At the end of the lecture, the student should be able to describe:

 Classification of irritant poisons

 Common metallic irritant poisons
 The physical appearance of Copper and Mercury
 Its uses
 Mechanism of action
 Fatal dose
 Fata period
 Signs and symptoms
 Treatment
 Postmortem appearance
 Medicolegal importance
 IRRITANT POISONS
Irritant poisons cause symptoms of gastroenteritis and exert marked depressant action
after absorption.
Chronic poisoning leads to lingering death, also known as slow poison

Classification
1. Inorganic irritants i) non-metals
ii) metals

2. Organic irritants i) vegetables

ii) animals

3. Mechanical irritants powdered glass, pins, needles, nails, hairs, etc

 General sign & symptoms of irritant poisons
• Onset: within ½ hour -1 hour

• Burning sensation: mouth, throat, oesophagus, stomach and abdomen.

• Followed by: intense thirst, difficulty in swallowing, retching, painful vomiting and diarrhea

• Initially vomiting contains stomach contents, later contains blood and dark brown in colour.

• Severe diarrhea with tenesmus and loose stools and later with mucus and blood
• Shock with cold clammy skin, pale anxious face, rapid feeble pulse and sighing
respiration

• Consciousness retained.

• Convulsions and coma may follow

• Death within 24 hours from shock or in few days due to exhaustion

• Patient may recover and death may ensue later due to esophageal stricture
 Common Metallic Irritant Poisons
• Important poisons in this group are:
i. Arsenic
ii. Mercury
iii. Lead
iv. Copper
v. Thallium
vi. Iron
vii. Antimony
viii. zinc
 Metallic irritants (Copper) appearance
• Metallic copper non-poisonus except its some salts are poisonus, e.g.

BLUE VITRIOL (Nila Tutia) or copper sulphate: present in the form of large blue crystals.

Verdigris (Zangal): present in the form of bluish green mass or powder

Copper arsenite (Scheel's green) , in the form of yellowish green pigment

Copper acetoarsenite, (Paris green or Emerald green) in the form of crystalline powder
 USES
• Copper sulphate; used as fungicide, algaecide, root killer, and herbicide in both agriculture
and non-agricultural settings.
• Verdigris; used as a patina to protect copper or bronze objects, especially in architecture
• Copper acetoarsenite or Copper arsenite ; used as rodenticides and insecticides and
also as a pigment in some paints
• In medicine used in TPN
• Also used in IUCDs
• As an antidote in phosphorus poisoning
 Mechanism of Action

• Copper is a powerful inhibitor of enzymes.

FATAL DOSE: 30 grams of copper sulphate / verdigris

FATAL PERIOD: 12-24 hours. May be delayed for 3-5 days or even a week.
 Signs and symptoms of Copper poisoning
• Its starts within 15-30 minutes
• In addition to general sign and symptoms, vomitus may appear greenish blue.
• stools not bloody and brown in colour
• Urine inky in appearance
• Uremia may occur
 Treatment

• Stomach wash with 1% potassium ferrocyanide solution

• Demulcent fluids also essential.

• Penicillamine, BAL or EDTA are helpful

 Postmortem Appearances
• Skin may be yellow due to jaundice

• Greenish blue froth at mouth and nostrils

• Bliush or greenish gastric mucosa and stomach is diagnostic.

• Mucous membrane congested, inflamed, and occsasionally eroded in patches

• Liver may be soft and fatty

• Parenchymatous injury to heart, kidney and liver

 Chronic Copper poisoning
• Metallic taste

• Green line on the gums at the base of the teeth; called Clapton’s Line

• Gastrointestinal symptoms

• Progressive emaciation

• Peripheral neuritis, with wrist drop or foot drop in some cases;

• Wilson’s disease; is a rare genetic disorder characterized by excess copper stored in various
body tissues, particularly the liver, brain, and corneas of the eyes.
The disease is progressive and, if left untreated, it may cause liver (hepatic) disease, central
nervous system dysfunction, and death.

• Bronzed diabetes ; Hemochromatosis has been called “bronze diabetes” due to

the discoloration of the skin and associated disease of the pancreas.
Clinical signs of the condition depend on which organ system is most affected. Often a
diagnosis will not be made until multiple systems are affected including liver, heart, pancreas,
endocrine glands, and joints.
 Medicolegal Aspects
• Used as an antidote in phosphorus poisoning

• Sometimes used as suicidal agent

• Accidental poisoning when copper added to keep vegetables green.

• Rarely as a cattle poison

• Improper tinned copper vessels leads to copper subacetate formation results in food
contamination
 MERCURY(PARA)
APPEARANCE
• Also named as quicksilver, a liquid metal with a bright silver lustre.(cinnabar, ras sindoor)
• Metallic mercury is not poisonus if swallowed because it is not absorbed.
• Vaporises at room temperature and causes poisoning if vaporized mercury is inhaled,
swallowed, or rubbed into the skin.
USES
• As a germicide (mercuric chloride)
• Fungicide in seed commerce
• In the past used as a diuretics
• Mercurous chloride (Calomel) is used as a standard in electrochemical measurements and
• In medicine as a purgative.
 Mechanism
• Mercury depresses cellular enzymatic mechanism by combining with sulphydryl groups.
• Mercuric compounds more poisonous than Mercurous compounds.

FATAL DOSE: 1 to 2 grams

FATAL PERIOD: few hours, may be delayed for 3-5 days.

Delayed death due to uremia
 Sign and symptoms
General sign and symptoms of irritant poison.
Metallic taste, mouth, tongue and fauces become corroded and mucus membrane appears
grayish white.

If death delayed, on 2nd or 3rd day the gums swollen, inflamed with foul breath.

Teeth loosening and ulcerative glossitis.

Nephrotoxicity: Albuminuria, hematuria and death from uremia.

Re-excretion of mercury; caecum and large intestine show areas of erosion, corrosion, and
necrosis
 Treatment
• Stomach wash with sodium formaldehyde sulphoxylate (250 ml of 5%), about 100 ml
solution left in the stomach. Reduces the perchloride to less soluble Mercurous compound

• Egg albumin forms insoluble albuminate, therefore be removed without delay gastric lavage
or by emetics.

• Medicinal charcoal with magnesium sulphate increases its absorption, hastens the removal
of ingested poison

• Antidotes :BAL and Penicillamine.

• Peritoneal dialysis or haemodialysis in case of renal damage.

• General treatment of shock, and symptomatic treatment

 Postmortem appearance
• If the poison is taken in concentrated form, signs of corrosion appears.

• In case of dilute form, signs of irritant poisoning present.

• Tongue, white and sodden.

• Mouth greyish white hard crust over a raw surface; called eschar.

• Caecum and large intestine: severe inflammation, ulceration and gangrene.

• Toxic nephritis

• Subendocardial haemorrhages

• Fatty liver degeneration

 Chronic mercury poisoning
• May appear after acute attack.

• Injudicious medical administration

• Accidentally, absorption in workers of manufacturing; thermometers, barometers, fur felt,

mirrors, ultraviolet apparatus or police officers in finger print detection.
 Symptoms and signs

Metallic taste with loosening of teeth, painful inflamed gums.

Blue-black lines on the gums (occasionally)

Skin irritation

Nephritis

Abortion

Discolouration of capsule of the lens due to mercury deposition; called Mercuria lentis.
It has no effect on visual acuity.
• Hatter’s shake: Tremors that effect hands, arms, tongue and later legs; in the workers
exposed to mercury in the industries.

• Erethism: Mental symptoms of personality disturbance cheracterised by shyness, irritability,

tremors, loss of memory and insomnia. Common in workers of mirror industry.

Treatment
• Removed from the source.
• Peritoneal dialysis and hemodialysis
• Symptomatic treatment
Erethism
 Postmortem appearance

Large whole intestine shows necrosis

Tubular nephritis

Fatty degeneration of the liver

In addition to routine viscera, teeth, bone, hair and nails should be sent for chemical analysis.
 Medicolegal aspects of Mercury

Accidental ingestion of antiseptic solutions, e.g. containing cyanide, iodide

Vaginal douches

Skin whitening creams

Diuretics (in past)

Accidental swallowing of sulfocyanide of mercury tablet containing Pharoah’s serpents

It passes rapidly to the foetal circulation through placenta and causes abortion.

Suicidal and homicidal poisoning is rare.

 ARSENIC & LEAD POISONING
At the end of lecture, the student should be able to describe:
• Mechanism of action
• Symptoms and signs of acute and chronic poisoning
• Fatal dose
• Fatal period
• Treatment
• Postmortem appearance
• Medicolegal importance
 ARSENIC-irritant(metallic poison)
• Grey arsenic is non-poisonus. Water insoluble, cannot be absorbed from alimentary canal.

• White arsenic or arsenious oxide tasteless, very poisonus.

• Arsenic combines with sulphydryl enzymes, interfering with cell metabolism and causes
toxicity. It causes irritation of the mucus membrane locally. Remotely depresses the
nervous system.
 Absorption, Excretion and Metabolism

• Arsenic is absorbed through all routes viz. through skin, inhalation, and GIT
mucosa.
• However, cutaneous absorption is low except in cases of damaged skin.
• The inorganic pentavalent forms are absorbed at higher rate than bivalent
forms.
• The absorbed inorganic arsenic undergoes methylation mainly in liver to
monomethyl arsenic acid and dimethylarsinic acid and excreted in urine.
• After absorption, arsenic is redistributed to the liver, lungs, intestinal wall,
spleen, and kidneys. It has minimal penetration in blood-brain-barrier
• Symptoms in acute poisoning starts within 15-30 minutes.

• General symptoms and signs of acute arsenic poisoning with rice

watery stool of cholera and contain shreds of mucous membrane and
fragments of poison in 3-4 hours.

• Skin eruptions in later stages.

• Remission occur in many cases.

• The patient becomes progressively weak and may die of heart failure
and weakness in 7 to 10 days.
• In large doses, poison absorbed quickly, narcotic symptoms present; such, as;
vertigo, headache, spasms, followed by stupor and vascular collapse. Death
occurs in 2 to 3 hours.

• FATAL DOSE: 120 - 200 mg

• FATAL PERIOD:
• 2-3 hours in narcotic form
• 12-48 hours in gastrointestinal form
• 7-10 days in subacute poisoning and heart failure or weeks later from chronic
poisoning with kidney and liver damage.
 Treatment

• Stomach wash: with warm water and milk.

• Antidote : hydrated ferric oxide to form ferric arsenite, in tablespoon full at short
intervals; for 2 – 3 days.

• As a substitute: calcined magnesia or charcol.

• Butter and greasy substances to prevent absorption

• Sodium sulphate (white arsenic) left in stomach is beneficial.

• No alkalis by mouth to prevent the solubility of white arsenic.

• Dimercaprol (BAL) I/M in oily solution to treat systemic effects

• I/V fluids for dehydration, glucose to prevent liver damage, sodium bicarbonate
to regulate acid-base balance.

• Morphine for pain relief and ice for thirst.

• Hemodialysis for anuria

 Postmortem appearance
• Mainly depend upon the amount taken and time elapsed before death.

• Externally: In acute poisoning; dehydrated, cyanosed with wrinkled skin and

jaundiced.

• Internally: Red velvety appearance of the stomach; Mucosa appear red,

oedematous and swollen, covered with tenacious mucus tinged with blood.
Pyloric end of stomach show small ulceration or large erosions. Small intestine
in its upper part and large intestine in its lower part(rectum) shows
inflammation.
• Petechial haemorhages in submucosa of stomach, endocardium of
the left ventricle. Haemorhages in abdominal organs; larynx, trachea
and lungs occasionally.

• Liver, heart and kidney shows fatty degeneration changes.

• Arsenic retarded decomposition changes.

 Chronic Arsenic Poisoning
• It may result from
1. After an acute attack.
2. Accidental ingestion in small doses repeatedly
3. Excretory function interfered with the body capacity.
Symptoms and Signs

Classical state of ill represented by 4 stages.

1) Gastrointestinal disturbances
2) Catarrhal changes
3) Skin rashes
4) Nervous disturbances
First Stage of Gastrointestinal disturbances:
Gradual emaciation is the earliest. Loss of appetite, nausea, vomiting and
diarrhea are common.
Second Stage of Catarrhal changes:
Like common cold. Mucous membrane causing conjunctivitis, running nose and
eyes, cough, hoarseness of voice and bronchial catarrh
Third Stage Skin rashes:
Skin irritation with vesicular eruption and form a nettle rash.
“Rain Drop” pigmentation; patchy brown skin pigmentation after long exposure
followed by hyperkeratosis of palms and soles.
Mee’s Lines: crossing the nails of fingers and toes.
Mee's line
Fourth Stage of Nervous Disturbances:
• Tingling and numbness of hands and feet with tenderness of muscles
with paresis.
• Arsenical neuritis resembles chronic alcoholism, it also includes
headache, drowsiness, vision impairment and mental activity.
There may be liver, kidney damage and bone marrow depression.
Heart is also effected. No symptom or sign is diagnostic.
Treatment
• Removal from the source.
Dimercaprol(BAL), vitamin B complex and sodium thiosulphate.
• Rest of the treatment is symptomatic.
• Compete recovery may require 6 months to I year.
• Postmortem appearance: In chronic poisoning, emaciated body with anemia,
fatty degeneration in heart, liver and kidney and congestion of gastrointestinal
tract. Microscopy shows peripheral neuropathy.
• Nails, hairs and bone should be taken.
Plucked hairs with their bulbs, nails as a whole and lower end of femur(few
centimeters) should be taken
 Poisoning by Organic Arsenical Compounds
• Also known as arsphenamines. Nitritoid crisis an anaphylactic reaction due to
its I/V use. in the treatment of syphilis, parasitic blood disease and
trichomonas vaginalis previously.
• Exfoliative dermatitis, toxic jaundice, nephritis, agraulocytosis, optic atrophy
and arsenical encephalopathy occurs due to its medicinal use in small doses.
• Death may results from convulsions and coma with cyanosis and anuria.
Tolerance: In the habit of arsenic as a tonic or as an aphrodisiac, built up
tolerance up to 250mg or more in a single dose. Chronic poisoning may occur in
due course.

Absorption: rapidly absorbed from skin and G I tract. Irritation, corrosion when
applied to skin.

Distribution: Found in liver in highest quantity.

Present in muscles for days
In bones for weeks
In hair, skin, nails and keratin tissues for months.
• Elimination: mainly by urine and also in faeces, bile and sweat and other
secretions.
In urine ½ an hour to about 10 to 14 days after a single dose.
In chronic poisoning; excreted in keratin tissues, bones; hairs and nails deposits.
Persist in hairs for long period of time even all traces left the viscera.
 USES
In arts, industry and agriculture:

As a preservative of timber and leather from white ants.

Various cosmetic preparations, depilatories

Colouring artificial flowers, toys, wall papers.

As a fungicides, insecticides and herbicides.

As a quack, common cold, for animals as a fodder.

 Medicolegal Aspects
• It was commonly used as a homicidal agent.
Administered in paan, tobacco, tea, coffee or some food articles.
Fly papers, weed killers soaked in tea or wine.
Mass homicidal poisoning occurred when mixed in some food or in drinking
water.
Applied locally in the form of paste or to abortion stick to procure abortion

• Accidental poison:
Sometimes may occur in children; when they take vermin, chew paint or ant
syrup. From injudicious medicinal use as an aphrodisiac or its used by quacks.
 Postmortem imbibition of arsenic
• Arsenic derived from arsenical weed killers in the ground. When dead body
buried in such earth, small quantities of arsenic may enter the dead body.
Where arsenic poisoning is suspected, samples of earth around the dead body
should be collected for chemical analysis at the time of exhumation.
• In arsenic poisoning, concentration of arsenic in various organs should be more
than that in earth.
 Lead (shisha)

• Lead poisoning occurs by inhalation, ingestion or by absorption from skin or

mucus surfaces.

• Its main effect is to cause spasm of the capillaries and arterioles.

• Its fixation in brain and peripheral nervous system results in toxic effects.

• Lead compounds are more poisonus than lead itself except when it is in a
volatile state.
 sources

• Automobile exhaust.
• Battery making
• Glass manufacture.
• Plastic manufacture.
• House paints.
• Steel welding and cutting.
Hookah smoke contains high levels of toxic compounds, including tar, carbon monoxide,
heavy metals and cancer-causing chemicals (carcinogens) In fact, hookah smokers are
exposed to more carbon monoxide and smoke than are cigarette smokers.

)
There are three commonly used types of hookah tobacco,
Mouassal,
Jurak, and
Tumbak, each contains different ingredients.
In brief, Mouassal which is an Arabic translation for “honeyed” contains 30% tobacco and around 70%
honey/sugarcane as well as glycerol and flavors
Hookah tobacco and smoke contain several toxic agents known to cause lung, bladder, and oral cancer
At least 82 toxic chemicals and carcinogens have been identified in hookah smoke.
 Sources of lead – Lead Salts

• Lead acetate
• Lead carbonate
• Lead oleate
• Lead oxide
• Lead sulphide
• Lead tetroxide
• Tetraethyl lead
• Lead is also used in storage batteries, printing, plumbing, firearm bullets etc.
 Symptoms and signs
• Like irritant poisons. Except diarrhea is to be replaced by constipation.
• Stool blackened and offensive.
• Mainly gastrointestinal and central nervous system are involved.
• Scanty urine.
• Leg cramps and arthralgia.
• Headache, drowsiness, and paralysis of the limbs finally collapse and death.
• Acute lead poisoning is not common; and may survive leads to chronic
poisoning.
• Lead encephalopathy by tetraethyl lead poisoning. Headache, sleeplessness,
tremors of the eye, mouth and fingers, sometimes paralysis or vision loss,
hallucinations, excitement and delirium or apathy and convulsions. May lead to
insanity. Gastric symptoms are absent or slight.
• FATAL DOSE:
Lead acetate 20 grams
Lead carbonate 4 grams
Tetraethyl lead (pure) 1 or 2 drops.

• FATAL PERIOD:
In 2 to 3 days death may occurs.
Acute poisoning rare, leads to chronic poisoning.

• Toxicity Rating: 3 or 4 for most lead salts.

 Treatment
• Gastric lavage with 1% magnesium solution or sodium sulphate.
To eliminate lead sulphate formed, adequate wash with plain water.

• Morphine and atropine to relieve colic.

• Milk, calcium salts and vitamin D are helpful

• Antidotes; Calcium versenate (EDTA) and Penicillamine.

• Peritoneal and haemodialysis

• Symptomatic treatment.
 Postmortem appearance

• Gastric mucosa congested

• Eroded patches

• Large gut contains black coloured faeces.

 Chronic lead poisoning- plumbism, saturnism

• Lead poisoning almost always chronic type. Its used in different industries and
ingestion, inhalation as follows:
Typesetting, plumbing, battery work, glazing pottery.
White lead manufacture, smelting, from paint in oxyacetylene, ship breaking,
diamond cutting, file making, car welding and polishing, turning.
In painting, coach building, lacquering, tinning, vitreous enameling, colour and
dye manufacture and use.
At home; from ghee use stored in tins or cooked food in tinned vessels and
were also from drinking water supplied through lead pipes.
From mobilization of stored lead in body tissues; like bones in acidosis.
 Symptoms and signs

The main symptoms and signs are due to prolong exposure but its
manifestations are acute and include;

Facial pallor: The earliest and most consistent sign especially around the mouth.
May be due to local vasospasm.

Anemia with punctate basophilia: Hypochromic, microcytic type with increased

reticulocytes and basophilic stippled RBC (i.e. RBC showing bluish dotted
appearance in the cytoplasm)

Metallic taste: Anorexia, constipation with blackish stool

Lead line: Bluish-black line/ stain on the gums at the junction with the teeth (not
on the teeth) also called Burtonian line
It present on the gums of carious teeth on the upper jaw especially.
Lead line is due to lead sulphide granules deposition.
Similar lines may also be seen in mercury, copper, bismuth, iron and silver
poisoning.

Colic and constipation: generally effects intestine, ureters, uterus and blood
vessels usually at night. Relieved by abdominal pressure. Constipation also called
dry belly ache.

Paralysis / Lead palsy: In less than 10% of the cases. May be gradual or sudden
onset. Commonly wrist drop (extensor muscles of the wrist) and foot drop
(peroneal muscles).
Encephalopathy: Commonly in children, manifested by recurrent convulsions
and progressive mental deterioration. Optic atrophy may occur.
More commonly in tetraethyl lead poisoning.

Renovascular manifestations: Arteriosclerotic nephritis and renal failure.

Hypertension and arteriolar degeneration.

Reproductive system manifestations: Menstrual disorders. Toxic action on the

trophoblastic epithelium and tonic contraction of the uterus results in either in a
dead foetus or abortion. It causes sterility in both genders.
General symptoms: weakness, anorexia, dyspepsia, metallic taste, foul breath,
headache, vertigo, irritability, drowsiness and arthralgia.

Diagnosis: Clinically:
Colic, punctate basophilia (>200 cells/ cmm ) and a bluish-black line on the
gums.
Prophyrins in urine (0.25mg of lead/ litre of urine)
Radiologic:
Transverse opaque bands at the end of long bones in children; (increase in the
metaphyseal density of bones)
Liver may be abnormally opaque in tetraethyl lead poisoning. (Opacities in the
GI tract)
 Treatment

• EDTA: Combines with lead and enhance its urinary excretion in inactive form.

• EDTA and BAL combination is more effective

• Penicillamine

• In lead paralysis muscle massage helpful.

 Postmortem appearance

• Manifest in the dead body as per the clinical signs.

• Bone marrow: hyperplasia of erythroblasts and leucoblasts with decrease in fat

cells.

• A long bone, teeth, hair and nails should be preserved in case analysis
required.
 Medicolegal aspects of lead poisoning

 Acute poisoning is rare

 Lead poisoning is usually accidental
In children from eating paint on crib, bed or toys.
Chronic poisoning caused by food or drink contamination
Use of lead monoxide for syphilis by quacks
Use of Diachylon paste to procure abortion
From Lead missiles of gunshot injury embedded in the tissues
 Red lead occasionally as a cattle poison alone or mixed with white arsenic
 Lead rarely used as a homicidal and suicidal poison