Chemistry and crime

Toxicity and Poisons
Brief History of Poisons
Poisons have been known from antiquity, and were used by ancient tribes and civilizations as hunting tools to quicken and ensure the death of their prey or enemies. This use of poison grew more advanced, and many of these ancient peoples began forging weapons designed specifically for poison enhancement. Later in history, particularly at the time of the Roman Empire, one of the more prevalent uses was for assassination. As early as 331 BC, poisonings executed at the dinner table or in drinks were reported, and the practice became a common occurrence. The use of fatal substances was seen among every social class; even the nobility would use it to dispose of unwanted political or economic opponents.

Toxicity of Phosphorus and the chemistry of the match

Classic Poisons

Until the 19th century, most poisons were undetectable as well as common and this meant that poisoners could expect to escape detection and punishment. Family members or neighbours might be suspect if an unloved wife or husband or a rich parent died suddenly, but no one could prove that such a person had been poisoned. As a result, historians say, poisoning was widespread in some places and times, such as in Italy and France in the late 1600s.

The most popular poison seems to have been arsenic. The human body needs tiny amounts of this metallic element, but arsenic is poisonous in most doses. Arsenic was most commonly found in the form of arsenic oxide, a white powder that had respectable uses ranging from improving the complexion to poisoning rats. Because white arsenic, as the powder was called, was odourless and tasteless as well as easy to buy, however, some people applied it to less legitimate purposes. Secretly mixed into food, the powder caused stomach pains, vomiting, diarrhea, and other signs of illness just like the symptoms of cholera and several other common, deadly diseases. Only a minute dose of arsenic (about 0.25 g) was needed to kill a person. White arsenic was supposedly used so often to poison rich relatives in late 17th-century France that it was nicknamed "inheritance powder".

Mathieu Orfila, born 1787 in Minorca, is considered the father of toxicology. In 1813, not long after he graduated as a doctor, he was living in Paris and giving private lessons in Chemistry to help cover his bills. After he failed several times to show his students the precipitate that was claimed to form when arsenic acid was mixed with various substances - a common test for arsenic at the time - he decided to examine other standard tests for poisons in fluids such as soup, wine, and coffee. He found that most of the tests were unreliable. He learnt that the detection of many poisons was achieved by feeding suspected substances to animals and waiting to see whether the animals died. Orfila went on to create new techniques and refined existing techniques in his first treatise, Traité des poisons, greatly enhancing their accuracy. The book divided poisons into several groups and described their effects on the living body, the symptoms of illness they produce, the signs they leave in a dead body, and the ways of identifying them. The first volume of this exhaustive work appeared in 1813, and a second volume in 1815.

Traite by Orfila Marsh apparatus for detection of arsenic
1818 publication by Orfila and Marsh apparatus for the detection of arsenic
a= funnel, b= escape tube, C= stand

In 1832, James Marsh was called as a chemist by the prosecution in a murder trial, wherein a certain John Bodle was accused of poisoning his grandfather with arsenic-laced coffee. Marsh performed the standard test by mixing a suspected sample with hydrogen sulfide and hydrochloric acid. While he was able to detect arsenic as yellow arsenic trisulfide, when it came to show it to the jury it had deteriorated, allowing the suspect to be acquitted due to reasonable doubt. Annoyed by this, Marsh developed a much better test. The material to be tested was mixed with zinc and sulfuric acid in the flask at the left (A). If the sample contained arsenic, hydrogen from the acid combined with the arsenic to form arsine gas. The gas passed into the horizontal calcium chloride drying tube (B). Near the end of the tube, the gas was heated by a flame (f). The heat broke down the arsine and released metallic arsenic, that formed a black, shiny deposit (called the arsenic mirror) at the end of the tube. So sensitive was the test that it could detect as little as one-fiftieth of a milligram of arsenic.

Maria LaFarge case

Marie-Fortunée Lafarge, née Capelle (January 15, 1816 - November 7, 1852) was a Frenchwoman said to be a descendant of Louis XIII (27 Sept 1601-14 May 1643) of France through her grandmother. She gained notoriety in 1840 since she was convicted of murdering her husband by arsenic poisoning. Her case became notable, because it was one of the first trials to be followed by the public through daily newspaper reports, and because she was the first person convicted largely on direct forensic toxicological evidence.

After several tests had been carried out by local chemists, Orfila was called to perform the Marsh Test at the courthouse in the presence of the local chemists. He confirmed the presence of arsenic in the deceased's body as well as food material gathered from the household. Marie was convicted and given a life-sentence.

See as well the article on arsenic detection and the Moreau and LaFarge cases.

Arsenic in drinking water
The World Health Organisation (WHO) notes that Arsenic in drinking-water is a hazard to human health. The contamination of groundwater by arsenic in Bangladesh is the largest poisoning of a population in history. With a total population of around 125 million, they estimated that between 35-77 million people were at risk from exposure. It occurs less extensively in many other countries as well. Studies have shown that where the population has had long-term exposure to arsenic in groundwater 1 in 10 people who drink water containing 500 mg of arsenic per litre may ultimately die from cancers caused by arsenic, including lung, bladder and skin cancers.

Magnitude of arsenic poisoning in Bangladesh
Population of Bangladesh 125 million
Total population in regions where some wells are known to be contaminated 35-77 million
Maximum concentration of arsenic permitted in drinking-water according to WHO recommendations 10 mg/l
Maximum concentration allowed in Bangladesh 50 mg/l (similar to many countries worldwide)
Number of tube-wells sampled by the British Geological Survey (1998) 2022
Proportion of wells with arsenic concentrations >50 mg/l 35%
Proportion of wells with arsenic concentrations >300 mg/l 8.4%

In the USA, the EPA is required by Congress (1974 Safe Drinking Water Act) to determine the level of contaminants in drinking water at which no adverse health effects are likely to occur. These non-enforceable health goals, based solely on possible health risks and exposure over a lifetime with an adequate margin of safety, are called maximum contaminant level goals (MCLG).

Based on the MCLG (for As = ZERO), the EPA has set an enforceable regulation called a maximum contaminant level (MCL), at 0.010 mg/L or 10 ppb. MCLs are set as close to the health goals as possible, considering cost, benefits and the ability of public water systems to detect and remove contaminants using suitable treatment technologies.

Approximately 90 percent of industrial arsenic used in the U.S. is as a wood preservative, but arsenic is found in paints, dyes, metals, drugs, soaps, and semi-conductors as well. Agricultural applications, mining, and smelting can contribute to arsenic releases in the environment. The major sources of arsenic in drinking water are erosion of natural deposits; runoff from orchards; and runoff from glass and electronics production wastes.

Recently a group in Florida have devised a method for As removal from drinking water using a "Biochar" filter method. A magnetic, porous biochar absorbent was prepared from the thermal pyrolysis of FeCl3 treated biomass. Batch sorption experimental results showed that the composite had strong sorption abilities towards aqueous arsenic. Due to its excellent ferromagnetic properties, the arsenic-laden biochar/γ-Fe2O3 composite could be readily separated from the solution by a magnet at the end of the sorption experiment.

A November 2014 follow-up report on iron-enhanced carbon cooked from hickory chips noted that ground wood chips were heated in nitrogen gas, but not burned. The resulting biochar, that had the consistency of ground coffee, was then treated with a saltwater bath to impregnate it with iron. Homeowners might eventually be able to use a small filter attached to their tap.

Common poisonous cyanide compounds include hydrogen cyanide gas and the crystalline solids potassium cyanide and sodium cyanide. The cyanide ion halts cellular respiration by inhibiting an enzyme in the mitochondria called cytochrome c oxidase.

John Tawell (1784-1845) was a British murderer who was eventually hanged in public in front of a crowd of around 10,000 people. In 1845, he became the first person to be arrested as the result of telecommunications technology. It was also the first known homicide case where the criminal attempted to flee the scene of the crime by a railway train.

Cyanide compounds are found naturally in the stones of apricots, cherries, plums, peaches, and the cores of apples where it may have evolved as a plant protection mechanism against grazing animals. A number of bacteria, fungi and algae are able to produce cyanide as well. Ingestion of moderate amounts of these natural substances causes headaches accompanied by mild heart palpitations, providing a warning that they should be avoided. Middle Eastern people of ancient times made the discovery that the distillation, by evapouration of laurel leaves, produced lethal concentrations of this innocent plant product.

Some millipedes release HCN as a defense mechanism and certain insects such as day-flying moths contain a deadly dose of cyanide to deter predators. Cassava root contains linamarin, a natural molecule containing both glucose and cyanine groupings and perhaps the cyanide is present to protect the plant, although since we recognise that cassava is the third-largest source of food carbohydrates in the tropics, it is no longer working very well against humans!!

structure of linamarin

Cassava is a major staple food in the developing world, providing a basic diet for around 502 million people, some eating as much as 0.5 kg a day in the form of porridge. It is one of the most drought-tolerant crops, capable of growing on marginal soils. Nigeria is the world's largest producer of cassava.

Cassava is prepared by peeling and grating the root, soaking it in water for at least 3 days, drying in the sun and finally grinding it into a flour that can be used to make the porridge. Too much though can give rise to a disease called konzo.

The onset of paralysis (hypertonic paraparesis) is sudden and symmetrical and if the symptoms do not disappear within a few days the resulting disability is permanent, but does not progress. The disease onset is associated with high dietary exposure from cyanide liberated from the naturally occurring glucosides that normally are removed by processing (washing and drying) before consumption of bitter cassava roots. However, during food shortage, war and other severe disruptions of life in poor rural cassava growing communities, the population is forced to make short-cuts in the established procedures for removing the cyanide.

Fresh cassava root contains 300 mg of cyanide per kg, but if it is peeled and soaked in water for ONE day then sun-dried for four days, this falls to 80 mg per kg. If peeled and soaked for FIVE days and then sun-dried for a week this figure is further reduced to 30 mg per kg. Grating before soaking can reduce this amount even further to 10 mg per kg and this is the value recommended by the WHO as the MAXIMUM limit for cyanide in cassava flour. This value was chosen so that anyone eating 500 g of cassava would still be one tenth the estimated lethal dose of around 50 mg.

Cyanide has been used in gold-mining industry and even more exotically by butterfly collectors (who use NaCN - in their collection bottles so that the butterfies die quickly without much fluttering of wings), its most notable use throughout history was as a poison. One of the first administrators of cyanide was said to be Livia, 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 including: Adolf Hitler, Eva Braun, Hermann Goering, Wallace Carothers and Alan Turing.

Some people claim that cyanide has a sweet, sickly almond smell. People who have been exposed to the poison sometimes describe a faint bitter almond taste in the breath and stomach - a sure sign of cyanide poisoning. Note though that 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.

The extent of a person's exposure to cyanide can be assessed by determining the amount of thiocyanate in their urine, since this is a metabolic product in the bodies attempt at detoxification by the liver. Generally SCN- is present at under 6 mg per litre but in villages affected by konzo, for example, the level may reach 60 mg per litre.

The toxicity of cyanide is due to it's binding to iron in the enzyme, cytochrome oxidase which is present in the membrane of cell mitochondria. This enzyme is critical in the oxidation of glucose by di-oxygen, and is vital for the generation of energy. Without it the energy processes cannot proceed and so life ends very quickly. The heart and central nervous system are immediately affected and because the oxygen being transported by the haemoglobin is not used up a symptom of cyanide poisoning is that those affected often show the bright red colour of oxygenated blood.

The seeds and bark of many plants of the genus Strychnos, Family Loganiaceae and in particular the strychnine tree (Strychnos nux-vomica L.) contains the powerful poison strychnine. The seeds contain approximately 1.5% strychnine, and the dried blossoms contain 1.0%. However, the tree's bark contains brucine and other poisonous compounds.

Strychnine is a highly toxic colourless crystalline alkaloid used for years to get rid of rodents and birds. In September 2006 the EU banned its use for killing moles, as it caused them unnecessary suffering.

Death by strychnine must truly be 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 unravelling horrors.

It operates by blocking a glycine receptor that stops motor nerves in the spinal cord from operating normally. It heightens sensitivity to stimuli, resulting in excessive muscular contractions. Death is a result of either suffocation by paralysis of breathing, or of exhaustion from the continuous convulsions. Since strychnine does not cross the blood-brain barrier, the victim remains conscious throughout and because the symptoms are enhanced by noise and light, victims must be kept quiet to ease their suffering.

Plants are brilliant synthetic organic chemists, and the Strychnos nux vomica tree is one of the most talented, as strychnine has a fiendishly complicated structure, containing seven rings fused together. The plant makes it from the amino acid tryptophan; no one is sure why, though this toxic and bitter-tasting molecule could be a deterrent to predators.

structure of L-tryptophan structure of strychnine
L-tryptophan is the biosynthetic precursor to strychnine

The toxic and medicinal effects of strychnine have been well known from the times of ancient China and India. In Europe, historic records indicate that the strychnine alkaloid had been used to kill dogs, cats, and birds as far back as 1640. The structure of strychnine was first determined in 1946 by Sir Robert Robinson and in 1954 the first total synthesis by Robert B. Woodward was reported. This is one of the most famous syntheses in the history of organic chemistry. Both chemists won the Nobel prize (Robinson in 1947 and Woodward in 1965). In a 1963 publication, Woodward quoted Sir Robert Robinson who said "for its molecular size, it is the most complex substance known".

Some of the worlds most toxic substances
Toxic Compound Occurrence Type ~RMM LD50 *
Most Toxic
maitotoxin dinoflagellum polyketide 3422 0.050
ciguatoxin dinoflagellum polyketide 1061 0.35
palytoxin coral species polyketide 2679 0.45
taipoxin Australian taipan snake glycoprotein 45600 2
batrachotoxin Columbian poison dart frog steroid alcohol 539 2
tetrodotoxin pufferfish saccharide derivative 319 10
Plant poisons
ricin castor bean glycoprotein (lectin) 62400 0.1
nicotine tobacco plant alkaloid 162 300
strychnine poison nut alkaloid 334 750
cymarine tropical creeping shrub digitalis glycoside 549 25000
tubocurarine chloride tropical woody vine alkaloid 682 33200
atropine deadly nightshade alkaloid 289 400000
Fungal poisons
L-(+)-muscarine "fly agaric" alkaloid 174 230
α-amanitin "death cap" bicyclic octapeptide 919 300
penitrem A mould polycyclic indole derivative 634 1050
aflatoxin b1 mould difuran coumarin derivative 312 1700
Inorganic and synthetic poisons
2,3,7,8-TCDD (dioxin) polychlorinated dibenzo-p-dioxin 320 22
parathion (E605) organophoshate 291 3600
potassium cyanide 66 10000
arsenic oxide 198 15100
* LD50 generally given as μg kg-1

Animal derived toxins
Reef stonefish
The reef stonefish, or simply stonefish, is a fish species (Synanceia verrucosa) that is sometimes lethal to humans. They are carnivorous ray-finned fish with venomous spines that live on reef bottoms, camouflaged as a rock.

Reef Stonefish

The Reef Stonefish is the most venomous fish in the world. Its dorsal area is lined with 13 spines that release venom from two sacs attached to each spine. Its venom causes severe pain with possible shock, paralysis, and tissue death depending on the depth of the penetration. This level can be fatal to humans if not given medical attention within a couple of hours. Immediate first aid treatment requires immersion of the affected limb in hot water, ensuring that it is not so hot that skin damage may occur.

The venom consists of a mixture of proteins, including the hemolytic stonustoxin, the protinaceous verrucotoxin and the cardioactive cardioleputin; an antivenom is available.

Red Lionfish
The red lionfish (Pterois volitans) is a venomous coral reef fish in the family Scorpaenidae, order Scorpaeniformes. P. volitans is natively found in the Indo-Pacific region, but has become a huge invasive problem in the Caribbean Sea and along the East coast of the United States along with a similar species, Pterois miles. Red lionfish are clad in white stripes alternated with red, maroon, or brown. Adults can grow as large as 43 cm (17 inches) in length while juveniles may be shorter than 2.5 cm (1 inch). They can live up to 10 years. The fish has large venomous spines that protrude from the body like a mane, giving it the common name of the lionfish. The venomous spines make the fish inedible or deter most potential predators. Lionfish reproduce monthly and are able to quickly disperse during their larval stage for expansion of their invasive region. There are no definitive predators of the lionfish, and many organizations are promoting the harvest and consumption of lionfish in efforts to prevent further increases in the already high population densities.


The most distinguishable characteristic of the red lionfish, as well as all scorpionfishes, are the venomous spines protruding from the body. An extremely showy and ornate fish such as the lionfish should be an easy target for predators, but the large spines act as a great defense. The spines are incorporated into certain fins of the fish, and have venom glands at the base of the spine. These glands protect the fish from predation, delivering a painful and potentially fatal venomous "sting" to predators or a human that may come in contact with a lionfish.

Puffer fish
Tetraodontidae is a family of primarily marine and estuarine fish of the Tetraodontiformes order. The family includes many familiar species which are variously called pufferfish, balloonfish, blowfish, bubblefish, globefish, swellfish, toadfish, toadies, honey toads, sugar toads, and sea squab. They are morphologically similar to the closely related porcupinefish, which have large external spines (unlike the thinner, hidden spines of Tetraodontidae, which are only visible when the fish has puffed up). The scientific name refers to the four large teeth, fused into an upper and lower plate, which are used for crushing the shells of crustaceans and mollusks, their natural prey.

Puffer Fish

(Maple) Puffer fish are generally believed to be the second-most poisonous vertebrate in the world, after the Golden Poison Frog. Certain internal organs, such as liver, and sometimes their skin are highly toxic to most animals when eaten, but nevertheless the meat of some species is considered a delicacy in Japan (Fugu), Korea and China when prepared by chefs who know which part is safe to eat and in what quantity. Although the liver is considered to have the best taste, it was found to be the most toxic so has been banned in restaurants in Japan since 1984.

Pufferfish can be lethal if not served properly. Puffer poisoning usually results from consumption of incorrectly prepared puffer soup, fugu chiri, or occasionally from raw puffer meat, sashimi fugu. While chiri is much more likely to cause death, sashimi fugu often causes intoxication, light-headedness, and numbness of the lips, and is often eaten for this reason. Puffer's (tetrodotoxin) poisoning deadens the tongue and lips, and induces dizziness and vomiting, followed by numbness and prickling over the body, rapid heart rate, decreased blood pressure, and muscle paralysis. The toxin paralyzes diaphragm muscles and stops the person who has ingested it from breathing. People who live longer than 24 hours typically survive, although possibly after a coma lasting several days. Some people claim to have remained fully conscious throughout the coma, and can often recount events that occurred while they were supposedly unconscious. The paralysis reduces oxygen demands of the body dramatically, but because the toxin does not cross the blood-brain barrier, neural activity in the brain and from the eyes and ears are generally intact. In Voodoo, puffer's poison may be part of the mixture given to the victim to make them a "zombie", most likely because the paralysis and pseudo-comatose effect simulate the death portion of traditional zombie creation.

tetrodotoxin structure

Although tetrodotoxin was discovered in these fish and found in several other animals (e.g., blue-ringed octopus, rough-skinned newt, and Naticidae) it is now believed that puffers do NOT produce toxins themselves, as puffer fish kept in tanks or fish farms are totally free of the toxin. The toxin is now believed to be produced by certain symbiotic bacteria, such as Pseudoalteromonas tetraodonis, certain species of Pseudomonas and Vibrio, as well as some others that reside within these animals. The gastric contents of shellfish prey are believed to carry the toxins or their precursors, which are stored in the puffers organs.

Saxitoxin, the cause of paralytic shellfish poisoning and red tide has also been found in certain puffers.

A recent study involving "spy-cams" disguised as turtles has found that young dolphins can antagonise puffer-fish so that they release the toxin and this has a narcotic effect on the dolphins.

Poison arrow frog.
Poison dart frog (also dart-poison frog, poison frog or formerly poison arrow frog) is the common name of a group of frogs in the family Dendrobatidae which are native to Central and South America. These species are diurnal and often have brightly-colored bodies. Although all wild dendrobatids are at least somewhat toxic, levels of toxicity vary considerably from one species to the next and from one population to another. Many species are critically endangered. These amphibians are often called "dart frogs" due to the Amerindians' indigenous use of their toxic secretions to poison the tips of blowdarts. However, of over 175 species, only three have been documented as being used for this purpose (curare plants are more commonly used), and none come from the Dendrobates genus, which is characterized by the brilliant color and complex patterns of its members.

blue poison dart frog
Blue poison arrow frog

Many poison dart frogs secrete lipophilic alkaloid toxins through their skin. Alkaloids in the skin glands of poison frogs serve as a chemical defense against predation, and they are therefore able to be active alongside potential predators during the day. About 28 structural classes of alkaloids are known in poison frogs. The most toxic of poison-dart frog species is Phyllobates terribilis. It is argued that dart frogs do not synthesize their poisons, but sequester the chemicals from arthropod prey items, such as ants, centipedes and mites. This is known as the dietary hypothesis. Because of this, captive-bred animals do not contain significant levels of toxins. Despite the toxins used by some poison dart frogs, there are some predators that have developed the ability to withstand them, including the Amazon ground snake (Liophis epinephelus).

Chemicals extracted from the skin of Epipedobates tricolor may be shown to have medicinal value. One such chemical is a painkiller 200 times as potent as morphine, called epibatidine, that has unfortunately demonstrated unacceptable gastrointestinal side effects in humans. Secretions from dendrobatids are also showing promise as muscle relaxants, heart stimulants and appetite suppressants. The most poisonous of these frogs, the Golden Poison Frog (Phyllobates terribilis), has enough toxin on average to kill ten to twenty men or about ten thousand mice. Most other dendrobatids, while colorful and toxic enough to discourage predation, pose far less risk to humans or other large animals.

epibatidine and batrachotoxin
Plant derived toxins
Ricin is produced by the castor bean plant Ricinus communis. It makes this highly toxic, naturally occurring protein in its seeds, possibly as a deterrent to predators, since once the seed has germinated the toxin disappears. The LD50 for ricin in rodents is listed as 0.1 microgram/kilogram and for humans as 20 microgram/kilogram.
structure of ricin
Ricin is an example of an holotoxin, consisting of heterodimeric glycoproteins, the A and B chains.

The ricin molecule consists of two long chains (A and B) neither of which are considered toxic by themselves. The A chain for example can be found in barley. The B chain is the critical component since it is able to bind to the outside of the cell membrane via a carbohydrate component. The A chain is then able to pass through the cell membrance and once inside it blocks an essential enzyme so the cell dies. In principle, a single ricin molecule can kill a cell so that 3 ug ricin, containing over 1010 molecules, would be sufficient to poison every cell in a human body.

Accidental deaths due to castor beans are not common and while a single bean has the potential to poison a child this is rare, possibly since the coating of the bean is sufficiently hard so that it remains unbroken if swallowed, passing through the system undigested.

For an adult, under 500 microgam is needed to cause death by inhalation or injection (less than would fit on the head of a pin!). There is no antidote although vaccines have been produced for those who might be susceptible to contact with the toxin. The effects are generally observed within six hours and following inhalation there is fluid build up in the lungs so breathing becomes more difficult. Following ingestion, vomiting and diarrhoea and internal bleeding may result and within days the liver, spleen and kidneys stop working. Following injection, death occurs withing thirty-six to seventy-two hours.

The use of castor oil to relieve severe constipation is perhaps due to trace amounts of ricin that it contains. It is worth noting the similarity in structure to enterotoxin produced by E coli and responsible for intestinal problems when travelling.

Deliberate ricin poisoning
During the period October 2003 to February 2004, three letters containing powdered ricin were sent through US mail to addresses including the White House and the Washington office of a Republican Senator. No-one has ever been prosecuted for these attacks.

In September 1978, Georgi Markov, an exiled Bulgarian was murdered in London by what was thought to have been an attack by the Bulgarian secret police. The method employed was that he was prodded with an umbrella gun on the street and it contained a platinum (90%), iridium (10%) pellet (an alloy that is not rejected by the body) of about 0.45 mg ricin that was injected into his right leg. He died five days after the attack, having spent several of them in hospital in critical condition.

Tubocurare is a naturally occurring mono-quaternary alkaloid obtained from the bark of the South American plant Chondrodendron tomentosum, a climbing vine known to the European world since the Spanish conquest of South America. Curare had been used as a source of arrow poison by South American Natives to hunt animals, and they were able to eat the animals' contaminated flesh subsequently without any untoward effects because tubocurarine cannot easily cross mucous membranes.
poison dart with curare structure of Tubocurarine

Amanita mushrooms
The genus Amanita contains about 600 species of agarics including some of the most toxic known mushrooms found worldwide. This genus is responsible for approximately 95% of the fatalities resulting from mushroom poisoning, with the Amanita phalloides, "death cap" accounting for about 50% on its own.

As the common name suggests, the fungus is highly toxic, and its biochemistry has been intensively researched for decades, and it is estimated that only 30 gram (1 oz), or half a cap, of this mushroom is enough to kill a human. In 2006, a family of three in Poland was poisoned, resulting in one death and the two survivors requiring liver transplants. Some authorities strongly advise against putting suspected death caps in the same basket with fungi collected for the table and to avoid touching them. Furthermore, the toxicity is not reduced by cooking, freezing, or drying.

Amatoxins are a subgroup of toxic compounds found in several genera of poisonous mushrooms, most notably Amanita phalloides and several other members of the genus Amanita. The most potent toxin present in these mushrooms is α-amanitin.
The structures of at least nine amatoxins are known:
Name R1 R2 R3 R4 R5
α-Amanitin OH OH NH2 OH OH
β-Amanitin OH OH OH OH OH
γ-Amanitin H OH NH2 OH OH
ε-Amanitin H OH OH OH OH
Amanullin H H NH2 OH OH
Amanullinic acid H H OH OH OH
Amaninamide OH OH NH2 H OH
Amanin OH OH OH H OH
Proamanullin H H NH2 OH H
structure of alpha-amanitin

A simple field test developed by Meixner for detecting poisonous amatoxins is based on their acid-catalyzed reaction with the complex biopolymer lignin to form a blue product. Lignin is a constituent of wood pulp which is generally removed in the processing of pulp to high-grade cellulose paper, but remains in cheaper grades such as newsprint. As described by Meixner, the test is performed by expressing the juice from a piece of fresh mushroom tissue onto a piece of newsprint, allowing the spot to dry, and then applying one drop of concentrated hydrochloric acid. Formation of a blue color constitutes a positive test. The test can detect amatoxin concentrations as low as 0.2 mg/mL and this is substantially smaller than the concentration found in most toxic species.

In addition to amatoxins there are at least 7 phallotoxins that have been isolated from the "death cap".

Jamaica's poisonous plants.
In the book "Poisonous plants of Jamaica" by Lowe, H.I.C, Morrison, E.Y. StA, Magnus, K.E and Grizzle, H., published by FlexPak Printers Ltd, Jamaica in 2002,
fifty poisonous plants are identified.
Family Name Plant Name Common Name
Aizoaceae Trianthema portulacastrum Horse Purslane
Amaryllidaceae Haemanthus mulitflorus Blood Lily
Apocynaceae Adeniuzn spp. Desert Rose
Catharanthus roseus Periwinkle, Rain Goat Rose
Nerium oleander Oleander
Rauvolfia nitida Glasswood
Thevetia peruviana Milk Bush, Yellow Oleander, Lucky Beans
Urechites lutea Nightsage, Yellow Nightshade
Aristolochiaceae Aristolochia grandiflora Poisoned Hog Meat
Asclepiadaceae Asciepias curassavica Red Head, Red Top, Blood Flower
Calotropis procera French Cotton, Dumb Cotton
Cryptostegia grandiflora Purple Allamanda, India-rubber Vine
Araceae Dieffenbachia seguine Dumb Cane
Boraginaceac Heliotropium indicuni Scorpion Weed, Wild Clary
Caesalpiniaceae Cassia alata Ringworm Shrug
Campanulaceae Hippobroma longiflora Madame Fate, Horse Poison, Star Flower
Cannabinaceae Cannabis sativa Ganja, Marijuana, Indian Hemp
Chenopodiaceae Chenopodium ambrosioides Semicontract, Mexican Tea, Bitter Weed
Compositae (Asteraceae) Erechtites hieraciifolia Fireweed
Senecio discolor Whiteback
Cucurbitaceae Luffa aegyptiaca Strainer Vine, Loofah Gourd
Euphorbiaceae Hippomane mancinella Manchineel Tree
Jatropha curcas Physic Nut Tree
Manihot esculenta Cassava, Tapioca
Ricinus communis Castor Oil Plant, Oil Nut Plant
Tragia volubilis Twining Cowitch
Lauraceae Cassytha filiformis Love Bush
Liliaceae Gloriosa rothschildiana Gloriosa Lily
Loganiaceae Spigeia anthelmia Pink Weed, Worm Grass
Loranthaceae Phoradendron piperoides Godbush, Scorn-the-Earth
Malvaceae Sida acuta Broomweed
Meliaceae Melia azedarach Neem, China Berry, Persian Lilac
Menispermaceae Cissampelos pareira Velvet Leaf
Mimosaceae Albizia saman or Samanea saman Guango, Rain Tree, Cow Tamarind
Papaveraceae Argemone mexicana Mexican Poppy, Yellow Thistle
Papiionaceae Abrus precatorius John Crow Bead Vine, Crab's eyes, Red Bead Vine
Andira inermis Cabbage Bark Tree
Crotalaria fulva Consumption Weed
Mucuna pruriens Cowitch
Ormosia jamaicensis Red Nickel
Portulacaceae Portulaca oleracea Pussley, Pursiane
Punicaceae Punica granatum Pomegranate
Rubiaceae Borreria verticillata Button Weed, Wild Scabious
Cinchona pubescens Quinine Tree
Sapindaceae Blighia sapida Ackee
Solanaceae Cestrum diurnum Wild Jasmine
Datura stramonium Devil's Trumpet, Thorn Apple, Jimson Weed
Nicotiana tabacum Tobacco
Solanium ciliatum Cockroach Poison
Verbenaceae Lantana camara Whitesage, Wild Sage

A comment on alkaloids
Alkaloid Isolation Structure Synthesis
    (yrs to det.)
Morphine 1805 1925 (120) 1952
Strychnine 1818 1947 (129) 1954
Atropine 1819 1883 (64) 1902
Quinine 1820 1908 (88) 1944/2003
Caffeine 1820 1882 (62) 1895
Nicotine 1828 1893 (65) 1904
Cocaine 1860 1898 (38) 1898
The structure of many alkaloids can now be determined in a day or less!

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The Department of Chemistry, University of the West Indies,
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Created September 2011. Links checked and/or last modified 21st November 2014.