What is Sodium Fluoroacetate

also known as
compound 1080?

Most of the nation knows little or nothing about compound 1080.

Who is ADC and what connection does it have to this lethal poison?
Should you be concerned?.........you betcha!!
Most citizens sit back and trust the agencies who claim to protect them and our
wildlife population......indeed as tax payers we have every right to expect that.
Read on and no doubt you will leave with a little bit different outlook and for
sure you will be a much more informed citizen.
Consider this scenario:
A coyote goes after a ewe. Bites the collar and gets a dose of 1080. Two hours
later, while drinking from a creek, the poison begins to take effect. After he
thrashes around in extreme agony, he dies. His body collapses in the creek.
1080 is unleashed.
Down stream, a bear visits the stream and grabs a fish. He eats the fish, leaves
the skeletal remains on the shore and wanders off to die. A raccoon finds the
remains and scavenges what's left. A doe stops to get a drink of water. Two
hours and 25 miles later, she dies. Wolves raid the carcass. Ravens come to
feast then fly further away. Warblers ... and so on and so on...
Now for the icing on the cake. This poison is chemically stable. That means
that a decade from now, the ground it is spilled on is toxic. It has the ability to
kill x-potentially.
Thank you to
North American Wolf Association for this scenario.

The Livestock Protection Collars are handled and distributed by Animal

Damage Control (ADC) agency and Animal Damage Control (ADC), NOW
CALLED WILDLIFE SERVICES is a branch of the Animal and Plant Health
Inspection Service (APHIS) of the U.S. Department of Agriculture (USDA).

An excerpt taken from:

http://www.fund.org/facts/adc.html
A BRIEF HISTORY!
In 1931, Congress established the Animal Damage Control program, and
animal control became institutionalized at the federal level within the
Department of Interior (in the U.S. Fish & Wildlife Service). Sheep ranchers
and other livestock interest groups convinced Congress to pass the legislation,
which calls for "campaigns for the destruction" of "animals injurious to
agriculture, horticulture, forestry, animal husbandry, wild game animals, fur
bearing animals, and birds." ***In 1985, as a result of pressure from western
states, Congress transferred the ADC program to the Department of
Agriculture, thereby putting predator control into the hands of an agency
wedded to the livestock industry.***
In 1996, ADC agents killed 82,243 coyotes, primarily in western states. The
U.S. Department of Agriculture's own statistics indicate that the government
spends $2.60 on predator control for every $1 lost in livestock.
ADC represents an immense drain of taxpayer dollars to cover the losses of
very few citizens. Ranchers suffering livestock losses graze their animals on
publicly owned land at very cheap rates. Thus, American taxpayers are
subsidizing grazing for ranchers who demand that they further subsidize, at
enormous cost, the destruction of predators killing relatively small numbers of
their livestock. This corporate welfare ignores the suffering of ADC's victims
and the vital ecological role that species play in their habitats.
ADC DOES NOT require PUBLIC Input before beginning a CONTROL
PROGRAM in ANY area. They are at the "Beck and Call" of Ranchers, Sheep
Farmers etc. who pay part of their bill and GUESS what - an animal doesn't
even have to be going after any Livestock. Every year, ADC kills tens of
thousands of coyotes, and many bears, mountain lions, bobcats, wolves and
other predators . ADC also kills animals for eating flowers and pet food,
digging in gardens, frightening people, and other concerns that could easily be
addressed by nonviolent methods.
One of the MAIN means by which ADC accomplishes their KILLS is through
the use os a substance known as COMPOUND 1080 chemically known as:
SODIUM FLUOROACETATE!
WHAT IT IS AND WHAT IT DOES!

Compound 1080 is a highly toxic, slow-acting poison that causes immense

suffering in its victims. The federal agency authorized to kill predators with
Compound 1080, the ADC, reports that death "occurs in TWO to FIVE hours
OR MORE" and "may result from gradual cardiac failure; progressive
depression of the central nervous system with either cardiac or respiratory
failure as the terminal event; or respiratory arrest following severe
convulsions." IN OTHER WORDS, THE ANIMAL WILL EXPERIENCE
PROLONGED SUFFERING, BUT NOT BEFORE WANDERING AND
DYING FAR FROM THE POISON SITE.
THE REAL DEATH FACTS FROM FIELD OBSERVATIONS!
Coyotes which ingest a few drops of the 1080 from the LPC may not show
immediate symptoms, and often linger between 2 to 7 hours before dying.
Throughout this time symptoms reveal extensive suffering including
convulsions, dry heaves, disoriented running, biting their flanks and yipping.
Death occurs slowly, as the victim succumbs to cardiac or respiratory failure, or
progressive failure of their nervous system.
Secondary deaths may result when animals feed on poisoned victims. The death
scene described above will be repeated when other animals feed on the
poisoned carcass because most -- 90 percent according to one government
report -- poisoned animals will not be recovered. Likely victims of this
secondary poisoning include domestic dogs, birds, and other wildlife. The U.S.
Fish and Wildlife Service notes. PLEASE NOTE other wildlife WILL include
HAWKS, EAGLES, RACCOON, to say nothing of WOLVES, BOBCATS,
BEARS etc. OH ALMOST FORGOT, there is ONE other potential
SECONDARY VICTIM YOU! Compound 1080 is extremely dangerous to
people and their environment. An EPA-labeled "super" poison, Compound
1080 poses significant threats to human beings. The manufacturer reports
that each livestock collar contains enough poison to kill SIX 150-pound
adults or 26 children weighing 35 pounds each.

THERE IS NO KNOWN ANTIDOTE!

The poison can leak from collars and contaminate the environment. Two
government studies showed that more collars are punctured by wire, vegetation
or other objects, than by coyotes, and a fair number of collars are reported as
"missing." Although required that collars and wastes contaminated by
Compound 1080 be disposed under three feet of soil at least one-half mile
from human habitations and water supplies, nothing can be done about

undetected leakage, missing collars, and unrecovered carcasses. KEEP in mind

the estimate for UNRECOVERED carcasses is 90% and BECAUSE this poison
is ODORLESS and TASTELESS, (making its presence in the environment
extremely difficult to detect), COMPOUND 1080 maintains the SAME
LEVELS l of toxicity in water, meat, or grain. It remains in the tissue of the
victim, killing all animals in the food chain.
NOW WHAT HAPPENS TO THOSE ANIMALS THAT 1080 IS
SUPPOSED TO PROTECT!
Regarding the sheep and goats that are supposedly "protected" by the 1080
collars -- the law requires that any animal whose collar is punctured,
(Remember now, a puncture can often occur from Barbed Wire, Vegetation
such as a Broken Tree Branch, or maybe even just a Rub against a Rock etc.),
must be destroyed; and any animal that forages where the poison has leaked
will suffer the same agonizing death as the predator.
There are a lot of other non-lethal methods that can be used to prevent livestock
loss yet still ADC (Wildlife Services) keeps pushing for the use of Compound
1080 a substance originally developed in Poland, and initially patented as a
MOTH-PROOFING AGENT and was also tested as a chemical warfare agent
and insecticide. WHY?
OTHER NON-LETHAL CONTROL METHODS AVAILABLE!
http://www.enviroweb.org/pdi/alternat.htm
HERD MANAGEMENT!
Changing lambing times - ie. Farmers in Kansas have succeeded in cutting
losses by switching to fall instead of spring lambing.
CARRION REMOVAL - Dead livestock attracts coyotes and accustoms them
to the taste of domestic livestock. Carcasses should be removed and buried.
VARIABLE GRAZING - ie. rough rocky pastures or those with much cover
should be avoided during lambing time.
SHEPHERDS
BETTER HUSBANDRY - ie. A study in Montana found that visibly
handicapped sheep were selected by coyotes over healthy sheep. Thus,

improving herd health and removing diseased or injured animals for treatment
helps both to raise the heath status of the sheep flock and to avert predation.
CONFINEMENT!
Confinement close to residences - ie. penning at night time.
Shed lambing - a safe area for lambing time.
Predator-resistant fencing - especially appropriate for night penning and
lambing areas. There are two types "exclusion fencing" that prohibits entry and
"drift fencing" that redirects coyote movements away from sheep pens. Though
more expensive then electrical fencing, the maintenance costs are lower.
Electric fencing more costly maintenance wise but is very effective in deterring
coyote predation.
FRIGHTENING DEVICES!
Nighttime lighting - ie. Mercury-vapor lights with electric-eye sensors that turn
on at sunset and off at dawn.
Propane exploders - produce a loud explosion (resembling a gunshot) at
random intervals. They are most effective when the interval is fairly short and
the location of the devices is changed every few days.
Bells - A study in Kansas found that coyotes never attacked belled sheep in a
flock.
Parking a vehicle in the area of losses - may temporarily deter coyotes,
especially if moved frequently.
Radios - talk radio is at least temporarily effective at deterring coyotes.
GUARD ANIMALS!
Guard dogs - Guard dogs are one of the most promising techniques in predation
prevention, especially in larger, unconfined flocks. Although guard dog breeds
are ancient, their use in the United States is recent.Flock guardian breeds do not
herd the sheep, as a Border Collie or Australian Shepherd does. Instead, they
aggressively protect their sheep from any threats. They bond with their sheep
much as a wolf bonds with its pack. Guard dog breeds are large and
predominantly white-coated. Breeds include the Komondor, Maremma,

Slovensky Cuvac, Polish Tatra Sheepdog, Anatolian Shepherd, Kuvasz, Shar

Planinetz, and Great Pyrenees.
Aggressive livestock - donkeys, horses and llamas with donkeys are usually
considered to be the best species for this.
COMPENSATION to farmers and ranchers for CONFIRMED KILLS!
Bottom line - Yes, coyotes are predators.
Yes they will take down a sheep, goat, chicken etc. but
COMPOUND 1080 IS NOT the answer
and it is HIGH TIME ADC (Wildlife Services) be told ONCE and for ALL NO MORE USE OF COMPOUND 1080 EVER!
It is up to YOU to make sure that this horrendous poison NEVER be used in
your STATE - get involved, find out if it has been approved for use - write your
legislator, your congressman/woman, let them know the RISKS are FAR TOO
HIGH and NO ANIMAL deserves such a horrible fate.
There is ONE other way you can help.
SUPPORT "Predator-Friendly" Wool - SEE:
http://www.enviroweb.org/pdi/wool.htm
WHY SO MUCH ATTENTION ON ADC AND IT'S METHODS?
Today, ADC exemplifies bureaucracy out of control. In 1997, the agency began
calling itself "Wildlife Services" in a public relations attempt to appear that it is
doing something positive for wildlife. Instead, the rogue agency relies on the
same brutal, archaic management practices, and the
program remains a misdirected attempt to resolve animal/human conflicts. With
a misguided focus on killing, ADC does not promote long-term resolution of
conflicts, but often worsens them. And it completely fails to address the
ecological imbalance it creates by destroying integral parts of native
ecosystems.
BRUTAL METHODS STILL USED!
Trapping with painful devices such as the steel-jaw leghold trap and the wire
neck snare.
"Denning" of coyote pups (i.e. forcing them from their dens by hooking,
gassing, or other methods, and clubbing them to death).
Aerial shooting from helicopters and airplanes.

Using sheep collars containing Compound 1080, an extremely lethal poison

that causes extended convulsions and suffering prior to death.
Spraying a chemical detergent on roosting birds, sometimes numbering in the
hundreds of thousands, that destroys the insulating properties of their feathers
and leads to death by freezing.
Using M-44, an explosive device often baited with sodium cyanide powder that
explodes in an animal's mouth when bitten.

Ricin
From Wikipedia, the free encyclopedia
Jump to: navigation, search

Castor beans
Ricin (pronounced / ra s n/) is a protein toxin that is extracted from the castor bean
(Ricinus communis).

The U.S. Centers for Disease Control (CDC) gives a possible minimum figure of 500
micrograms (about the size of a grain of salt)[citation needed] for the lethal dose of ricin in
humans if exposure is from injection or inhalation.[1]

Contents
[hide]

1 Toxicity
2 Biochemistry
o 2.1 Structure
o 2.2 Entry into the Cytosol
o 2.3 Ribosome Inactivation
o 2.4 Depurination reaction
3 Manufacture
o 3.1 Patented extraction process
4 Potential medicinal use
5 Use as a chemical/biological warfare agent
6 Detected ricin incidents
o 6.1 1978 assassination of Georgi Markov
o 6.2 2000 discovery in Irvine, California home
o 6.3 2003 arrests in Britain
o 6.4 2003 envelope in South Carolina
o 6.5 2003 White House mail
o 6.6 2006 home in Richmond, Virginia
o 6.7 2008 hotel room in Las Vegas, Nevada
7 See also
8 References
9 External links

[edit] Toxicity

Ricin structure. The A chain is shown in blue and the B chain in orange.
Ricin is poisonous if inhaled, injected, or ingested, acting as a toxin by the inhibition of
protein synthesis. While there is no known antidote, the US military has developed a
vaccine.[2] Symptomatic and supportive treatment is available. Long term organ damage
is likely in survivors. Ricin causes severe diarrhea and victims can die of shock. Abrin is
a similar toxin. To cover 25 km2 area with 50% toxicity, about 1 metric ton of ricin is
required (estimated by the United States Department of Cultural and Biological Society
in service to the United States Biological and Technological threat survey).
Deaths caused by ingestion of castor oil plant seeds are rare.[3] Eight beans are considered
toxic for an adult.[4] A solution of saline and glucose has been used to treat ricin
overdose.[5] The case experience is not as negative as popular perception would
indicate.[6]

[edit] Biochemistry
Ricin is classified as a type 2 ribosome inactivating protein (RIP). Whereas Type 1 RIPs
consist of a single enzymatic protein chain, Type 2 RIPs, also known as holotoxins, are
heterodimeric glycoproteins. Type 2 RIPs consist of an A chain that is functionally
equivalent to a Type 1 RIP, covalently connected by a single disulfide bond to a B chain
that is catalytically inactive, but serves to mediate entry of the A-B protein complex into
the cytosol. Both Type 1 and Type 2 RIPs are functionally active against ribosomes in
vitro, however only Type 2 RIPs display cytoxicity due to the lectin properties of the B
chain. In order to display its ribosome inactivating function, the ricin disulfide bond must
be reductively cleaved.[7]

[edit] Structure
The tertiary structure of ricin was shown to be a globular, glycosylated heterodimer of
approximately 60-65 kDA.[5] Ricin toxin A chain (RTA) and ricin toxin B chain (RTB)
are of similar molecular weight, approximately 32 kDA and 34 kDA respectively.

Ricin A Chain is an N-glycoside hydrolase composed of 267 amino acids.[8] It

has three structural domains with approximately 50% of the polypeptide arranged
into alpha-helices and beta-sheets.[9] The three domains form a pronounced cleft
that is the active site of RTA.
Ricin B Chain is a lectin composed of 262 amino acids that is able to bind
terminal galactose residues on cell surfaces.[10] RTB form a bilobal, barbell-like
structure lacking alpha-helices or beta-sheets where individual lobes contain three
subdomains. At least one of these three subdomains in each homologous lobe
possesses a sugar-binding pocket that gives RTB its functional character.

Many plants such as barley have the A chain but not the B chain. People do not get sick
from eating large amounts of such products, as ricin A is of extremely low toxicity as
long as the B chain is not present.

[edit] Entry into the Cytosol

The ability of ricin to enter the cytosol depends on hydrogen bonding interactions
between RTB amino acid residues and complex carbohydrates on the surface of
eukaryotic cells containing either terminal N-acetyl galactosamine or beta-1,4-linked
galactose residues. Additionally, the mannose-type glycans of ricin are able to bind cells
that express mannose receptors.[11] Experimentally, RTB has been shown to bind to the
cell surface on the order of 106-108 ricin molecules per cell surface.[12]
The profuse binding of ricin to surface membranes allows internalization with all types of
membrane invaginations. Experimental evidence points to ricin uptake in both clathrincoated pits, as well as clathrin-independent pathways including caveolae and
macropinocytosis.[13][14] Vesicles shuttle ricin to endosomes that are delivered to the
Golgi apparatus. The active acidification of endosomes are thought to have little effect on
the functional properties of ricin. Because ricin is stable over a wide pH range,
degradation in endosomes or lysosomes offer little or no protection against ricin.[15] Ricin
molecules are thought to follow retrograde transport through the Golgi and enter the
endoplasmic reticulum (ER).
For ricin to function cytotoxically, RTA must be reductively cleaved from RTB in order
to release a steric block of the RTA active site. Currently, it is unknown whether this
takes place in the ER or in the cytosol. It is speculated that within the ER, RTA utilizes
the endoplasmic reticulum-associated protein degradation (ERAD) pathway that exists to
eject misfolded proteins to the cytosol.[16] Chaperones participating in ERAD may
recognize RTA as misfolded native protein and translocate it into the cytosol.
Additionally, RTA resists degradation by ubiquitination that often occurs with misfolded

proteins by maintaining a low content of lysine residues, the usual attachment sites for
ubiquitin.[17] In the cytosol, RTA is free to exert its toxicity on ribosomes.

[edit] Ribosome Inactivation

Study of the N-glycosidase activity of ricin was pioneered by Endo and Tsurugi[18] who
showed that RTA cleaves a glycosidic bond within the large rRNA of the 60S subunit of
eukaryotic ribosomes. They subsequently showed RTA specifically and irreversibly
hydrolyses the N-glycosidic bond of the adenine residue at position 4324 (A4324) within
the 28S rRNA, but leaves the phosphodiester backbone of the RNA intact.[19] The ricin
targets A4324 that is contained in a highly conserved sequence of 12 nucleotides
universally found in eukaryotic ribosomes. The sequence, 5-AGUACGAGAGGA-3,
termed the sarcin-ricin loop, is important in binding elongation factors during protein
synthesis.[20] The depurination event rapidly and completely inactivates the ribosome,
resulting in toxicity from inhibited protein synthesis. A single RTA molecule in the
cytosol is capable of depurinating approximately 1500 ribosomes per minute.

[edit] Depurination reaction

Within the active site of RTA, there exist several invariant amino acid residues involved
in the depurination of ribosomal RNA.[15] Although the exact mechanism of the event is
unknown, key amino acid residues identified include tyrosine at positions 80 and 123,
glutamic acid at position 177, and arginine at position 180. In particular, Arg180 and
Glu177 have been shown to be involved in the catalytic mechanism, and not substrate
binding, with enzyme kinetic studies involving RTA mutants. The model proposed by
Mozingo and Robertus,[21], based x-ray structures, is as follows:
1. Sarcin-ricin loop substrate binds RTA active site with target adenine stacking
against tyr80 and tyr123.
2. Arg180 is positioned such that it can protonate N-3 of adenine and break the bond
between N-9 of the adenine ring and C-1 of the ribose.
3. Bond cleavage results in an oxycarbonium ion on the ribose, stabilized by
Glu177.
4. N-3 protonation of adenine by Arg180 allows deprotonation of a nearby water
molecule.
5. Resulting hydroxyl attacks ribose carbonium ion.
6. Depurination of adenine results in a neutral ribose on an intact phosphodiester
RNA backbone.

[edit] Manufacture
Ricin is easily purified from castor-oil manufacturing waste. The aqueous phase left over
from the oil extraction process is called waste mash. It contains about 5-10% ricin by
weight. Separation requires only simple chromatographic techniques.

[edit] Patented extraction process

The process for extracting ricin is well known and has been described in a patent.[22] The
described extraction method is very similar to that used for the preparation of soy protein
isolates.
The patent was removed from the United States Patent and Trademark Office (USPTO)
database sometime in 2004, but it is still available online through international patent
databases.[23][24] Modern theories of protein chemistry cast doubt on the effectiveness of
the methods disclosed in the patent.[25]

[edit] Potential medicinal use

Some researchers have speculated about using ricins in the treatment of cancer, as a socalled "magic bullet" to destroy targeted cells:[26] Ricin could be linked to a monoclonal
antibody to target malignant cells recognized by the antibody. The major problem with
ricin is that its native internalization sequences are distributed throughout the protein. If
any of these native internalization sequences are present in a therapeutic, then the drug
will be internalized by, and kill, untargeted epithelial cells as well as targeted cancer
cells.
Some researchers hope that modifying ricin will sufficiently lessen the likelihood that the
ricin component of these immunotoxins will cause the wrong cells to internalize it, while
still retaining its cell-killing activity when it is internalized by the targeted cells.
Generally, however, ricin has been superseded for medical purposes by more practical
fragments of bacterial toxins, such as diphtheria toxin, which is used in denileukin
diftitox, an FDA-approved treatment for leukemia and lymphoma. No approved
therapeutics contain ricin.
A promising approach is also to use the non-toxic B subunit as a vehicle for delivering
antigens into cells thus greatly increasing their immunogenicity. Use of ricin as an
adjuvant has potential implications for developing mucosal vaccines.

[edit] Use as a chemical/biological warfare agent

The United States investigated ricin for its military potential during the First World War.
At that time it was being considered for use either as a toxic dust or as a coating for
bullets and shrapnel. The dust cloud concept could not be adequately developed, and the
coated bullet/shrapnel concept would violate the Hague Convention of 1899. The war
ended before it was weaponized.
During the Second World War the United States and Canada undertook studying ricin in
cluster bombs. Though there were plans for mass production and several field trials with
different bomblet concepts, the end conclusion was that it was no more economical than
using phosgene. This conclusion was based on comparison of the final weapons rather

than ricin's toxicity (LCt50 ~40 mgmin/m3). Ricin was given the military symbol W or
later WA. Interest in it continued for a short period after the Second World War, but soon
subsided when the U.S. Army Chemical Corps began a program to weaponize sarin.
The Soviet Union also had ricin. There were speculations that KGB even used it outside
of the Soviet bloc; however, this was never proven. In 1978, the Bulgarian dissident
Georgi Markov was assassinated by Bulgarian secret police who surreptitiously 'shot' him
on a London street with a modified umbrella using compressed gas to fire a tiny pellet
contaminated with ricin into his leg.[27] He died in a hospital a few days later; his body
was passed to a special poison branch of the British Ministry of Defence (MOD) that
discovered the pellet during an autopsy. The prime suspects were the Bulgarian secret
police: Georgi Markov had defected from Bulgaria some years previously and had
subsequently written books and made radio broadcasts which were highly critical of the
Bulgarian communist regime. However, it was believed at the time that Bulgaria would
not have been able to produce the pellet, and it was also believed that the KGB had
supplied it. The KGB denied any involvement although high-profile KGB defectors Oleg
Kalugin and Oleg Gordievsky have since confirmed the KGB's involvement. Earlier,
Soviet dissident Aleksandr Solzhenitsyn also suffered (but survived) ricin-like symptoms
after a 1971 encounter with KGB agents.[28]
Despite ricin's extreme toxicity and utility as an agent of chemical/biological warfare, it
is extremely difficult to limit the production of the toxin. Under both the 1972 Biological
Weapons Convention and the 1997 Chemical Weapons Convention, ricin is listed as a
schedule 1 controlled substance. Despite this, more than 1 million metric tonnes of castor
beans are processed each year, and approximately 5% of the total is rendered into a waste
containing high concentrations of ricin toxin.[29]
To put ricin used as a weapon into perspective, it is worth noting that as a biological
weapon or chemical weapon, ricin may not be considered very powerful in comparison
with other agents such as botulinum or anthrax. Furthermore, the quantity of ricin
required to achieve LD50 over a large geographic area is significantly more than an agent
such as anthrax (metric tons of ricin vs. only kilogram quantities of anthrax)[30]. Hence, a
military willing to use biological weapons and having advanced resources would rather
use either of the latter instead. Ricin is easy to produce, but is not as practical nor likely
to cause as many casualties as other agents. Ricin is inactivated (the protein changes
structure and becomes less dangerous) much more readily than anthrax spores, which
may remain lethal for decades. (Jan van Aken, an expert on biological weapons explained
in an interview with the German magazine Der Spiegel that he judges it rather reassuring
that Al Qaeda experimented with ricin as it suggests their inability to produce botulin or
anthrax.)
The major reason it is dangerous is that there is no specific antidote, and that it is very
easy to obtain (the castor bean plant is a common ornamental, and can be grown at home
without any special care). There have been several reported incidents where ricin has
been involved with infanticide where small children have been tricked into eating castor
beans because of their striking resemblance to chocolate-covered coffee beans.[citation

needed]

Ricin is actually several orders of magnitude less toxic than botulinum or tetanus
toxin, but those are more difficult to obtain.

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Cute Killers: 16 Unassuming-but-Lethal Poison Plants

Written by Sara on September 16th, 2008 - Topics: Animals and Habitats, Featured
Articles, Food and Health, Home and Garden, Nature and Ecosystems

(Part of an Exclusive WebEcoist Series on Amazing Trees, Plants, Forests and Flowers)

Most plants contain some level of toxins (like alkaloids) for defense. After all, they re
plants. They can t go anywhere. Through millennia of trial and error, both animals and
human beings have figured out which plants are safe, which are lethal, and which are
somewhere in between. For example, did you know that many grain-bearing plants
contain a toxin known as lectins? And that the African staple, cassava, must be
thoroughly boiled and soaked to separate it from its poisonous compound, cyanide? Even
the humble lima bean has been bred to contain less cyanide. Cherries, potatoes, peaches
and apple seeds are all toxic - eat enough of the latter, in fact, and it will prove fatal.
Fortunately, artificial selection and cooking methods have all but eliminated the threat of
toxins in everyday foods. But you may be surprised to find out the incredibly lethal plants
often hanging around the neighborhood park - or gracing your tabletop in the form of a
centerpiece.

Castor Bean

Images via UCC, My Sunshine Garden and remarc

Castor oil - for anyone unlucky enough to have been force spoon-fed this healthy yet
disgusting fluid as a child, you may be surprised to learn that an ingredient in the castor
bean just happens to be the deadliest plant poison on earth. Literally. Just one tiny castor
bean is enough to kill an adult within a few minutes. Castor oil is made safe (but not
palatable) with the removable of the lethal compound known as ricin. Amazingly, castor
bean plants are grown for decorative purpose all over the place, particularly in California.
Rosary Pea

Image source unknown

As if a deadly legume weren t bad enough, the pulses aren t so benign, either. The rosary
pea may sound sweet and downright pious, but it s actually one of the most dangerous
plants on earth. Its seeds contain a particular lectin known as abrin; if chewed and
swallowed, death will follow shortly. The seeds are easily identified with their distinctive
bright red jacket and single black dot (almost like a reverse Black Widow spider). Abrin,
which does its damage by inactivating ribosomes, is one of the most fatal toxins on earth.
After the vomiting, fever, nausea, drooling and G.I. dysfunction but before the bizarre
hyperexcitability, edema and fatally convulsive seizures, renal tubular degeneration,
bladder and retinal hemorrhage and widespread internal lesions typically develop.
Monkshood

Image via About.com

Another unassuming plant - until you learn that the nickname for monkshood is actually
wolfsbane. That s owing to its once common use by farmers as a very effective wolf
extermination tool. (Not to be left out, fowl are also fatally affected by the related
hensbane.) The monkshood has the distinction of evidently being the bane of many
creatures: its nicknames include womensbane and leopard s bane, though it is also known
as blue rocket and devil s helmet. It is technically part of the aconitum genus, of which
there are more than 250 species. The wolfsbane used to be a popular werewolf detection
tool, by the way. (Status was determined by holding the flower near the alleged s chin; a
yellow-tinged shadow on the skin was thought to be confirmation.)
Bushmans poison

Images via plantzafrica

The aptly-named Bushman s poison has famously been used by the Khoisan of South
Africa to poison the tips of their arrows. Though the plant produces pleasantly scented
flowers and a tasty plum-like berry, the milky sap can be fatal. The leaves, however, have
medicinal properties. Bushman s poison is also known as the wintersweet.
Angels trumpet

Images via Direct Gardening and Wikimedia

What could be sweeter than the sound of an angel s trumpet? Perhaps the moaning agony
of a trip that won t end. Related to petunias, tomatoes and potatoes, the angel s trumpet
(datura stramonium) is a highly effective hallucinogen, but should not be consumed for
recreational purposes as it can also be lethal. According to wikipedia: The active
ingredients are atropine, hyoscyamine and scopolamine which are classified as deliriants,
or anticholinergics. Due to the elevated risk of overdose in uninformed users, many
hospitalizations, and some deaths, are reported from recreational use. This common
plant also goes by many other names, including jimson weed, stink weed, loco weed, and
devil s snare. One 18-year-old who was house-sitting alone for his uncle recounts how he

decided to prepare some angel s trumpet tea in curiosity and almost died (a friend burst in
on him convulsing on the bathroom floor and the authorities assumed he was on an acid
trip).
Water hemlock

Image via Rutgers

The poison hemlock famously drunk by Socrates is deadly, but the water hemlock is just
as fatal. According to the USDA, water hemlock or poison parsnip is the most violently
toxic plant in North America. The flowers and stems are safe, but the stalky roots
contain chambers that are full of a deadly sap containing the convulsant cicutoxin. Grand
mal seizures are followed by a quick death if even a tiny amount is consumed.
English Yew

Images via greenlover, c-r-alpacas, bomengids, and Britannica

The English Yew, or taxus baccata (taxus meaning toxin), is one of the deadliest trees
on the planet. The evergreen has a majestic and lush appearance and is fairly common in
forests of Europe. The yew is considered by scientists to be an odd and primitive conifer
along with the monkey puzzle tree of Chile and Gingko biloba tree of Asia. The yew has
a rather sad history. All parts - save for the flesh of the berries - are extremely poisonous.
Because the toxin causes convulsions and paralysis, it was once used as an abortifacient.
Apothecaries would dry and powder the leaves and stems and give desperate women
minute amounts in the days before birth control was available. Unfortunately, death
would often result. The yew has been quite popular throughout history for a number of
medicinal purposes at extremely dilute levels, but it is deemed too dangerous in modern
medical practice to be of use. The yew s primary toxin is taxine, a cardiac depressant.
The yew acts rapidly and there is no antidote.
Snakeroot

Images via Sonja Keohane and canalphotos

Snakeroot is most dangerous for livestock such as cattle and sheep. When cows consume
the attractive fluffy white blooms and stems of the snakeroot, their milk and bones
become saturated with the toxin tremetol and humans who consume these contaminated
animal products will develop milk sickness (tremetol poisoning). In fact, milk sickness is
what killed Abraham Lincoln s mother, Nancy Hanks.
Strychnine tree

Images via motherherbs, BRAIN and wikipedia

Queen Cleopatra famously forced servants to commit suicide by means of a strychnine

tree s fruit seeds, which contain lethal levels of strychnine and brucine, in order to
determine if it would be the best means for her own suicide. Upon seeing their agony
(which included painful vomiting, facial contortions and convulsions) she opted for the
apparently less horrific choice of the asp. (The asp was actually an ancient term for any
number of poisonous snakes, but experts think it was probably the cobra that Cleopatra
chose to end her life.)
Moonseed

Images via Missouri plants and paradisegardentx

A otherworldly name and a plant with often fatal effects. The seeds of this Eastern North
American drupe (stone fruit) are extremely toxic to humans, although birds can eat them.
Moonseeds first cause paralysis but are fatal in larger doses and/or if treatment is not
sought immediately.
Daphne

Images via Bonnie Day and Island Net

This plant, also called the spurge laurel, is a favorite ornamental shrub in Europe. This
drupe-producing evergreen with waxy, attractive foliage and gorgeously fragrant blooms
is also highly toxic. Consumption of the leaves or red or yellow fruits will first cause
nausea and violent vomiting, followed by internal bleeding, coma and death. The daphne
plant is rich in the toxin mezerein.
Narcissus

Images via the Guardian and the flower expert

Narcissists are toxic enough when they come in human form, but the plant for which they
are named, also called the daffodil, is highly poisonous. Poet s narcissus is more toxic
than daffodil, but in both cases it is the bulbs, not the flower or stems, that cause illness.
One famous fatal case in Toulouse in the early 1900s occurred when the bulbs were
mistaken for onions and consumed. According to Botanical.com, Socrates called this
plant the Chaplet of the infernal Gods, because of its narcotic effects. An extract of the
bulbs, when applied to open wounds, has produced staggering, numbness of the whole
nervous system and paralysis of the heart. Yet, there are medicinal properties, and some
cultures even believe they can cure baldness and serve as a potent aphrodisiac. (Do not
try at home.)

Oleander

Image via Bay Area Hiker

The oleander is the most deadly plant in the world. It is also tremendously popular as a
decorative shrub. Just one leaf can kill an adult, and fatal poisonings have resulted from
minimal exposure to the twigs, blooms and berries. The plant contains numerous toxins,
including nerioside, oleandroside, saponins, and cardiac glycosides. Though native to
parts of the Mediterranean and Asia, it is now widely cultivated throughout the world.
Fatalities among horses and other livestock are common. Once ingested, oleander goes to
work simultaneously on the nervous system, the cardiovascular system, and the digestive
tract.
Rhododendron

Images via SOUL, Netstate and Kew

The toxic rhododendron, a stalky tree-like evergreen shrub with large, brilliant blooms, is
famously seen throughout much of the Pacific Northwest and is the state flower of
Washington. Its relative, the popular garden shrub azalea, is also poisonous. Both plants
contain andromedatoxin, which can cause severe pain, lethargy, depression, vomiting and
nausea, progressive paralysis, coma and eventual death. All parts are deadly.
Choke cherry

Images via Why Oh Why and BC

Chokecherry, or wild cherry, is a North American plant that is known for its large sprays
of tiny white flowers. The cherries are small and not eaten. The plant s woody stalks and
leaves are full of hydrocyanic acid, which is fatal if consumed. The poison affects the
respiratory system, and rapid breathing, choking and asphyxiation result.
Nightshade

Image via PBase

Also known as the devil s cherry, black cherry, great morel and belladonna, the
nightshade is toxic from tip to top. Containing atropine, a deadly alkaloid, those who
ingest even a small amount of the plant will soon notice they have lost their voice.
Respiratory trouble and convulsions follow. The plant is problematic because its cherries
are so sweet and children are frequently attracted to the wild fruit. Strangely, horses,
birds, sheep, goats and pigs seem to be immune to the effects of nightshade. Nightshade
poisoning is treatable with an emetic if treatment is sought swiftly. Plutarch spoke of
armies being wiped out by nightshade, and legend has it that Macbeth s soldiers poisoned
the invading Danes with wine made from the sweet fruit.