The dose makes the poison, Paracelsus once said. And there is no truer statement about the nature of poisons. The toxicity of many medicinal substances were discovered only when a slip of the hand or experiments driven by curiosity revealed the lethality of these substances in large (or, in the case of antimony, small) quantities. It is perhaps fitting then, that this next section be dedicated to the classical 'ancient' poisons, whose properties were discovered in centuries past, and which have endured to present time as the poisoner's choice of homicide weapon.
Please note that in the biological context, poison usually refers to substances that cause injury, illness or death to organisms by chemical reaction or molecular activity, while toxin refers to naturally produced substances that will kill quickly in small quantities. (These include both plant and bacterial substances, such as belladonna and botulinum toxin). However, for the poisoner and toxicologist, both terms are synonymous as substances that, when administered, bring an unnatural end to life, and that is how it will be considered in this article.
The superstitious called it wolfsbane, leopard's bane, women's bane, Devil's helmet, blue rocket. The Greeks hailed it as the Queen of Poisons, created from the saliva of three-headed Cerberus, mythical guardian of the underworld. And until the 20th century, it was the deadliest toxin known to man.
The name aconite is derived from the garden plant monkshood, Aconitum anglicum, whose leaves and root yield its active ingredient, a potent alkaloid called aconitine, which was frequently used to poison the tips of hunting darts or javelins. Until its toxic properties were discovered, tincture or liniment of aconite was used to relieve sciatica, neuralgia and rheumatism, for the heat-production and mild anaesthetic properties of the potion gave comfort to many an aching joint. However, its popularity took a plunge when it was discovered that the mere rubbing of preparations on skin produced symptoms like poisoning by ingestion, and thereafter was sought primarily by those who had more sinister uses for the plant. The author Nicander of Colophon (fl 130 BC) said of aconite toxicity:
'It is established that of all poisons the quickest to act is aconite, and that death occurs on the same day if the genitals of a female creature are but touched by it.'
In solid form, aconite is a white powder with no definite crystalline structure, which will only dissolve in alcohol and weak acid. One-fiftieth of a grain is deadly; at one-tenth of a grain, it will stop anything living. Even a weak thousand-fold dilution produces discomfiting tingling sensations where it is applied.
The poison works by targetting the cardiovascular and central nervous system, and gastrointestinal tract. The aconite alkaloids modify the cell membrane to sodium and potassium ions, inhibiting repolarisation, activate the sodium channel, and affect the excitable membranes of cardiac, neural and muscular tissue.
The poison takes effect quickly. The victim will experience numbness and tingling in the mouth and throat within minutes of consuming the poison, both of which will feel parched. If the dose is large, it produces a severe burning sensation from throat to abdomen. The tingling feeling soon spreads to the hands and feet, and subsequently the whole body; the skin and extremities cold and clammy to the touch; yet at the same time the victim will feel as though his limbs are being flayed. This is followed by a loss of power in the legs and the dulling of sight and hearing, although the victim will be clear-headed until death comes. Muscular twitching may result in convulsions, the pulse will weaken and pupils dilate, and the slightest exertion brings a fatal syncope. Acotine will poison all organs in turn, but death is usually from failure of the respiratory system – between eight minutes and four hours after the symptoms begin.
The name antimony is derived from the Greek word anthemonium, which means flowerlike (referring to the shape of the crystals). It is fitting a name for something once used for delicate purposes – ancient Egyptian women used it as cosmetic for darkening their eyelids and eyebrows, under the name stibium. One Urs-maat-Ra princess who probably fancied herself as an experimenter fed her handmaid an oral dose – and that was how the ancient world came to realise that stibium was a deadly poison.
In its natural metallic state, antimony is often mixed with arsenic and silver, and the greatest problem in purifying the metal in the past was getting rid of the arsenic. The extracted metal is often obtainable as tartar emetic (antimony tartrate), a white powder which leaves a strong taste of metal in the mouth.
The early Romans found great use for antimony in their gourmand practices. The metal was fashioned into little goblets, which would be filled with wine and left to ferment on the banquet table. When a bloated reveller had eaten all he could, he would simply reach out for the emetic cup and take a swig of the wine – whereupon he would throw up all the food in his stomach, thus making room for more gorging.
The reason why merrymaking Romans were able to go on partying into the night instead of collapsing dead on the banquet table was that, although antimony is highly poisonous in small quantities, a dose of more than one grain at a time induces severe vomitting, causing the poison to be ejected before it can do harm. However, if repeated low dosage of antimony is administered, it will produce the symptoms of poisoning with a strong irritant. Indeed it is because of this that antimony was favoured by poisoners of old who wished to kill their victims without attracting attention, as the symptoms of antimony poisoning were compatible with common diseases of the stomach.
The typical symptoms of antimony poisoning are as follows: a burning sensation in the throat and difficulty in swallowing, followed by violent stomach pains, incessant vomitting and diarrhea. This is accompanied by fainting and extreme depression brought on by the victim's premonition of death. The pulse accelerates, but the decrease of blood pressure eventually causes the pulse to become slow and irregular. The victim will perspire profusely, and his skin will be cold and clammy to the touch, with the extremities exhibiting cyanosis. Sometimes cramps in the calves lead to spasmodic contraction. Vertigo and repeated syncope eventually causes loss of consciousness. Death comes as a result of heart failure.
If aconite is the Queen of Poisons, then arsenic, which has probably claimed more victims than any other poison, would be King. Occurring commonly in many living organisms – especially fish and crustaceans – and in ores, coal and soil, arsenic is a metallic ore once thought by alchemists to be a source of gold. (And indeed it is, to many poisoners). Although it was administered1 as yellow sulphide in the old days, it is more commonly found in its white oxide form. Its production involves roasting the metallic ore, putting the product into a vessel and applying even greater heat to form a deadly vapour that condenses as heavy white powder or a crystalline mass.
Although arsenic is poisonous at high levels, we are constantly exposed to low levels of the metal. The average person ingests about 8 mg of arsenic daily, and the toxin finds its way into the blood, heart, lungs, liver, hair and fingernails. The lethal dose is 0.6 mg per kg per day – which means that the ingestion of 42 mg in a day would bring down a 70-kg adult.
The symptoms of arsenic poisoning vary according to dose and form. However, the typical symptoms are: initial irritation and burning sensation in the throat, faintness, nausea and depression accompanied by sickness. This is followed by the regurgitation of food, and subsequently mucous specked with blood. Abdominal pain follows, which may be aggravated by the merest touch, and which feels as though red hot coals have been applied to the stomach. By now the victim experiences throat constriction, and the tongue is covered by a layer of white 'fur'. Within 12 to 18 hours the symptoms progress to violent diarrhoea accompanied by pain – especially from the cramp in the calves – and tenesmus. The pulse becomes weak, rapid, and irregular. By this stage, collapse will come rapidly, and the patient dies while still conscious. There is a marked manifestation of cyanosis, caused by lack of oxygen, and post mortem will reveal that the lining membrane of the stomach is badly inflamed and ulcerated.
The popularity of arsenic as a murder weapon lies in its virtual tastelessness (its reported faintly sweet and metallic taste is easily masked by food) and its cumulative effect, especially in the kidneys and liver, which means that a victim may be slowly fed small doses until there is enough poison to strike a fatal blow. It also does not matter how the arsenic is administered – however you do it, the results are the same. Furthermore, its symptoms resemble cholera and dysentery, thus causing many a homicide case to be misreported as food poisoning.
And what's more - never was there a more widely used poison in domestic life in the history of civilisation, especially during the Victorian age. Arsenic was in flypaper and curtains, in fabric and floor covering, in ornaments, in candles and tobacco. It was virtually everywhere, and in practically everything, that even if you could not walk right up to the apothecary to buy a pound of arsenic powder (which you could), you could always find it someplace else.
Said William Farr, the statistic head of the General Register Office, in 1840:
'It is generally asked for to kill 'rats', but it is questionable whether arsenic kills more rats than human beings.'
Because of the unnerving rise in the number of arsenic homicide cases in England during the 19th century, the government was driven to introduce the 1851 Arsenic Act, which forbids the sale of arsenic compounds unless the purchaser was known to the pharmacist. Moreover, manufacturers were required to mix each pound of arsenic powder with one ounce of colouring (soot or indigo), which further made it difficult for poisoners to slip arsenic into food and beverages.
Found naturally in the stones of cherries, plums and peaches, the cores of apples and the leaves of the laurel plant, cyanide evolved as a plant protection mechanism of grazing animals. (Interestingly, a number of bacteria, fungi and algae are also found to produce the chemical). Ingestion of moderate amounts of these natural substances cause headaches accompanied by mild heart palpitations, more than enough to steer animals – two-legged or four – clear. However, the Middle Eastern people of ancient times made the discovery that the distillation by evaporation of laurel leaves produced lethal concentrations of this innocent plant product.
Although cyanide has found usage in the gold industry2 and butterfly collection (collectors used hydrocyanic acid – produced by the fermentation of crushed laurel leaves – in their collection bottles), its most notable use throughout history was as a poison. One of the first administrators of cyanide was said to be Livia3, the wife of Augustus who, in AD 14 killed her husband by soaking his figs in the poison. A number of people elected to end their lives by cyanide: Adolf Hitler, Eva Braun, Hermann Goering, and Alan Turing. The poison was stockpiled by both the United States and the Soviet Union during the 50s and 60s – indeed, it was thought that the Soviet Union had plans to use them to clear their way right into enemy territory.
The common misconception, especially by the murder-romance story crowd, is that cyanide has a sweet, sickly almond smell. People who have been unfortunate enough to come into contact with the poison describe a faint bitter almond taste in the breath and stomach – a sure sign of cyanide poisoning. (Nevertheless there are some people who cannot smell cyanide at all, due to a genetic trait). However it smells, its actions are brutal and deadly: as little as 50 mg causes death by anoxia within five minutes.
Symptoms will be slow to reveal in the case of chronic poisoning, and may include general weakness, confusion, bizarre behaviour, excessive sleepiness, shortness of breath, dizziness, headache and seizures. If a large dose is taken at one go, the heart will immediately be affected, causing a sudden collapse; the brain may also be affected, causing a seizure or a coma. Death follows rapidly as the poison prevents oxygen from reaching the cells. Post mortem will reveal healthy lungs whose coverings show signs of inflammation, and the skin of a poisoned victim may sometimes be pink or cherry-red in colour as oxygen remains in the blood.
Cyanide compounds include prussic acid (hydrocyanic acid), cyanide salts, potassium ferricyanide4 and Scheele’s acid (copper (II) arsenite).
In 399 BC the philosopher Socrates was found guilty by the Athenian jury of corrupting the youth and interfering with the religion of the city. Socrates gracefully accepted the verdict and, in the presence of his friends and disciples, ended his own life with a goblet of poison.
Hemlock is a poison hailing from the ancient world. Its poisonous properties were fully realised by the Greek, who not only devoted much of their literature to it, but also sanctioned the use of the 'suicide cup' in situations where suicide was considered a noble act, and used it as a form of capital punishment.
There are two varieties of hemlock: the water hemlock (Cicuta maculate) and the poison hemlock (Conium maculatum)5. Both plants are impregnated from leaves and fruit right down to the roots with a poisonous, volatile oily alkaloid, of which only a few drops are sufficient to down a small animal.
In spite of its poisonous properties, hemlock is also popular as medicine. The extract from the poison hemlock is sedative and antispasmodic, and thus is the recommended antidote for several conditions including strychnine poisoning, tetanus and hydrophobia. Its juice has also been prescribed in treatment of undue nervous motor excitability, such as epilepsy from dentition, cramps, spasms of the larynx and gullet, and teething in children. The ancient Greek and Arabic physicians used it to cure tumours6, rheumatisms and skin conditions. It was also inhaled to relieve coughs brought about by bronchitis, whooping cough and asthma. In all cases it is stressed that the juice is to be administered with utmost care, as an overdose may cause paralysis. Lethal doses results in complete paralysis, loss of speech, failure of the respiratory system, and death resulting from suffocation, while the victim is conscious.
The symptoms for hemlock poisoning are: dullness, paralysis of the motor centres (first of muscular power, and then complete paralysis), stumbling and falling, nausea and – in the case of Socrates – loss of sensation. The onset of symptoms occurs as quickly as 12 minutes after ingestion of the poison, and death occurs within 2 to 3 hours. However, a variety of antidotes exist for the poison, ranging from coffee and tannic acid, to zinc emetics and mustard and castor oil. In desperate situations, artificial respiration may be administered. The plant also loses much of its potency upon cutting and drying; cooking destroys its poison altogether. Thankfully for our ancestors, its unpleasant odour has prevented them from eating it raw. Its poison appears not to affect larks and quails, although thanks to ingestion of the deadly plant and subsequent impregnation of the tissues with the poison, it is best to avoid these birds as food.
Witches believed that the nightshade, ruled by Hecate, Queen of the Night, conferred flying abilities. Hamlet was visited by the ghost of his father, who tells him that his uncle7 killed him by pouring hebenon into his ear. Early Sanskrit writings spoke of datura, or Jimson Weed. All of them different plants, but with one chemical property in common: hyoscine.
Hyoscine (commonly called scopolamine to distinguish it from hyoscyamine) is a vegetable drug found in a number of plants. Its toxic properties, regardless of whether it is administered internally or externally, makes it a highly useful drug for physicians and poisoners alike. Its depressive action of the central nervous system8 makes it suitable for use in very tiny amounts in the treatment of anxiety-related problems and travel-sickness (in the form of hyoscine hydrobromide, which is a type of anticholinergic drug). In larger doses, it breaks down a person’s ability to discriminate and make reasoned judgment, making it a potential 'truth drug'. Hyoscine in the form of nightshade was also used by practitioners of witchcraft in the concocting of flying potions – large amounts of it caused hallucination and a sensation of floating. And for the aspiring poisoner, fatal doses of hyoscine causes the heart to cease functioning, which results in death. Indeed, it was because of its sedative properties that Dr. Hawley Harvey Crippen, the man notorious for introducing hyoscine as a murder weapon, decided upon it as a homicide tool, not realizing that the drug's unpredictable effect in different people made it hazardous to administer even in small quantities. Alas for Dr. Crippen, he learnt the hard way that dosage was everything.
Mercury is a metal that is liquid at room temperature, whose soluble compounds and vapours are extremely dangerous. Its salts are much used in medicine9, horticulture, paint manufacture and as wood preservatives; the metal itself is mostly used for scientific instruments. Over the years, however, there has been growing concern about the association between mercury amalgams with conditions such as autism and chronic fatigue syndrome, as well as mercury contamination of the environment. While some of the associations are controversial and hard to prove (or disprove), it is nevertheless known that mercury is a potent neurotoxin, as evidenced by the case of the 'mad hatters' of the 19th century who inhaled the mercury used to cure the fur used to make their hats and subsequently developed personality changes, uncontrollable muscular tremors and twitches, nervousness, distorted vision, hallucinations and even dementia.
We are constantly exposed to mercury in the environment, although these levels of exposure are seldom harmful. When ingested, the metal is rapidly absorbed by the intestinal tract and stored in the kidney and liver, and is subsequently slowly excreted through the faeces, urine and other bodily secretions10. Less than 10 µg/dL mercury in the bloodstream corresponds with mild mercuric poisoning effects; 300 µg/dL means certain death.
The clinical symptoms of mercury poisoning varies with dosage. Chronic exposure to the metal or its derivatives primarily affects the digestive tract, nervous system and kidneys. The gums, tongue and oral mucosa may become sore, swollen, bloody and ulcerated; degeneration of the nervous system may result in blindness and coordination difficulties, even coma; anaemia, edema and wasting are common. It is possible for death to follow after a prolonged period. On the other hand, acute mercury poisoning take effect quickly, damaging tissues11 by disrupting cellular process, causing gastrointestinal disorders (such as stomach pains, vomitting, diarrhoea and haemorrhage) and renal failure, and finally death. Shock and cardiovascular collapse have also been attributed to acute mercury poisoning. Some people may even develop a hypersensitive reaction to mercuric compounds, exhibiting dilation of the blood vessels, excessive sweating and abnormal growth of the horny layer of the skin.
The most famous (alleged) murder case by mercury poisoning is one that involves two of the biggest names in the history of astronomy. But more on that later.
Opiate abuse was a lifestyle of the 19th century. Originally used as a universal panacea12, opium was introduced by Chinese sailors to both Europe and America in the 1800s, where it was smoked in dimly lit dens and houses of dubious repute in Chinatown districts of seaports. In China, the opium trade with Westerners – particularly the British – boomed, although the government became increasingly concerned that the foreigners seemed 'intent on bringing down the Chinese through the opium trade'. To discourage the trade, heavy custom duties were imposed and attempts were made to stop the trade alltogether. However, political problems in China caused her to lose the upper hand in the trade, giving the British the chance to force the issue of increased trade rights. This culminated in the burning of the British opium stock and the subsequent Opium Wars of 1839-42 and 1856-60. China lost both wars, was forced to open a total of 16 ports, permit foreign legations in Beijing, sanction Christian missionary activity and legalise the opium trade – and lost Hong Kong to Britain in the process.
The drug responsible for these wars comes from the poppy (Papaver somniferum), an annual plant with white or red flowers growing on a central bulbous pod. The harvest season begins when all the petals have dropped from the flower. Harvesters make slits on either side of the pod twice daily, allowing the white liquid to ooze out and dry to browning gummy matter on its sides. Up to six incisions can be made before the flower begins to die. The dried juice is then collected, warmed, rolled into ball and are covered with leaves. This gives crude opium. Refinement of the drug involves careful mixing with water and filtering and drying and subsequently treating the resulting product with other solvents, after which it is ready for conversion into other compounds.
The active constituent in opium is the drug morphine, a fine white crystalline alkaloid. First extracted in 1805 by the German chemist Friedrich Sertner, it is a powerful analgesic and is used today in pain-relief medication. Because of its properties, it was widely available to medical practitioners, some of whom, it must be said, had intentions in mind other than curing their patients. Alas for the law, there were no means of proving the drug's presence in the bodies of victim back in the early days, allowing goodness knows how many poisoners to get off scot-free.
The fatal dose varies among individuals, but about 5 grains is generally sufficient to cause respiratory failure within a few hours. The symptoms take 10-30 minutes to manifest when the drug is consumed, and faster if it is introduced directly into the bloodstream. At the onset, the victim becomes drowsy, and sometimes mildly euphoric, but also experiences nausea and, on occasion, vomitting. The face may become swollen and highly coloured. As the victim gradually slips into unconsciousness, his skin becomes cool and clammy to the touch. Often the victim will feel cold, and his face will display signs of cyanosis while his extremities become livid. Coma follows, during which time the muscles become increasingly weak and flabby, and the breathing becomes slow and noisy. The pulse will gradually weaken and slow down until the victim stops breathing alltogether.
It may be of interest to note that morphine poisoning may also be achieved through the mixing of morphine with poultice applied over broken skin, and that anal administration of the drug has resulted in death.
The characteristic symptom of morphine poisoning is the pinpoint contraction of pupils until the conjunctival reaction degenerates and the pupils cease reacting to light and darkness. It is the first thing the doctors and police check for in cases of suspected morphine poisoning; however, more than one murder has circumvented this problem by an ingenious method that will be discussed later on.
If you have ever picked up a tube of lipstick, chances are that you would have seen the innocuous words 'castor seed oil' listed under ingredients13. While this is no cause for panic, it is worth pointing out that the seed also yields a deadly compound common to the homicide world, known as ricin.
Ricin is obtained from the waste 'mash'14 left over from the production of castor oil by the simple process of chromatography (hence its popularity). It is a stable substance, affected little by extreme conditions, with a basic structure similar to those of the botulinum, tetanus, cholera and diphtheria toxins. One gramme of it is sufficient to kill about 36,000 people. Because of its availability and sheer lethality, ricin was under serious consideration for use in chemical warfare during World War II. The toxin has recently also been linked with terrorist activity among anti-government militia in the US as well as the Al Qaeda, and was supposedly used by the Bulgarian secret service15 in 1978 to assassinate a Bulgarian dissident in what is known as The Case of the Umbrella Murder.
There are many routes of exposure to ricin, all of which will cause poisoning: inhalation, ingestion and injection. The toxin works by inhibiting protein synthesis in cells16, thus causing their death. In the case of ingestion, the symptoms of poisoning will manifest within a few hours of exposure, beginning with abdominal pain, vomiting and diarrhoea (which is sometimes bloody). Within the next few days the victim suffers from severe dehydration, a decrease in urine output, and a drop in blood pressure; death comes when multiple organs cease functioning. Inhalation of the toxin, on the other hand, causes respiratory distress, fever, cough, nausea and tightness in the chest, accompanied by heavy sweating caused by fluid accumulating in the lungs. Death is by respiratory failure.
The mortality rate varies according to the method of exposure – it takes 30 microgrammes/kg of ingested ricin to kill 50% of the exposed population; introduction of the poison into the bloodstream is rapidly fatal, and one-tenth of the amount is required to kill (the same is true of the inhalation exposure). If death has not occurred within 3-5 days, there is usually a good chance of recovery.
It may be worth pointing out that ricin was the murder weapon of choice in the 1962 comedy Kill or Cure, in which an inept policeman is called to investigate the strange goings-on in a health club.
Though the active component of the poison called strychnine wasn't determined until the 19th century17, the qualities of the poison berry, Nux vomica, have been known to the Arabs as early as the 5th century. The first reliable record of Strychnos nux vomica, documented in 17th century medicine textbooks, highlights the use of the berries for poisoning vermin and birds; but even before then strychnine was already being used as a tonic and to treat fever, in the form of 'St. Ignatius' Bean', a berry brought back from India by Jesuit missionaries, which contained a safe level of 1% strychnine.
Strychnos nux vomica is a plant with dark shiny leaves and long cylindrical pods with disc-shaped seeds about the size of a 5-pence coin. The seeds are slightly convex on one side and correspondingly concave on the other, and are covered with fine silky hairs radiating from the centre to the edge. They may be light brown, greenish-grey or silver grey in colour, depending on the state of maturity at the time of collection, and are tough to break or powder. They are largely found in Malabar, India, where the inhabitants are said to use it as a prophylactic for snake bites.
When powdered strychnine is dissolved, it produces a colourless solution with a strong bitter taste that still remains detected in dilutions as high as one part in 600,000. It is highly poisonous: one-third18 of a grain administered orally or one-twentieth of a grain administered intravenously will bring about poisoning; one and a half grains (100 mg) will bring death.
Death by strychnine is truly one of the most horrific ways to die. It begins with a general feeling of restlessness and a feeling of impending suffocation. As the poison spreads through the body, the facial muscles contract, and the face is drawn into a gruesome characteristic grin called risus sardonicus. Other muscles of the body will subsequently become similarly affected, causing the body to be violently and spasmodically jerked into all sorts of contortions – bent backward like a bow one minute, with the head and heels resting on the surface (a condition known as opisthotonos), and twisted in the other direction off the bed in the next. These paroxysms will last for several minutes, after which there is a period of relative quiet, during which time the victim will often complain of exhaustion and great thirst. But this is no sign of convalescence, for the next attack begins right after, and even more violently. The stomach muscles will harden and tense, the face will grow livid, with the jaws clenched shut in the fashion of lockjaw; observers will perceive the victim's eyeballs to be staring and prominent in a disturbing manner. Through all this agony, the victim remains fully conscious of the unraveling horrors.
The attacks will succeed one another with increasing rapidity, until the victim eventually dies from suffocation due to the paralysis of respiratory muscles – while still conscious. There may be an interval of up to 2 or 3 hours between the time of administration and the onset of the symptoms, but once the horror begins, there is only a speedy death or a speedy recovery for the victim.
Until the turn of the 20th century, there was no method for accurately detecting strychnine in the body, and it was because of this insurance that the Rugeley murderer Dr Palmer employed strychnine as a murder weapon. Strychnine had also claimed the life of Mrs Jane Stanford, the co-founder of Stanford University, although it still remains a mystery as to who slipped her the poison. But perhaps the most eyebrow-raising point is the latest speculation regarding Alexander the Great's death – rumour has it that Alexander’s wife Roxane had poisoned both her husband and his homosexual lover Hephaestian.
The least well known of the classical poisons, thallium, is a heavy metal discovered by Sir William Crookes in 1861. It is closely related to mercury and lead, but more toxic, and is used in industry in the manufacture of pesticides (although the sale of thallium-based products are no longer permitted in many cases). Its salts are colourless, almost tasteless, and will readily dissolve in water-based liquids; the symptoms tend to be confused with that of many viral diseases including influenza, thus impeding its detection. Despite this convenience, however, it has rarely been used in homicide, with the case of Graham Young being an exception.
The poison works by taking the place of potassium (which is essential for the sustenance of cells and nerves) in the body, thereby interfering with several different systems simultaneously. Within the first few hours it becomes distributed throughout the vascular space; by 48 hours it begins entering the central nervous system and other tissues, causing, among other things, the upset of vitamin B metabolism, inhibition of the absorption of iron and calcium, and the disturbance of nerve cells. Because it causes hair to fall out, it was used by dermatologists to remove body hair in the treatment of fungal diseases, until its toxic properties were discovered. The lethal dose of thallium is 15-20 mg per kg of body weight. The manifestation of thallium poisoning include digestive tract-related symptoms such as nausea, vomitting, diarrhoea and gastritis within the first two days; within the next three days the victim will suffer from headaches, respiratory depression, nystagmus, damage to the optic nerves, muscle-related problems, convulsions, coma, delirium dementia and psychosis. If death does not occur, the patient will experience hair loss within 2 to 3 weeks of the poisoning, and heartbeat irregularities for up to two months following the poisoning, due to damage to the controlling autonomic nerves or direct toxicity.
As a protective reaction towards thallium, the body attempts to excrete the poison by secreting about two-thirds of it in the intestine, where much of it is reabsorbed into the system, and about one-third in the urine.
Thallium poisoning is treatable if the condition is traced within six hours of ingestion. Gastric lavage and induced emesis is frequently administered to impede absorption of the poison into the body. An antidote also exists, known as potassium ferrihexacyanoferrate (also known as Prussian blue or Berlin blue), which acts to sequester the ions in the intestine, thus preventing their absorption. Activated charcoal may also be administered to disrupt the circulation of the poison in the liver, and reduce the severity of the poisoning.
Bartrip, P. 1992. A 'pennurth of arsenic for rat poison': the Arsenic Act, 1851 and the prevention of secret poisoning. Medical History 36(1): 53-69.
Lane, B. 2004. The Encyclopaedia of Forensic Science. Magpie Books, London.
Nicander. Alexipharmaca. Translated by Giovanni Gorreo (1557). Scanned by Bibliotheca Antiqua.
- Aconite poisoning
- Aconitum napellus spp
- ATSRD ToxFAQs for arsenic
- CBRNE – Ricin
- Facts about ricin
- The history of poisoning timeline
- Livia (Wife of Augustus)
- Opium poppy
- The Opium Wars
- Plant poisoning, hemlock
- Ricin toxin from castor bean plant Ricinus communis
- The Risk Assessment Information System
- Toxic effects of arsenic