Bittersweet nightshade Berries and leaves of the bittersweet nightshade (Solanum dulcamara) plant.
They may look harmless enough, but plantscan harbor some of the most deadly poisonsknown. From the death of Socrates by poison hemlock to the accidental ingestion of deadly nightshade by children, poisonous plants have been responsible for human deaths throughout history. Get to know some of the most infamous plants and their poisons with this macabre list.
Water Hemlock (Cicuta maculata)

Water hemlockCommon water hemlock, or cowbane (Cicuta maculata). The plant is common throughout much of North America and can be lethal if ingested.
Closely related to poison hemlock (the plantthat famously killed Socrates), water hemlock has been deemed “the most violently toxic plant in North America.” A large wildflower in the carrot family, water hemlock resembles Queen Anne’s lace and is sometimes confused with edible parsnipsor celery. However, water hemlock is infused with deadly cicutoxin, especially in its roots, and will rapidly generate potentially fatal symptoms in anyone unlucky enough to eat it. Painful convulsions, abdominal cramps, nausea, and death are common, and those who survive are often afflicted with amnesia or lasting tremors.
Deadly Nightshade (Atropa belladonna)

Deadly nightshadeBelladonna, or deadly nightshade (Atropa belladonna). The leaves and berries contain several toxic alkaloids and are extremely poisonous to humans.
According to legend, Macbeth’s soldiers poisoned the invading Danes with winemade from the sweet fruit of deadly nightshade. Indeed, it is the sweetness of the berries that often lures children and unwitting adults to consume this lethal plant. A native of wooded or waste areas in central and southern Eurasia, deadly nightshade has dull green leaves and shiny black berries about the size of cherries. Nightshade contains atropine and scopolamine in its stems, leaves, berries, and roots, and causes paralysis in the involuntary muscles of the body, including the heart. Even physical contact with the leaves may cause skin irritation.
White Snakeroot (Ageratina altissima)

White snakerootDainty flower clusters of white snakeroot (Ageratina altissima).
An innocuous plant, white snakeroot was responsible for the death of Abraham Lincoln’s mother, Nancy Hanks. White snakeroot is a North American herb with flat-topped clusters of small white flowers and contains a toxic alcohol known as trematol. Unlike those who have died from directly ingesting deadly plants, poor Nancy Hanks was poisoned by simply drinking the milk of a cow who had grazed on the plant. Indeed, both the meat and milk from poisoned livestock can pass the toxin to human consumers. Symptoms of “milk poisoning” include loss of appetite, nausea, weakness, abdominal discomfort, reddened tongue, abnormal acidity of the blood, and death. Luckily farmers are now aware of this life-threatening hazard and make efforts remove the plant from animal pastures.
Castor Bean (Ricinus communis)

Castor bean seedsThe source of castor oil, castor bean seeds are used to make oil cakes. Unprocessed seeds also contain the poison ricin.
Widely grown as an ornamental and naturalized in many places, the castor beanis an attractive plant native to Africa. While the processed seeds are the source of castor oil, they naturally contain the poison ricinand are deadly in small amounts. It only takes one or two seeds to kill a child and up to eight to kill an adult. Ricin works by inhibiting the synthesis of proteins within cells and can cause severe vomiting, diarrhea, seizures, and even death. The poison was used in 1978 to assassinate Georgi Markov, a journalist who spoke out against the Bulgarian government, and has been mailed to several U.S. politicians in failed terrorism attempts. Most fatalities are the result of accidental ingestion by children and pets.
Rosary Pea (Abrus precatorius)

Jequirity beanThe distinctive and highly poisonous seeds of the jequirity bean, or rosary pea (Abrus precatorius).
Also called jequirity beans, these piously-named seeds contain abrin, an extremely deadly ribosome-inhibiting protein. Rosary peas are native to tropical areas and are often used in jewelry and prayer rosaries. While the seeds are not poisonous if intact, seeds that are scratched, broken, or chewed can be lethal. It only takes 3 micrograms of abrin to kill an adult, less than the amount of poison in one seed, and it is said that numerous jewelry makers have been made ill or died after accidentally pricking their fingers while working with the seeds. Like ricin, abrin prevents protein synthesiswithin cells and can cause organ failure within four days.
Oleander (Nerium oleander)

OleanderCommon oleander, or rosebay (Nerium oleander).
Described by Pliny the Elder in Ancient Rome, oleander is a beautiful plant known for its striking flowers. Though commonly grown as a hedge and ornamental, all parts of the oleander plant are deadly and contain lethal cardiac glycosides known as oleandrin and neriine. If eaten, oleander can cause vomiting, diarrhea, erratic pulse, seizures, coma, and death, and contact with the leaves and sap is known to be a skin irritant to some people. Indeed, the toxins in oleander are so strong that people have become ill after eating honey made by honeybees that visited the flowers! Fortunately, fatalities from oleander poisoning are rare, as the plant is very bitter and thus quickly deters anyone sampling the vegetation.
Water hemlock is the most violently toxic plant that grows in North America. Only a small amount of the toxic substance in the plant is needed to produce poisoning in livestock or in humans. The toxin cicutoxin, acting directly on the central nervous system, is a violent convulsant. Clinical signs of poisoning occur when a threshold dose is reached after which grand mal seizures and death occur.
Water hemlock has small, white flowers that grow in umbrella like clusters. Side veins of the leaves lead to notches, not to tips at the outer margin. The thick rootstalk of water hemlock contains a number of small chambers. These hold a highly poisonous brown or straw-colored liquid that is released when the stem is broken or cut. Thick, fleshy tubers and slender individual roots grow from the bottom of the rootstalk. Water hemlock grows in wet seepage areas of meadows, pastures, and in streams. It reaches a height of 0.5 to 1.0 meters. The plant is a perennial in the carrot family.
Water hemlock may be confused with poison-hemlock because of the similarity in names; however, these two are different plants that cause different types of poisoning. It has also been confused with wild parsnips, other herbs, and medicinal plants. In cases of water hemlock poisoning in humans, contact a poison control center and obtain emergency medical assistance as quickly as possible. Poisoning results in severe seizures and convulsions that must be controlled to preserve normal ventilation and cardiovascular function.

Animals will eat water hemlock early in spring and graze on the green seed heads later in the season. The roots; however, are more palatable and animals have been poisoned when the roots are exposed by plowing or cleaning ditches or when animal tramp in the streambeds. The underground portions of the plant, especially the tuberous roots, are highly toxic and very dangerous. Green seed heads have caused death losses in cattle.
The toxic substance in water hemlock is cicutoxin, a highly poisonous unsaturated alcohol that has a strong carrot-like odor. It is found principally in the tubers, but is also present in the leaves and stems during early growth. Leaves and stems lose most of their toxicity as they mature; however, green seed heads are poisonous.

Where and When It Grows Water hemlock, a wetland plant, is commonly found in wet meadows and pastures and along the banks of streams. It starts growing in the spring. In the higher elevations, water hemlock flowers in June or July.
How It Affects Livestock Livestock usually show signs of poisoning 15 minutes to 6 hours after they eat the plant; they may die within 15 minutes to 2 hours after signs appear. Cicutoxin is a severe convulsant and most animals die as a result of the asphyxia and cardiovascular collapse that occurs during the convulsions.
Signs and Lesions of Poisoning
Nervousness
Excessive salivation and frothing
Muscle twitching
Dilation of the pupils
Rapid pulse
Rapid breathing
Tremors
Violent convulsions, grand mal seizures
Coma
Death may occur as early as 15 minutes after a lethal dose is consumed
Skeletal and cardiac myofiber degeneration and necrosis
How to Reduce Losses The toxic substances act so rapidly that an affected animal can seldom be saved. Treatment consists of preventing seizures with barbiturates or tranquilizers and supporting respiration. Gastric lavage, activated charcoal, or saline cathartic may be helpful.
To reduce losses, keep animals away from places where water hemlock grows. The stems and leaves of water hemlock increase in palatability immediately after being sprayed with herbicide. Therefore, keep animals away from treated plants for 3 weeks after spraying. Most losses occur early in the spring or after the plants have been sprayed with 2,4-D.
The plants, which usually grow in small patches, are easy to locate. Spraying or grubbing can eradicate them. Actively growing plants can be controlled with 2,4-D applied at the rate of 1 kg per acre of acid equivalent. Repeat spray treatments until eradication is completed. Follow all precautions for handling herbicides. If you grub water hemlock, be sure to get all of the plant, including roots. Gather and burn every part.
All parts of the plant are toxic, particularly the seeds and roots, and especially when ingested. Hemlock is well-known as the poison that killed the philosopher Socrates after his trial in Ancient Greece
Toxicology Case Files from the Utah Poison Control Center
Teaching Points
Intentional ingestion of large quantities of oleander may cause toxicity similar to digoxin
Serum digoxin concentration may be used in a qualitative, but not quantitative, manner
Treatment with digoxin-specific antibody fragments (Digifab) may be helpful in management using typical indications
Case Presentation
A 32 y/o F presented to the ED about 30 minutes after ingestion of a large quantity of oleander leaves in a suicide attempt.
She was pale and vomited. Her initial vitals were normal. Activated charcoal was administered.
EKG and telemetry monitoring showed a Mobitz I AV block and premature atrial contractions. Initial labs showed a potassium of 3.8 and negative digoxin concentration.
However, about 30 minutes later the patient became bradycardic to the 40s. Four vials of Digifab were administered and the patient’s heart rate improved. She was admitted to the hospital and where she remained stable and did not require further Digifab. Unfortunately, additional digoxin concentrations were not measured.
Oleander Toxicity
There are numerous natural sources of cardioactive steroids, or cardiac glycosides, in addition to the well-known foxglove (Digitalis purpurea) and the pharmaceutical derivative digoxin. Other examples include red squill, lily of the valley, oleander (Nerium oleander), yellow oleander (Cascabela thevetia), dogbane, pong pong tree, milkweed, and sea mango. Ingestion of yellow oleander seeds is a common method of suicide in southeast Asia.1
Oleander (Figure 1) grows across the southern United States (Figure 2). The toxic cardenolide oleandrin is found in all parts of the plants with the greatest concentrations in the leaves. Toxicity has occurred with ingestion of multiple leaves or decoction of oleander. Toxicity is unlikely from small pediatric exposures.
Toxicity is similar to digoxin: nausea, vomiting, and cardiac abnormalities including bradycardia, various AV blocks, and ventricular dysrhythmias .2 Oleandrin is similar to digoxin and inhibits Na+/K+ ATPase leading to increased intracellular Na+ concentrations. This leads to diminished function of the Na+/Ca2+ antiporter causing increased intracellular Ca2+.
Digoxin immunoassays often cross-react with other structurally similar cardiac glycosides. However, the resulting concentrations should only be interpreted as “positive” and cannot be used to specifically guide treatment or quantify the amount of toxin present.
Instead, management will be based on clinical factors such as bradycardia, hypotension, and serum potassium. Serum potassium reflects the amount of inhibition of Na+/K+ATPase. In a series of acute digoxin overdoses, no patient died with a potassium < 5.3 Conversely, no patient survived with a potassium >5.5. Thus a potassium of 5-5.5 is often used as a threshold for treatment Digifab.
Dosing of Digifab is empiric. Patients with mild bradycardia and/or hypotension could be given 2-4 vials of Digifab. Unstable patients or those in cardiac arrest likely warrant higher doses but there is no data to guide therapy.
As Digifab is specific to digoxin, it may not completely reverse the effects of other cardiac glycosides. Other standard resuscitative measures for treatment of bradycardia, hypotension, and dysrhythmias may be used as well.
Digoxin is known to undergo enterohepatic recirculation. Thus, multidose activated charcoal may be useful in removing other cardiac glycosides if Digifab is unavailable or ineffective. There is no role for hemodialysis.
Oleander poisoning occurs when someone eats the flowers or chews the leaves or stems of the oleander plant (Nerium oleander), or its relative, the yellow oleander (Cascabela thevetia).
This article is for information only. DO NOT use it to treat or manage an actual poison exposure. If you or someone you are with has an exposure, call your local emergency number (such as 911), or your local poison control center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere in the United States.

Oleander (Nerium oleander) is a common ornamental evergreen shrub. It is used as a freeway median divider in warmer states, such as California. This plant is extremely toxic, and a single leaf may kill an adult. This photograph shows oleander not yet in bloom.
Poisonous Ingredient
Poisonous ingredients include:
Digitoxigenin
Neriin
Oleandrin
Oleondroside
Note: This list may not include all poisonous ingredients.
Where Found
The poisonous substances are found in all parts of the oleander plant:
Flowers
Leaves
Stems
Twigs
Symptoms
Oleander poisoning can affect many parts of the body.
HEART AND BLOOD
Irregular or slow heartbeat
Low blood pressure
Weakness
EYES, EARS, NOSE, MOUTH, AND THROAT
Blurred vision
Vision disturbances, including halosaround objects
STOMACH AND INTESTINES
Diarrhea
Loss of appetite
Nausea and vomiting
Stomach pain
NERVOUS SYSTEM
Confusion
Death
Depression
Disorientation
Dizziness
Drowsiness
Fainting
Headache
Lethargy
SKIN
Hives
Rash
Note: Depression, loss of appetite, and halos are most often seen in chronicoverdose cases.
Home Care
Seek immediate medical help. DO NOT make a person throw up unless told to do so by poison control or a health care provider.
Before Calling Emergency
Get the following information:
Person's age, weight, and condition
Name and part of the plant swallowed, if known
Time it was swallowed
Amount swallowed
Poison Control
Your local poison control center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere in the United States. This national hotline will let you talk to experts in poisoning. They will give you further instructions.
This is a free and confidential service. All local poison control centers in the United States use this national number. You should call if you have any questions about poisoning or poison prevention. It does not need to be an emergency. You can call for any reason, 24 hours a day, 7 days a week.
What to Expect at the Emergency Room
The provider will measure and monitor the person's vital signs, including temperature, pulse, breathing rate, and blood pressure. Symptoms will be treated as appropriate. The person may receive:
Activated charcoal
Blood and urine tests
Breathing support, including oxygen through a tube through the mouth into the lungs, and a breathing machine (ventilator)
Chest x-ray
ECG (electrocardiogram, or heart tracing)
Fluids through a vein (IV)
Medicines to treat symptoms including an antidote to reverse the effects of the poison
Tube through the mouth into the stomach to wash out the stomach (gastric lavage)
Outlook (Prognosis)
How well you do depends on the amount of poison swallowed and how quickly treatment is received. The faster you get medical help, the better the chance for recovery.
Symptoms last for 1 to 3 days and may require a hospital stay. Death is unlikely.
DO NOT touch or eat any plant with which you are not familiar. Wash your hands after working in the garden or walking in the woods
PREPARATION OF TOXIC RICIN Filed July 3, 1952 LSlurry with waterI pH of 3.8 sou using 5% u so,
LPrecipitate with N 80 pH of 7 using l2% Na,CO,
l Wash filter cake with |6.7% M0 80 I Single extraction Wash solution Extract with wateri pH of 3.8#O.l using H 80 iii Precipitate with Na IpH of 7 using i2% Na ()0 [E'E l Wash filter cake with l6.7% No.80 I
Wash solution Grind cake to 40 mesh Slurry with CCI.
| Settle and skim oft Ricin i Settled M0 reuse I N VEN TORS Harry L. Craig 0. h. A/derks Alsop/l H. 00min Sally h. Die/re 0h affe L. Karel BY 4 14 W ATTORNEY Dry and grind States. ate
This invention relates to the method of preparing toxic llClIl.
Ricin is a protoplasmic poison prepared from castor beans after the extraction of castor oil therefrom. It is most effective as a poison when injected intravenously or inhaled, the latter requiring extreme comminution and small particle size to be effective. It is believed that the toxic action is catalytic rather than stoichiometric which probably accounts for the high toxicity of the agent.
Because of its relative instability, ricin must be handled with extreme care. In neutral aqueous solution it is stable only up to 60-75 C., and in solid form up to 100110 0, although for short exposures, temperatures up to 130 may be tolerated. It is sensitive to acids, alkalis and halogen and may also be inactivated by mechanical working such as grinding or pulverizing. These factors are of great importance in developing a satisfactory method for preparing the material.
Although ricin has been prepared in crystalline condition in the laboratory in small quantities, it becomes necessary, for purposes of toxicological warfare, to prepare relatively large quantities in a high state of purity. This necessitates that as much as possible of the non-toxic material present be removed in the process.
In preparing the protein material, the castor beans are first ground and pressed to remove most of the oil. The pressed cake still retains about 15% oil and this may be removed by means of solvents which will extract an additional 150 pounds of oil per ton of beans and reduce the oil retained in the cake to a little over 1%. In the event that the expressing step is supplemented by solvent extraction, it is important to prevent detoxification of the protein during the solvent removal step. If residual solvent is removed from the ground beans by blowing with steam, considerable detoxification results. Blowing with nitrogen efiectively prevents detoxification but is expensive when carried out on a large scale.
After the oil has been removed, the pressed cake or pomace is extracted by agitating with water at a pH of 3.8101 at 25 C. which removes substantially all of the toxic protein. The extraction process is operative within a pH range of about 3 to 4.5 although the preferred range is about 3.5 to 4., The optimum operating point is a pH of 3.8-1.1, as indicated above. A careful pH control is essential in order that as much non-toxic protein as possible may be eliminated and also that the filtration rate may be held at a satisfactory value. Either HCl or H 80 may be used to get the desired pH for the extraction water, but H 50 is preferred due to its lower corrosion rate and ease of handling in concentrated form. The acid should be used in reasonably dilute form to prevent undue local concentrations during its addition. A 5% concentration is satisfactory.
Following the extraction, the slurry is filtered using either a conventional recessed plate filter or a continuous string discharge vacuum filter. With the latter about 7% of filter aid, based on meal weight, was found necessary for satisfactory filtration.
The filtrate from the water extraction step, which contains the ricin, was treated with a 16.7% solution of Na SO to precipitate the protein. This solution is com- "ice posed of 20 pounds of salt in 100 pounds of water and the amount used was such that the salt content equalled 20% of the filtrate weight. This amount and concentration of salt solution was about optimum considering the factors of cost and toxin recovery. Somewhat higher concentrations and larger amounts of solution can be used, however.
The precipitation process is not limited to the use of Na SO since a saturated solution of NaCl can be used successfully, but Na SO solution gives better nitrogen fractionation, more rapid precipitation, and can be operated under wider pH limits. It is desirable to raise the pH to about 7-8 before precipitation as this gives better ecovery and greater non-toxic nitrogen removal. The pH was raised to this value by using NaOH or Na CO the latter being preferred. The base used was quite dilute in order to prevent detoxification due to high local concentrations in the solution. A 5% solution of NaOH was used, whereas with Na CO a 12% solution was preferred. In general, this higher pH during precipitation gave a greater non-toxic nitrogen fractionation and at the same time maintained the toxin loss at less than 2%.
After precipitation, the slurry was filtered using from 1 to 4% filter aid, based on slurry weight, for satisfactory filtration; the amount of filter aid needed being dependent on the type of press used. Washing the filter cake with Na SO solution removed additional non-toxic nitrogen which is desirable. In this washing step a 16.7% solution of Na SO was again used. This washing step removed an additional 15% of non-toxic nitrogen from the cake.
After filtration the filter cake, which contains the ricin in combination with the Na SO may be dried and slurried with CCL, to separate the ricin by flotation. Separation of the ricin after a single precipitation and washing step is possible, but it is preferred to carry the process through an additional extraction and precipitation step. This is accomplished by slurrying the filter cake in three times its weight of water and the pH of the slurry is again brought to 3.8:.1 by means of 5% H The slurry is filtered and a second precipitation is brought about by adding Na SO solution. Although pH control here is not wholly essential it is advantageous to bring the pH to approximate neutrality by adding 12% Na CO A precipitation time of 45 minutes was necessary to obtain complete removal of the toxin. In filtering out the precipitate, no filter aid was used and the filter cake was washed with Na SO solution on the filter whereby an additional amount of nontoxic nitrogen was removed from the cake. This washing was effective only the first time and repeated washings had little effect in removing further non-toxic nitrogen.
The ricin-Na SO precipitate was dried at about 50 to 60 C. on a hot air tray dryer. The dried product was ground to pass a 40 mesh screen and agitated with 5 times its weight of CCl.;, which served the separate the ricin from the Na SO by flotation. After settling, the ricin was skimmed off the top. This reduced the Na SO content of the mixture from a previous 40 to 50% down to 15 to 18%. About 1 to 2% of nitrogen remained in the Na SO salt which could then be used for subsequent precipitations.
The final precipitation produced a particle size of 1-2 mu. On drying the wet cake, however, the ricin cemented together forming larger particles. These could not be broken down to their original size by ordinary grinding methods and since a very fine particle size was necessary in order that the product might be used as a toxic weapon, it was thought desirable to seek some method to prevent the agglomeration or cementing process that took place on drying.
To attempt to affect this result, physical conditions prevailing under the precipitation process were changed.
This included changing the temperature of precipitation and the rate of agitation. Other changes included precipitation with ony partial saturation of Na SO and the use of wetting and seeding agents. None of these expedients produced any significant improvement in particle size.
Ordinary dry ball and hammer milling of the dried ricin produced considerable detoxifiiation perhaps due to the generation of excess heat. The use of CCl slurry plus the use of low temperature and low moisture content of the ricin reduced detoxification during ball milling.
Spray drying proved to be an even better method of securing a reasonably small particle size. Best results Were achieved by using a solution having about 20% solids, an inlet temperature of 150 C. and an atomizing air pressure of 150 to 180 psi. The particle size secured was 6 to 8 mu.
The best means of securing a small particle size was by air grinding. This was carried out in an apparatus having a chamber with conical top and bottom. The material to be ground has been fed into this chamber and is withdrawn from the bottom and forced back into the center of the chamber tangentially through a venturi. Compressed air of about 100 psi. was fed to the venturi to provide the grinding force. The fines are drawn off the top and the large particles settle to the bottom to be recirculated and reground. This process produced particles having a mass median diameter of 2.5 to 3.5 mu.
Numerous variations are possible in the several steps of the process commencing with the water extraction and precipitation which may be a single or multiple step. Although a single extraction step can be used, as indicated before, some process modifications are necessary for its successful operation on a plant scale. Double extraction proved to be quite efiicien-t but additional steps beyond the second extraction step were not found necessary.
The drawing is self-descriptive and shows the various steps of the process described.
We claim:
1. In a method of preparing toxic ricin from castor beans comprising slurrying an expressed castor bean cake with water to remove the water soluble ricin and precipitating the ricin from the filtrate,
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Bittersweet nightshade Berries and leaves of the bittersweet nightshade (Solanum dulcamara) plant.
They may look harmless enough, but plantscan harbor some of the most deadly poisonsknown. From the death of Socrates by poison hemlock to the accidental ingestion of deadly nightshade by children, poisonous plants have been responsible for human deaths throughout history. Get to know some of the most infamous plants and their poisons with this macabre list.
Water Hemlock (Cicuta maculata)

Water hemlockCommon water hemlock, or cowbane (Cicuta maculata). The plant is common throughout much of North America and can be lethal if ingested.
Closely related to poison hemlock (the plantthat famously killed Socrates), water hemlock has been deemed “the most violently toxic plant in North America.” A large wildflower in the carrot family, water hemlock resembles Queen Anne’s lace and is sometimes confused with edible parsnipsor celery. However, water hemlock is infused with deadly cicutoxin, especially in its roots, and will rapidly generate potentially fatal symptoms in anyone unlucky enough to eat it. Painful convulsions, abdominal cramps, nausea, and death are common, and those who survive are often afflicted with amnesia or lasting tremors.
Deadly Nightshade (Atropa belladonna)

Deadly nightshadeBelladonna, or deadly nightshade (Atropa belladonna). The leaves and berries contain several toxic alkaloids and are extremely poisonous to humans.
According to legend, Macbeth’s soldiers poisoned the invading Danes with winemade from the sweet fruit of deadly nightshade. Indeed, it is the sweetness of the berries that often lures children and unwitting adults to consume this lethal plant. A native of wooded or waste areas in central and southern Eurasia, deadly nightshade has dull green leaves and shiny black berries about the size of cherries. Nightshade contains atropine and scopolamine in its stems, leaves, berries, and roots, and causes paralysis in the involuntary muscles of the body, including the heart. Even physical contact with the leaves may cause skin irritation.
White Snakeroot (Ageratina altissima)

White snakerootDainty flower clusters of white snakeroot (Ageratina altissima).
An innocuous plant, white snakeroot was responsible for the death of Abraham Lincoln’s mother, Nancy Hanks. White snakeroot is a North American herb with flat-topped clusters of small white flowers and contains a toxic alcohol known as trematol. Unlike those who have died from directly ingesting deadly plants, poor Nancy Hanks was poisoned by simply drinking the milk of a cow who had grazed on the plant. Indeed, both the meat and milk from poisoned livestock can pass the toxin to human consumers. Symptoms of “milk poisoning” include loss of appetite, nausea, weakness, abdominal discomfort, reddened tongue, abnormal acidity of the blood, and death. Luckily farmers are now aware of this life-threatening hazard and make efforts remove the plant from animal pastures.
Castor Bean (Ricinus communis)

Castor bean seedsThe source of castor oil, castor bean seeds are used to make oil cakes. Unprocessed seeds also contain the poison ricin.
Widely grown as an ornamental and naturalized in many places, the castor beanis an attractive plant native to Africa. While the processed seeds are the source of castor oil, they naturally contain the poison ricinand are deadly in small amounts. It only takes one or two seeds to kill a child and up to eight to kill an adult. Ricin works by inhibiting the synthesis of proteins within cells and can cause severe vomiting, diarrhea, seizures, and even death. The poison was used in 1978 to assassinate Georgi Markov, a journalist who spoke out against the Bulgarian government, and has been mailed to several U.S. politicians in failed terrorism attempts. Most fatalities are the result of accidental ingestion by children and pets.
Rosary Pea (Abrus precatorius)

Jequirity beanThe distinctive and highly poisonous seeds of the jequirity bean, or rosary pea (Abrus precatorius).
Also called jequirity beans, these piously-named seeds contain abrin, an extremely deadly ribosome-inhibiting protein. Rosary peas are native to tropical areas and are often used in jewelry and prayer rosaries. While the seeds are not poisonous if intact, seeds that are scratched, broken, or chewed can be lethal. It only takes 3 micrograms of abrin to kill an adult, less than the amount of poison in one seed, and it is said that numerous jewelry makers have been made ill or died after accidentally pricking their fingers while working with the seeds. Like ricin, abrin prevents protein synthesiswithin cells and can cause organ failure within four days.
Oleander (Nerium oleander)

OleanderCommon oleander, or rosebay (Nerium oleander).
Described by Pliny the Elder in Ancient Rome, oleander is a beautiful plant known for its striking flowers. Though commonly grown as a hedge and ornamental, all parts of the oleander plant are deadly and contain lethal cardiac glycosides known as oleandrin and neriine. If eaten, oleander can cause vomiting, diarrhea, erratic pulse, seizures, coma, and death, and contact with the leaves and sap is known to be a skin irritant to some people. Indeed, the toxins in oleander are so strong that people have become ill after eating honey made by honeybees that visited the flowers! Fortunately, fatalities from oleander poisoning are rare, as the plant is very bitter and thus quickly deters anyone sampling the vegetation.
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Water hemlock is the most violently toxic plant that grows in North America. Only a small amount of the toxic substance in the plant is needed to produce poisoning in livestock or in humans. The toxin cicutoxin, acting directly on the central nervous system, is a violent convulsant. Clinical signs of poisoning occur when a threshold dose is reached after which grand mal seizures and death occur.
Water hemlock has small, white flowers that grow in umbrella like clusters. Side veins of the leaves lead to notches, not to tips at the outer margin. The thick rootstalk of water hemlock contains a number of small chambers. These hold a highly poisonous brown or straw-colored liquid that is released when the stem is broken or cut. Thick, fleshy tubers and slender individual roots grow from the bottom of the rootstalk. Water hemlock grows in wet seepage areas of meadows, pastures, and in streams. It reaches a height of 0.5 to 1.0 meters. The plant is a perennial in the carrot family.
Water hemlock may be confused with poison-hemlock because of the similarity in names; however, these two are different plants that cause different types of poisoning. It has also been confused with wild parsnips, other herbs, and medicinal plants. In cases of water hemlock poisoning in humans, contact a poison control center and obtain emergency medical assistance as quickly as possible. Poisoning results in severe seizures and convulsions that must be controlled to preserve normal ventilation and cardiovascular function.

Animals will eat water hemlock early in spring and graze on the green seed heads later in the season. The roots; however, are more palatable and animals have been poisoned when the roots are exposed by plowing or cleaning ditches or when animal tramp in the streambeds. The underground portions of the plant, especially the tuberous roots, are highly toxic and very dangerous. Green seed heads have caused death losses in cattle.
The toxic substance in water hemlock is cicutoxin, a highly poisonous unsaturated alcohol that has a strong carrot-like odor. It is found principally in the tubers, but is also present in the leaves and stems during early growth. Leaves and stems lose most of their toxicity as they mature; however, green seed heads are poisonous.

Where and When It Grows
Water hemlock, a wetland plant, is commonly found in wet meadows and pastures and along the banks of streams. It starts growing in the spring. In the higher elevations, water hemlock flowers in June or July.
How It Affects Livestock
Livestock usually show signs of poisoning 15 minutes to 6 hours after they eat the plant; they may die within 15 minutes to 2 hours after signs appear. Cicutoxin is a severe convulsant and most animals die as a result of the asphyxia and cardiovascular collapse that occurs during the convulsions.
Signs and Lesions of Poisoning
Nervousness
Excessive salivation and frothing
Muscle twitching
Dilation of the pupils
Rapid pulse
Rapid breathing
Tremors
Violent convulsions, grand mal seizures
Coma
Death may occur as early as 15 minutes after a lethal dose is consumed
Skeletal and cardiac myofiber degeneration and necrosis
How to Reduce Losses
The toxic substances act so rapidly that an affected animal can seldom be saved. Treatment consists of preventing seizures with barbiturates or tranquilizers and supporting respiration. Gastric lavage, activated charcoal, or saline cathartic may be helpful.
To reduce losses, keep animals away from places where water hemlock grows. The stems and leaves of water hemlock increase in palatability immediately after being sprayed with herbicide. Therefore, keep animals away from treated plants for 3 weeks after spraying. Most losses occur early in the spring or after the plants have been sprayed with 2,4-D.
The plants, which usually grow in small patches, are easy to locate. Spraying or grubbing can eradicate them. Actively growing plants can be controlled with 2,4-D applied at the rate of 1 kg per acre of acid equivalent. Repeat spray treatments until eradication is completed. Follow all precautions for handling herbicides. If you grub water hemlock, be sure to get all of the plant, including roots. Gather and burn every part.
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All parts of the plant are toxic, particularly the seeds and roots, and especially when ingested. Hemlock is well-known as the poison that killed the philosopher Socrates after his trial in Ancient Greece
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Plants containing cardiac glycosides
FamilyRepresentative exampleBotanical nameCommon nameApocynaceaeCerbera thevetia or Thevetia peruvianaYellow oleanderNerium oleanderCommon or pink oleanderStrophanthusDogbaneAsclepiadaceaeAsclepiasMilkweedCalotropisCrown flowerCelastraceaeEuonymus europaeusSpindle treeCruciferaeCheiranthusWall flowerErysimumWall flowerLiliaceaeConvallaria majalisLily of the valleyUrginia maritima or Urginia indicaSquillRanunculaceaeHelleborus nigerHenbaneScrophulariaceaeDigitalis purpureaFoxgloveDigitalis lanataWoolly foxglove
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Toxicology Case Files from the Utah Poison Control Center
Teaching Points
Intentional ingestion of large quantities of oleander may cause toxicity similar to digoxin
Serum digoxin concentration may be used in a qualitative, but not quantitative, manner
Treatment with digoxin-specific antibody fragments (Digifab) may be helpful in management using typical indications
Case Presentation
A 32 y/o F presented to the ED about 30 minutes after ingestion of a large quantity of oleander leaves in a suicide attempt.
She was pale and vomited. Her initial vitals were normal. Activated charcoal was administered.
EKG and telemetry monitoring showed a Mobitz I AV block and premature atrial contractions. Initial labs showed a potassium of 3.8 and negative digoxin concentration.
However, about 30 minutes later the patient became bradycardic to the 40s. Four vials of Digifab were administered and the patient’s heart rate improved. She was admitted to the hospital and where she remained stable and did not require further Digifab. Unfortunately, additional digoxin concentrations were not measured.
Oleander Toxicity
There are numerous natural sources of cardioactive steroids, or cardiac glycosides, in addition to the well-known foxglove (Digitalis purpurea) and the pharmaceutical derivative digoxin. Other examples include red squill, lily of the valley, oleander (Nerium oleander), yellow oleander (Cascabela thevetia), dogbane, pong pong tree, milkweed, and sea mango. Ingestion of yellow oleander seeds is a common method of suicide in southeast Asia.1
Oleander (Figure 1) grows across the southern United States (Figure 2). The toxic cardenolide oleandrin is found in all parts of the plants with the greatest concentrations in the leaves. Toxicity has occurred with ingestion of multiple leaves or decoction of oleander. Toxicity is unlikely from small pediatric exposures.
Toxicity is similar to digoxin: nausea, vomiting, and cardiac abnormalities including bradycardia, various AV blocks, and ventricular dysrhythmias .2 Oleandrin is similar to digoxin and inhibits Na+/K+ ATPase leading to increased intracellular Na+ concentrations. This leads to diminished function of the Na+/Ca2+ antiporter causing increased intracellular Ca2+.
Digoxin immunoassays often cross-react with other structurally similar cardiac glycosides. However, the resulting concentrations should only be interpreted as “positive” and cannot be used to specifically guide treatment or quantify the amount of toxin present.
Instead, management will be based on clinical factors such as bradycardia, hypotension, and serum potassium. Serum potassium reflects the amount of inhibition of Na+/K+ATPase. In a series of acute digoxin overdoses, no patient died with a potassium < 5.3 Conversely, no patient survived with a potassium >5.5. Thus a potassium of 5-5.5 is often used as a threshold for treatment Digifab.
Dosing of Digifab is empiric. Patients with mild bradycardia and/or hypotension could be given 2-4 vials of Digifab. Unstable patients or those in cardiac arrest likely warrant higher doses but there is no data to guide therapy.
As Digifab is specific to digoxin, it may not completely reverse the effects of other cardiac glycosides. Other standard resuscitative measures for treatment of bradycardia, hypotension, and dysrhythmias may be used as well.
Digoxin is known to undergo enterohepatic recirculation. Thus, multidose activated charcoal may be useful in removing other cardiac glycosides if Digifab is unavailable or ineffective. There is no role for hemodialysis.
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Oleander poisoning occurs when someone eats the flowers or chews the leaves or stems of the oleander plant (Nerium oleander), or its relative, the yellow oleander (Cascabela thevetia).
This article is for information only. DO NOT use it to treat or manage an actual poison exposure. If you or someone you are with has an exposure, call your local emergency number (such as 911), or your local poison control center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere in the United States.

Oleander (Nerium oleander) is a common ornamental evergreen shrub. It is used as a freeway median divider in warmer states, such as California. This plant is extremely toxic, and a single leaf may kill an adult. This photograph shows oleander not yet in bloom.
Poisonous Ingredient
Poisonous ingredients include:
Digitoxigenin
Neriin
Oleandrin
Oleondroside
Note: This list may not include all poisonous ingredients.
Where Found
The poisonous substances are found in all parts of the oleander plant:
Flowers
Leaves
Stems
Twigs
Symptoms
Oleander poisoning can affect many parts of the body.
HEART AND BLOOD
Irregular or slow heartbeat
Low blood pressure
Weakness
EYES, EARS, NOSE, MOUTH, AND THROAT
Blurred vision
Vision disturbances, including halosaround objects
STOMACH AND INTESTINES
Diarrhea
Loss of appetite
Nausea and vomiting
Stomach pain
NERVOUS SYSTEM
Confusion
Death
Depression
Disorientation
Dizziness
Drowsiness
Fainting
Headache
Lethargy
SKIN
Hives
Rash
Note: Depression, loss of appetite, and halos are most often seen in chronicoverdose cases.
Home Care
Seek immediate medical help. DO NOT make a person throw up unless told to do so by poison control or a health care provider.
Before Calling Emergency
Get the following information:
Person's age, weight, and condition
Name and part of the plant swallowed, if known
Time it was swallowed
Amount swallowed
Poison Control
Your local poison control center can be reached directly by calling the national toll-free Poison Help hotline (1-800-222-1222) from anywhere in the United States. This national hotline will let you talk to experts in poisoning. They will give you further instructions.
This is a free and confidential service. All local poison control centers in the United States use this national number. You should call if you have any questions about poisoning or poison prevention. It does not need to be an emergency. You can call for any reason, 24 hours a day, 7 days a week.
What to Expect at the Emergency Room
The provider will measure and monitor the person's vital signs, including temperature, pulse, breathing rate, and blood pressure. Symptoms will be treated as appropriate. The person may receive:
Activated charcoal
Blood and urine tests
Breathing support, including oxygen through a tube through the mouth into the lungs, and a breathing machine (ventilator)
Chest x-ray
ECG (electrocardiogram, or heart tracing)
Fluids through a vein (IV)
Medicines to treat symptoms including an antidote to reverse the effects of the poison
Tube through the mouth into the stomach to wash out the stomach (gastric lavage)
Outlook (Prognosis)
How well you do depends on the amount of poison swallowed and how quickly treatment is received. The faster you get medical help, the better the chance for recovery.
Symptoms last for 1 to 3 days and may require a hospital stay. Death is unlikely.
DO NOT touch or eat any plant with which you are not familiar. Wash your hands after working in the garden or walking in the woods
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PREPARATION OF TOXIC RICIN Filed July 3, 1952 LSlurry with waterI pH of 3.8 sou using 5% u so,
LPrecipitate with N 80 pH of 7 using l2% Na,CO,
l Wash filter cake with |6.7% M0 80 I Single extraction Wash solution Extract with wateri pH of 3.8#O.l using H 80 iii Precipitate with Na IpH of 7 using i2% Na ()0 [E'E l Wash filter cake with l6.7% No.80 I
Wash solution Grind cake to 40 mesh Slurry with CCI.
| Settle and skim oft Ricin i Settled M0 reuse I N VEN TORS Harry L. Craig 0. h. A/derks Alsop/l H. 00min Sally h. Die/re 0h affe L. Karel BY 4 14 W ATTORNEY Dry and grind States. ate
This invention relates to the method of preparing toxic llClIl.
Ricin is a protoplasmic poison prepared from castor beans after the extraction of castor oil therefrom. It is most effective as a poison when injected intravenously or inhaled, the latter requiring extreme comminution and small particle size to be effective. It is believed that the toxic action is catalytic rather than stoichiometric which probably accounts for the high toxicity of the agent.
Because of its relative instability, ricin must be handled with extreme care. In neutral aqueous solution it is stable only up to 60-75 C., and in solid form up to 100110 0, although for short exposures, temperatures up to 130 may be tolerated. It is sensitive to acids, alkalis and halogen and may also be inactivated by mechanical working such as grinding or pulverizing. These factors are of great importance in developing a satisfactory method for preparing the material.
Although ricin has been prepared in crystalline condition in the laboratory in small quantities, it becomes necessary, for purposes of toxicological warfare, to prepare relatively large quantities in a high state of purity. This necessitates that as much as possible of the non-toxic material present be removed in the process.
In preparing the protein material, the castor beans are first ground and pressed to remove most of the oil. The pressed cake still retains about 15% oil and this may be removed by means of solvents which will extract an additional 150 pounds of oil per ton of beans and reduce the oil retained in the cake to a little over 1%. In the event that the expressing step is supplemented by solvent extraction, it is important to prevent detoxification of the protein during the solvent removal step. If residual solvent is removed from the ground beans by blowing with steam, considerable detoxification results. Blowing with nitrogen efiectively prevents detoxification but is expensive when carried out on a large scale.
After the oil has been removed, the pressed cake or pomace is extracted by agitating with water at a pH of 3.8101 at 25 C. which removes substantially all of the toxic protein. The extraction process is operative within a pH range of about 3 to 4.5 although the preferred range is about 3.5 to 4., The optimum operating point is a pH of 3.8-1.1, as indicated above. A careful pH control is essential in order that as much non-toxic protein as possible may be eliminated and also that the filtration rate may be held at a satisfactory value. Either HCl or H 80 may be used to get the desired pH for the extraction water, but H 50 is preferred due to its lower corrosion rate and ease of handling in concentrated form. The acid should be used in reasonably dilute form to prevent undue local concentrations during its addition. A 5% concentration is satisfactory.
Following the extraction, the slurry is filtered using either a conventional recessed plate filter or a continuous string discharge vacuum filter. With the latter about 7% of filter aid, based on meal weight, was found necessary for satisfactory filtration.
The filtrate from the water extraction step, which contains the ricin, was treated with a 16.7% solution of Na SO to precipitate the protein. This solution is com- "ice posed of 20 pounds of salt in 100 pounds of water and the amount used was such that the salt content equalled 20% of the filtrate weight. This amount and concentration of salt solution was about optimum considering the factors of cost and toxin recovery. Somewhat higher concentrations and larger amounts of solution can be used, however.
The precipitation process is not limited to the use of Na SO since a saturated solution of NaCl can be used successfully, but Na SO solution gives better nitrogen fractionation, more rapid precipitation, and can be operated under wider pH limits. It is desirable to raise the pH to about 7-8 before precipitation as this gives better ecovery and greater non-toxic nitrogen removal. The pH was raised to this value by using NaOH or Na CO the latter being preferred. The base used was quite dilute in order to prevent detoxification due to high local concentrations in the solution. A 5% solution of NaOH was used, whereas with Na CO a 12% solution was preferred. In general, this higher pH during precipitation gave a greater non-toxic nitrogen fractionation and at the same time maintained the toxin loss at less than 2%.
After precipitation, the slurry was filtered using from 1 to 4% filter aid, based on slurry weight, for satisfactory filtration; the amount of filter aid needed being dependent on the type of press used. Washing the filter cake with Na SO solution removed additional non-toxic nitrogen which is desirable. In this washing step a 16.7% solution of Na SO was again used. This washing step removed an additional 15% of non-toxic nitrogen from the cake.
After filtration the filter cake, which contains the ricin in combination with the Na SO may be dried and slurried with CCL, to separate the ricin by flotation. Separation of the ricin after a single precipitation and washing step is possible, but it is preferred to carry the process through an additional extraction and precipitation step. This is accomplished by slurrying the filter cake in three times its weight of water and the pH of the slurry is again brought to 3.8:.1 by means of 5% H The slurry is filtered and a second precipitation is brought about by adding Na SO solution. Although pH control here is not wholly essential it is advantageous to bring the pH to approximate neutrality by adding 12% Na CO A precipitation time of 45 minutes was necessary to obtain complete removal of the toxin. In filtering out the precipitate, no filter aid was used and the filter cake was washed with Na SO solution on the filter whereby an additional amount of nontoxic nitrogen was removed from the cake. This washing was effective only the first time and repeated washings had little effect in removing further non-toxic nitrogen.
The ricin-Na SO precipitate was dried at about 50 to 60 C. on a hot air tray dryer. The dried product was ground to pass a 40 mesh screen and agitated with 5 times its weight of CCl.;, which served the separate the ricin from the Na SO by flotation. After settling, the ricin was skimmed off the top. This reduced the Na SO content of the mixture from a previous 40 to 50% down to 15 to 18%. About 1 to 2% of nitrogen remained in the Na SO salt which could then be used for subsequent precipitations.
The final precipitation produced a particle size of 1-2 mu. On drying the wet cake, however, the ricin cemented together forming larger particles. These could not be broken down to their original size by ordinary grinding methods and since a very fine particle size was necessary in order that the product might be used as a toxic weapon, it was thought desirable to seek some method to prevent the agglomeration or cementing process that took place on drying.
To attempt to affect this result, physical conditions prevailing under the precipitation process were changed.
This included changing the temperature of precipitation and the rate of agitation. Other changes included precipitation with ony partial saturation of Na SO and the use of wetting and seeding agents. None of these expedients produced any significant improvement in particle size.
Ordinary dry ball and hammer milling of the dried ricin produced considerable detoxifiiation perhaps due to the generation of excess heat. The use of CCl slurry plus the use of low temperature and low moisture content of the ricin reduced detoxification during ball milling.
Spray drying proved to be an even better method of securing a reasonably small particle size. Best results Were achieved by using a solution having about 20% solids, an inlet temperature of 150 C. and an atomizing air pressure of 150 to 180 psi. The particle size secured was 6 to 8 mu.
The best means of securing a small particle size was by air grinding. This was carried out in an apparatus having a chamber with conical top and bottom. The material to be ground has been fed into this chamber and is withdrawn from the bottom and forced back into the center of the chamber tangentially through a venturi. Compressed air of about 100 psi. was fed to the venturi to provide the grinding force. The fines are drawn off the top and the large particles settle to the bottom to be recirculated and reground. This process produced particles having a mass median diameter of 2.5 to 3.5 mu.
Numerous variations are possible in the several steps of the process commencing with the water extraction and precipitation which may be a single or multiple step. Although a single extraction step can be used, as indicated before, some process modifications are necessary for its successful operation on a plant scale. Double extraction proved to be quite efiicien-t but additional steps beyond the second extraction step were not found necessary.
The drawing is self-descriptive and shows the various steps of the process described.
We claim:
1. In a method of preparing toxic ricin from castor beans comprising slurrying an expressed castor bean cake with water to remove the water soluble ricin and precipitating the ricin from the filtrate,
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