Poisonous plants with special

reference to Pakistan
by
Muhammad Khalil-ur-Rehman

 Plants which produce gastroenteritis

Plants producing cardiovascular problems
Plants producing central nervous system disturbances
Plants having atropine and atropine like actions
Plants having nicotine like actions
Plants having hydrogen cyanide (Cyanophore plants)
Plants having liver damaging effects

Plants which produce gastroentritis

Plants irritant to mouth and throat
Plants irritant to gastric mucosa
Plants irritant to intestinal mucosa
Plants producing delayed gastroenteritis

Plants which produce irritation of mouth and

throat
Arisaema triphyllum
Colocasoa esculenta
Arum jaquemontii
Family : Araceae
Leaves, stem and tubers may be poisonous

Arisaema triphyllum
Jack in the pulpit, Indian turnip

Arisaema triphyllum
Herbaceous perennial plant
Three parted leaves
Flowers contained in a spadix covered by a hood
Cultivated in Sind and NWFP

Arum Jaquemontii
Himalayas in Pakistan and N,W. India, Afghanistan.
Found in forests and open places up to 3000 m.
Mainly found in galliyat (Ayubia & Nathia gali)

Colocasia esculanta

Elephant ear

Colocasia esculenta
Wildly found in Gilgit-baltastan (Gilgit, Swat, Parachanar)
Distribution: Cultivated in the tropics everywhere, up to 2600 m.
Elephants ear is cultivated for its starchy tuberous corms,
which when boiled lose their poisonous nature and can be eaten.
The leaves are also edible and a source of vitamins A,B, and C.
The juice from the corm and the petioles is medicinal, being used as a
stimulant, rubifacient and as a styptic.

Toxic Principal
Water insoluble Ca-oxalate crystals
Present in special mucilaginous cells called Raphides
Which break open by mechanical process like chewing or masticating
plants parts
These crystals are produced by plant in detoxification of Ca ions
Oxalic acid is produced in plant as a by-product of protein
biosynthesis

Signs & symptoms of toxicity

Painful burning sensation of the lips and mouth results from the
ingestion of stem and leaves of the plant
Increased salivation
Inflammation occur often with edema and blistering on the tongue
Hoarseness, dysphonia and dysphagia

Management
Pain and edema settles slowly without therapy
Cool liquids and demulcents held in mouth may provide relief
Analgesic may be indicated
Antihistamine like diphenhydramine can be administered
Insoluble oxalates do not cause systemic poisoning
Consultation with poison control centre may be considered

Plants producing irritation of intestinal mucosa

Amaryllus vittata
Crinum asiaticum
Narcissus tazetta
FAMILY: Amaryllidaceae
Bulbs and other plant parts are toxic upon ingestion

Amaryllis vittata
Amaryllis
Cultivated in Punjab and Sind
Amaryllis (Amaryllis belladonna) is an
ornamental plant commonly sold for its
winter flowers. Ingesting the bulbs has
poisoned humans.

Crinum asiaticum
Spider lily, giant crinum lily
Cultivated in Punjab and Sind Province
All plant parts are toxic especially bulbs

Narcissus tazetta
Daffodil
Found in Gigit-Baltastan region wildly

Toxic Principal
These plants of Amaryllidaceae family mainly contained heat stable
alkaloid LYCORINE which produce irritation of gastric mucosa
The toxic alkaloid, lycorine, is the principal toxin, although small
quantities of related alkaloids are also present
It mainly cause severe vomiting (emesis) after ingestion of plant parts
Due to this reason severe intoxication never occur after ingestion of
plant parts

Lycorine

Signs and symptoms of toxicity

Usual signs of toxicity are nausea, vomiting and diarrhoea
In mild intoxication severe emesis followed by incoordination
between brain and muscles occur leading to shivering and fever
Severe intoxication in human have not been observed
Animal data show that insensibility, convulsions, muscle contraction
and lowering of blood pressure occur.

Management
Symptoms subsides within 24 hours
No need of specific treatment
Fluids can provide relief

Plants producing irritation of intestinal mucosa

After one hour of ingestion these plants produce emesis and colic
Aesculus indica
Podophyllum emodi
Taxus brevifolia

Aesculus indica (Horse chestnut)

Sapindaceae
Geographical source:
Himalayan region between Kashmir and
west Nepal at elevation of 900-3000 meter
Toxicity:
Nut of the plant contain toxic saponin glycoside
Aesculin
Ingestion of single nut can lead to
severe gastroenteritis

Symptoms of toxicity:
Severe sneezing and runny nose
Painful inflammation of eyes
Nausea and abdominal pain
Gastroentritis

Podophyllum emodi
Podophyllaceae

Geographical source:
Kashmir and swat, Chitral at elevation of
600-1200 feet
Toxicity:
Rhizomes of contain resinous principal podophyllin 0.3-1%
Podophyllin contain podophyllotoxin
Podophyllin cause contact dermatitis on contact and cathartic action
upon ingestion

Symptoms of toxicity:
Irritation of eyes and mucous membranes
Ingestion of plant parts especially rhizomes
cause colic, persistent vomiting, severe diarrhoea,
headache, fever
At low doses it produce cathartic action usually
at 0.01g but higher dose can lead to enteritis
followed by death

Taxus baccata
Taxaceae
Geographical source:
This plant is found in Gilgit baltastan
especially at swat & Chitral
Also in Murree and Azad Kashmir
Toxicity:
Plant contain alkaloids which are Poisonous
Mainly contain Taxane A & Taxane B
10-de-acetyl baccatin-III and Baccatin III
Leaves of the plant contain higher proportions of the alkaloids.
Ingestion of 50-100 leaves can lead to death due to cardiac & respiratory
depression

Symptoms of toxicity:
Taxane has irritant action on the intestinal mucosa producing
gastroenteritis
Cardiac depression
Straggling gait, muscle tremor followed by convulsions occur
Collapse occur due to difficulty in breathing, coldness, impaired
circulation and heart failure
Exposure to plant pollens leads to atopic manifestations

Plants producing delayed gastroentritis

After ingestion of these plants no sign and symptoms of toxicity
appear but after lapse of sum time varying from hours to days they
do. Intoxication occur in the form of severe gastroenteritis, vomiting
and diarrhoea.
Abrus precatorius
Ricinus communis
Colchicum luteum
Rheum webbianum or Rheum ribes

Rheum webbianum
Rheum ribes
(RHUBARB- rewend chini)
Family: Polygonaceae
Geographical source
This plant is found in Himalayan region
Especially in Kashmir and Gilgit Baltistan
Toxic Principle:
This plant contain OXALIC ACID and its salts
Which exerts corrosive action on the
gastrointestinal tract. Intoxication occur
due to formation of insoluble Ca-oxalate salts
Which leads to hypocalcemia

Sign & symptoms of toxicity

After ingestion of plant parts especially leaves, intoxication occur
after lapse of some time and characterised by
Nausea
Vomiting
Diarrhea
Gastroentritis
Disturbed functioning of heart and neuromuscular transmission

Abrus precatorius
Leguminosae

(Ratti-Abrus)

Geographical source
This plant is found in Kashmir and Sindh
Toxic Principle:
Seeds of the plant are toxic
Contain toxalbumin called Abrin
Death from abrin poisoning could take
place within 36 to 72 hours of exposure,
depending on the route of exposure
(inhalation, ingestion, or injection) and the dose received. If death has not
occurred in 3 to 8 days, the victim usually recovers.

 Sign and symptoms of toxicity

If someone swallows a small amount of abrin, vomiting and diarrhea
that may become bloody Severe dehydration may be the result,
followed by low blood pressure.
Other signs or symptoms may include hallucinations, seizures, and
blood in the urine.
Within several days, the persons liver, spleen and kidneys might stop
working, and the person will die.

Treatment:
No specific treatment
Abrin poisoning is treated by giving victims supportive medical care to
minimize the effects of the poisoning.
The types of supportive medical care would depend on several factors,
such as the route by which victims were poisoned (that is, whether
poisoning was by inhalation, ingestion, or skin or eye exposure).
Care could include such measures as helping victims breathe, giving them
intravenous fluids, giving them medications to treat conditions such as
seizure and low blood pressure, flushing their stomachs with activated
charcoal (if the abrin has been very recently ingested), or washing out their
eyes with water if their eyes are irritated.

Colchicum luteum & Colchicum autumnale

Colchicum luteum
Liliaceae

(Surunjan)

Geographical source
This plant is found in Hazara division, Gilgit Baltastan and Kashmir
Toxic Principle:
All the plant parts are toxic especially seeds
Contain toxic alkaloid colchicine.
Colchicine is a medication most commonly used to treat gout. It is a toxic
natural product and secondary metabolite, originally extracted from plants
of the genus Colchicum. Adverse effects are primarily gastrointestinal upset
at high doses.
Colchicine is a mitotic poison.
Colchicine is used in agriculture to induce polyploidy.

Signs and symptoms of toxicity

Colchicine poisoning has been compared to arsenic poisoning.
Symptoms start 2 to 5 hours after the toxic dose has been ingested and
include burning in the mouth and throat, fever, vomiting, diarrhea,
abdominal pain and kidney failure.
These symptoms may set in as many as 24 hours after exposure.
Onset of multiple-system organ failure may occur within 24 to 72 hours. This
includes hypovolemic shock due to extreme vascular damage and fluid loss
through the GIT, which may cause death.
In addition, sufferers may experience kidney damage that causes low urine
output and bloody urine, low white blood cell counts (persisting for several
days), anemia; muscular weakness, and respiratory. Recovery may begin
within six to eight days.
There is no specific antidote for colchicine.

Ricinus communis

Ricinus communis
Euphorbiaceae

(Arnid)

Geographical source
This plant is found in various parts of Pakistan
Toxic Principle:
The seeds of the plant are toxic
Contain toxic protein RICIN

 Ricin is a highly toxic, naturally occurring Lectin (a carbohydratebinding protein) produced in the seeds of the castor oil plant.
The LD50 of ricin is around 22micrograms per kilogram of body weight
(1.78 milligram for an average adult).
Oral exposure to ricin is far less toxic, and an estimated lethal dose in
humans is approximately 1 milligram per kilogram.
Because it is destroyed in GIT.
It act as toxin by inhibiting protein synthesis.

Signs & symptoms of toxicity

Most acute poisoning episodes in humans are the result of oral
ingestion of castor beans, 520 of which could prove fatal to an adult.
Often manifestations of poisoning are nausea, diarrhea, increases
heart rate, low BP and seizures persisting for up to a week.
Blood, plasma, or urine ricin or ricinine concentrations may be
measured to confirm diagnosis.

Treatment for ricin poisoning

There is no antidote for ricin poisoning in humans.
Existing treatments emphasize minimizing the effects of the poison.
Possible treatments include giving intravenous fluids, helping the
victim to breathe, or giving medications to deal with seizures and low
blood pressure.
If the ricin has been ingested recently, the stomach can be flushed by
ingesting activated charcoal.

Plants acting on Central Nervous System

Cicuta virosa
Cannabis sativa

Cicuta virosa
Apiaceae

Geographical source
This plant is found in Kashmir Valley
Toxic Principle:
Perennial herbaceous plant, 1-2m in height
The plant contains Cicutoxin which is a poisonous polyyne and alcohol. It
disrupts the workings of the central nervous system.
In humans, cicutoxin rapidly produces symptoms of nausea,
emesis and abdominal pain, typically within 60 minutes of ingestion.
Poisoning can lead to tremors and seizures.
A single bite of the root (which has the highest concentration of cicutoxin) can
be sufficient to cause death.

Cicutoxin (C17H22O2)
Heptadeca, 8,10,12 tri ene, 4,6 di yne, 1,14 di ol

MoA
Cicutoxin is a noncompetitive gamma-aminobytyric acid (GABA)
antagonist in the central nervous system (CNS).
GABA normally binds to the GABA receptor and activates the
receptor which causes a flow of chloride across the membrane.
Cicutoxin binds to the same place as GABA, because of this the
receptor is not activated by GABA. The pore of the receptor
wont open and chloride cant flow across the membrane.
Binding of cicutoxin to the receptor also blocks the chloride
channel.
Both effects of cicutoxin on the GABA-receptor cause a constant
depolarization. This causes hyperactivity in cells, which leads to
seizures.

Sign and symptoms of toxicity

First signs of cicutoxin poisoning start 1560 minutes after ingestion and
are vomiting, convulsions, widened pupils, salivation, excess sweating
and the patient may go into a coma.
Other described symptoms are cyanosis, amnesia, absence of muscle
reflexes, heart problems and central nervous system problems which
manifest themselves as convulsions and either an overactive or
underactive heart.
Due to an overactive nervous system respiratory failure occurs which
may cause suffocation and accounts for most of the deaths.
Dehydration from water loss due to vomiting can also occur.
If untreated, the kidneys can also fail, causing death.
Since there currently isn't any antidote for cicutoxin, the symptoms have
to be treated to prevent death and/or permanent damage

THC (Tetrahydrocannabinol)

Plants having atropine

Atropa belladonna
Hyocyamus niger
Datura stramonium

Plants having nicotine like actions

Conium maculatum
Lobellia inflata

Plants having Nicotine like actions

Nicotine
Alkaloidal drug
Nicotinic acetylcholine receptors (nAChR) agonist
Stimulant
Relaxant
Psychoactive
At higher doses produce toxicity
Readily cross Blood Brain Barrier, after inhalation within 10-20seconfs
Addictive
LD50 is 30-60mg for adults (0.5-1mg/kg body weight)

Conium maculatum (Poison hemlock)

Umbelliferae
Geographical source
This plant is found in Hazara division (Abottabad, Murree hills)
Toxic Principle:
All plant parts are toxic
Contain Nicotine like alkaloids

Coniine, N-methyl Coniine, Conhydrine and Pseudoconhydrin

Coniine is a poisonous alkaloid. It is a neurotoxin which disrupts the
peripheral nervous system.
It is toxic to humans and livestock; less than 0.1g is fatal to humans, with
death caused by respiratory paralysis.

Notably, Socrates was sentenced to death by drinking a

mixture containing Posion hemlock in 399 BC.

Coniine

Sign and symptoms of toxicity

Coniine paralyzes muscles by blocking the nicotinic receptors.
Symptoms of paralysis occur within a half hour, and death may take several
hours.
As the central nervous system is not affected the person remains conscious
and aware until respiratory paralysis results in cessation of breathing.
The muscular paralysis is an ascending paralysis as the lower limbs are
affected first. The person may have a hypoxic convulsion just prior to death.
The cause of death is lack of oxygen to the brain and heart as a
consequence of respiratory paralysis. A poisoned person will recover if
artificial ventilation (breathing) is maintained until the toxin is removed
from the receptor.
The LD50 (mouse; administered IV) 7-12 mg/kg

Lobellia inflata (Indian tobacco)

Lobellia frutescens
Lobelliaceae
Geographical source
This plant is found in Karachi near the seacoast
Toxic Principle:
It contain 14 alkaloids, most important is Lobeline.
It has same actions as that of Nicotine
It is mixed agonist-antagonist at nicotinic acetylcholine
receptors.
It is respiratory stimulant

Sign and symptoms of toxicity

Emesis
Paralysis
Respiratory depression
Death

Plants producing Cardiovascular problems

Digitalis purpurea
Digitalis lanata

Nerium indicum
Aconitum napellus
Aconitum heterophyllum

Digitalis purpurea
Digitalis lanata
Scrophulariaceae
Geographical source:
Hazara division and
Azad Kashmir

 Digoxins primary mechanism of action involves

inhibition of the Na+/K+ ATPase, mainly in the
myocardium.
This inhibition causes an increase in intracellular
sodium levels, resulting in a reversal of the action of
the sodiumcalcium exchanger, which normally imports
three extracellular sodium ions into the cell and
transports one intracellular calcium ion out of the cell.
The reversal of this exchange causes an increase in the
intracellular calcium concentration that is available to
the contractile proteins.

 Increased intracellular calcium lengthens phase 4

and phase 0 of the Cardiac action potential,
which leads to a decrease in heart rate
Overall, the heart rate is decreased while BP is
increased, resulting in a net increase in stroke
volume, leading to increased tissue perfusion.
This causes the myocardium to work more
efficiently

Nerium indicum
Apocyanaceae
Geographical source:
Gilgit-baltastan and Kashmir
Also cultivated in gardens of Punjab
Toxicity:
Oleandrin a poisonous cadioactive glycoside
Ingestion of this plant can affect the gastrointestinal system, the heart, and the central
nervous system. The gastrointestinal effects can consist of nausea and vomiting, excess
salivation, abdominal pain, diarrhea that may or may not contain blood and colic.
Cardiac reactions consist of irregular heart rate, sometimes characterized by a racing
heart at first that then slows to below normal further along in the reaction.
Extremities may become pale and cold due to poor or irregular circulation. The effect on
the central nervous system may show itself in symptoms such as drowsiness, tremors or
shaking of the muscles, seizures, collapse, and even coma that can lead to death.
Oleander sap can cause skin irritations, severe eye inflammation and irritation, and
allergic reactions characterized by dermatitis.

Aconitum napellus
Aconitum heterophyllum
Ranunculaceae
Geographical source:
Gilgit-baltastan and Kashmir
Toxicity:
Aconitine is a potent neurotoxin that opens tetrodotoxin sensitive
sodium channels. It increases influx of sodium through these channels
and delays repolarization, thus increasing excitability and promoting
ventricular dysrhythmias.

 Marked symptoms may appear almost immediately, usually not later

than one hour, and "with large doses death is almost instantaneous."
Death usually occurs within two to six hours in fatal poisoning (20 to
40 mL of tincture may prove fatal). The initial signs
are gastrointestinal including nausea, vomiting, and diarrhea. This is
followed by a sensation of burning, tingling, and numbness in the
mouth and face, and of burning in the abdomen. In severe poisonings
pronounced motor weakness occurs and cutaneous sensations of
tingling and numbness spread to the limbs. Cardiovascular features
include hypotension, sinus bradycardia, and ventriculararrhythmias.
Other features may include sweating, dizziness, difficulty in breathing,
headache, and confusion. The main causes of death are ventricular
arrhythmias and asystole, paralysis of the heart or of the respiratory
center.

Plants containing cyanide group

(Cyanophore plants)
These plants contain toxic compounds which on hydrolysis yield
cyanide group or HCN (Hydrogen cyanide)
Toxic Principle:
cyanogenic glycosides or cyanogens (amygdalin, prunasin)
Prunus amygdalus
Prunus serotine
Manihor utilisimma

 Hydrogen cyanide (HCN) is formed when the glycosides are

hydrolyzed by enzymes in plants or by rumen microorganisms.
The glycosides occur in vacuoles in plant tissue while the enzymes are
found in the cytosol. Damage to the plant from wilting, trampling,
mastication, frost, drought, bruising etc. results in the enzymes and
glycosides coming together causing hydrogen cyanide to be formed.
b-glycosideases are also produced by rumen microorganisms. The
optimal pH for enzyme activity is near neutrality, so release of HCN is
more rapid in the rumen than in the highly acid stomach of
monogastrics. For this reason, ruminants are more sensitive to
cyanogens than nonruminants.

Toxicity
Cyanide is lethal at dosages of 0.5 to 3 mg/kg b.w. Ingestion of 100 g
of wild cherry leaves with ~ 200 mg CN per 100 grams would be lethal
to a 100 lb. animal.
MoTA
Once free cyanide is released from the plant tissue and is absorbed it
reacts with ferric iron (+3) in cytochrome oxidase which halts cellular
respiration. Oxyhemoglobin cannot release oxygen for electron
transport in the cytochrome system since the cyanide cytochrome
oxidase will not function in electron transport.

Sign of toxicity:
Animals are commonly found dead due to rapidity of cyanides effects
When observed, signs may include excitement, general muscle
tremors, dyspnea, salivation, defecation, urination followed by clonic
convulsions and death.

 General
remove from source
Specific
sodium nitrite at 10 to 20 mg/kg with 500 mg/kg sodium thiosulfate
as needed. The treatment is directed at breaking the cyanide
cytochrome bond with the nitrite forming methemoglobin.
Methemoglobin has a greater affinity for cyanide than does
cytochrome oxidase, so it strips cyanide from the enzyme. The
thiosulfate then reacts with the cyanide via the enzyme rhodanase
forming thiocyanate which is readily excreted in the urine.

Prunus amygdalus
Roasaceae
Geographical source
This plant is cultivated in northern areas of Pakistan
Toxic Principle:
The seeds of the plant contain toxic glycosides which on hydrolysis yield HCN.
Hydrogen cyanide exert toxic action in human. Major toxic glycoside is
Amygdalin. Which is a glucoside and on hydrolysis yield Prunacin which
further undergo hydrolysis to yield HCN among the products of hydrolysis
Sign and symptoms of toxicity:
After ingestion hydrolysis takes place which lead to toxic sign and symptoms
like nausea, emesis, muscular weakness, difficulty in breathing and
convulsions

Prunus serotina
Roasaceae
Geographical source
This plant is found in Chitral, Gilgat Baltastan, Kaghan valley and other
parts of NWFP
Toxic Principle:
The seeds of the plant contain toxic glycosides which on hydrolysis yield
HCN. Hydrogen cyanide exert toxic action in human. Major toxic
glucoside is Prunacin which on hydrolysis yield HCN.
Sign and symptoms of toxicity:
After ingestion hydrolysis takes place which lead to toxic sign and
symptoms like nausea, emesis, muscular weakness, difficulty in
breathing and convulsions

Manihot ultilissima
Euphorbiaceae
Geographical source
This plant is cultivated in northern areas of Pakistan
Toxic Principle:
Tubers of the plant contain cyanogenocyte which produce liver
damage
Sign and symptoms of toxicity:
Nausea, vomiting, muscular weakness and convulsions

Plants having liver damaging effects

Melia azedarach
Manihot ultilissima
Ricinus communis
Sapindus trifoliatus

Melia azedarach (china berry/ white cedar) Darhek

Meliaceae
Geographical source
This plant is cultivated in Sind,
Punjab and KPK
Toxic Principle:
Ingestion of fruit causes
degeneration of liver

 Fruits are poisonous to humans if eaten in quantity.

The toxins are neurotoxins and unidentified resins, found mainly in the
fruits.
Azadirachtin, is thought to be the toxic principle

Leaves have been used as a natural insecticide to keep with stored food, but
must not be eaten as they are highly poisonous.
Chinaberry fruit was used to prevent insect larvae from growing in the fruit.
By placing the berries in drying apples (etc.) and keeping the fruit turned in
the sun without damaging any of the Chinaberry skin, the fruit will dry and
not have insect larvae in the dried apples.

Sign and symptoms of toxicity

The first symptoms of poisoning appear a few hours after ingestion.
They may include
loss of appetite,
vomiting,
constipation or diarrhea,
bloody faeces,
stomach pain,
pulmonary congestion, cardiac arrest,
rigidity, lack of coordination and general weakness.
Death may take place after about 24 hours.

Manihot ultilissima
Euphorbiaceae
Geographical source:
This plant is cultivated in northern areas
of Pakistan
Toxic Principle:
Tubers of the plant contain
cyanogenocyte which produce liver damage
Sign and symptoms of toxicity:
Nausea, vomiting, muscular weakness and convulsions

Sapindus trifoliatus (soapnut plant)

Sapindaceae
Geographical source
This plant is found in northern areas of
Pakistan
Toxic Principle:
The fruit and bark of the plant are
toxic.
Toxic principle is not known.
In past soapnut was used as surfactant
for washing purpose, in medicine as
mucolytic, contraceptive and for emesis.

Sign and symptoms of toxicity:

Vomiting
Hypoglycaemia
Degeneration of liver
Convulsions leading to coma

Ricinus communis

Ricinus communis
Euphorbiaceae

(Arnid)

Geographical source
This plant is found in various parts of Pakistan
Toxic Principle:
The seeds of the plant are toxic
Contain toxic protein RICIN

 Ricin is a highly toxic, naturally occurring Lectin (a carbohydratebinding protein) produced in the seeds of the castor oil plant.
The LD50 of ricin is around 22micrograms per kilogram of body weight
(1.78 milligram for an average adult).
Oral exposure to ricin is far less toxic, and an estimated lethal dose in
humans is approximately 1 milligram per kilogram.
Because it is destroyed in GIT.
It act as toxin by inhibiting protein synthesis.

Signs & symptoms of toxicity

Most acute poisoning episodes in humans are the result of oral
ingestion of castor beans, 520 of which could prove fatal to an adult.
Often manifestations of poisoning are nausea, diarrhoea, increased
heart rate, low BP and seizures persisting for up to a week.
Blood, plasma, or urine ricin or ricinine concentrations may be
measured to confirm diagnosis.

Treatment for ricin poisoning

There is no antidote for ricin poisoning in humans.
Existing treatments emphasize minimizing the effects of the poison.
Possible treatments include giving intravenous fluids, helping the
victim to breathe, or giving medications to deal with seizures and low
blood pressure.
If the ricin has been ingested recently, the stomach can be flushed by
ingesting activated charcoal.