One of the challenges facing agribiologists at the moment is to breed a strain of cassava with reduced amounts of linamarin while still retaining the disease resistance, high yield, and palatability of the original forms.
The science of the nineteenth century concentrated on identifying and detecting poisons; that of the twentieth century on developing antidotes to and syntheses of organic poison. The science of the future will be aimed at decreasing the natural and synthetic poisons in our foods and environments.
Before we look at poison as medicine, with its accompanying risk of “kill or cure,” it would perhaps be advantageous to investigate the science of poison through the ages.