554 Textbook of Forensic Medicine and Toxicology
8. Cattle poison: Red lead alone or when mixed
with Arsenic is used as a cattle poison.
9. It is used as to adulterate snuff (powdered
tobacco or medicine sniffed through the
nostrils) to improve its colour.
10. Lead is normally present in all human tissue,
deposited in the bones, nail, tooth and hair
and very poorly in lead. No lead is found in
ovary but is present in the testes. It has got
no affinity for fetal tissues.
Accidental poisoning occurs in the children by
eating pica, old paint, plaster; feeding bottles made
of glass contain lead, lead nipple shields, toys,
and street dirt. Also the cosmetics like face pow-
ders, hair dyes used by the mothers secreted in
the milk can cause accidental poisoning in the
children.
ARSENIC
Arsenic is a metallic poison known since ancient
times. The Greeks knew it as early as 500BC
and Hippocrates used it as an external remedy
for ulcers, although there is no record of it being
used as a poison this early. An eight-century Arab
alchemist Jabir ibn Hayyen was the first to obtain
white arsenic by heating realgar. It is thought that
it was around this time when criminals first emplo-
yed arsenic as a poison. Before white arsenic was
known, most of the poisons used had a distin-
guishing taste, smell or colour but arsenic has
very little smell or taste so it is undetectable by
the victim. It is the common environmental toxicant
and is found in soil, water and air. It ranks 20th in
elemental abundance in earth’s crust and 12th in
the human body.
Properties of Arsenic
Arsenic is element 33 in the periodic table and is
classically considered a heavy metal. It exists in
3 allotropic forms and in several ionic forms.
Environmental arsenic exists mainly as sulphide
complexes realgar (As2S2), Orpiment (As2S3) and
iron pyrites. On heating of these ores, arsenic
sublimes and oxidizes to form arsenic trioxide
(As2O3) a fine granular white powder also known
as white arsenic. Arsine gas (AsH3) is another
arsenic compound, formed by the hydrolysis of
metal arsenides and by the reduction of metals of
arsenic compounds in acidic solutions. The main
source of Arsenic is Arsenopyrites, realgar
(Arsenic di-sulphide, As2S2) orpiment (Arsenic
trisulphide, As2S3) and Arsenolite (Arsenic tri-
oxide, As2O3). It is usually obtained as a by-pro-
duct from smelting of copper, lead, zinc and ether.
Natural Sources of Arsenic
The average daily intake of arsenic in adults is
0.5-0.1mg. Arsenic is a widely distributed element
and is found in: (i) Rocks and soil in concentrations
of less than 1ppm (ii) Hot spring mineral waters
(iii) Drinking water supply (iv) Sea-water contains
2-5mg/L (v) Plant and plant products (vi) Vege-
tables, fruits and grains (vii) Seafood (Fish, Shell-
fish, crabs and Dover-sole) and meats. Marine
organisms particularly shellfish may contain large
amounts of well-absorbed trimethylated organo-
arsenic, arsenobentaine that exerts no known toxic
effects when ingested by mammals and is excre-
ted unchanged in the urine (viii) Poultry and meat
products: Arsenilic acid has been used as a food
additive for poultry and other livestock to promote
growth and weight gain. The poisoning may result
from regular consumption of such products but at
times accidental poisoning of livestock has occur-
red. There are instances of Beef or cattle being
poisoned by ingestion of field grass that has been
previously sprayed by herbicides.
The interaction of Arsenicals with bacteria is
thought to account for the changes in the oxidation
state and chemical form of arsenic.
Industrial Sources of Arsenic
Arsenic is used primarily in the production of glass
and semiconductors, in wood and hide preser-
vation, as an additive to metal alloys to increase
hardening and heat resistance. In the past Arsenic
was used as weed killer, rodenticide, in chemical
warfare and in the production of pigments and
enamels.
Arsenic may be introduced in to the environ-
ment through (i) Industrial process such as
smelting of other metals (ii) Application of arsenical

pesticides and herbicides (iii) Generation of power
from coal (iv) Geothermal sources (v) Coal and
combustion of coal.
In the metallic form Arsenic is not poisonous
as it is insoluble in water and cannot be absorbed
from alimentary tract, but when it is oxidized by
exposure to air becomes poisonous. But some
workers believe that the metallic form may undergo
oxidation in the GIT producing symptoms.
Compounds of Arsenic
The compounds of arsenic are organic as well as
inorganic. The inorganic compounds are Arsenate
(AS5+) and Arsenite (AS3+)
1. Arsenious oxide or Arsenious tri-oxide (AS2O3):
It is a heavy metal with a specific gravity 3.669.
Its curious property is that it floats in water as
a white film and is soluble in spirit. It is found
as impurity in iron ores, mineral acids. Also
found in soils, mineral water and coal smoke.
It is widely used in: (i) Calico-printing (ii)
Taxidermy (preparing, mounting skin of animals)
(iii) Preparation of artificial flowers (iv) Wall
papers preparation (v) Preservation of timber
and skin against Ants (vi) Used by Hakims and
Vaidhs to treat Rheumatism, skin diseases,
syphilis and impotence.
2. Copper Arsenite (Scheel’s green, Paris green)
3. Red Arsenic (Arsenic disulphide)
4. Yellow Arsenic (Arsenic trisulphide)
5. Arsine gas (AsH 3 )—is hemolytic and
nephrotoxic.
Organo-chemicals
Many organo-chemicals ranging in toxicity from
the war gas Lewisite to lead additives such as
Arsenilic acid. In general their toxicity is similar
to that of inorganic ones. These are: (i) Cacodylic
acid (ii) Sodium cacodylate (iii) Atoxyl (iv)
Salvarsan (v) Neo salvarsan.
Pharmacokinetics and General Toxicity of
Arsenicals
Arsenic can be inhaled and absorbed through the
skin or through GI tract after ingestion. After a
very small dose of arsenic (like that experienced
Metallic Poisons 555
daily by most people) most of the absorbed
inorganic arsenic undergoes methylation, mainly
in liver to monomethylarsonic acid and dimethy-
larsinic acid, which are excreted along with residual
inorganic arsenic in the urine. However, if the dose
of arsenic is very large, the elimination half-life is
prolonged. Once absorbed, arsenic rapidly com-
bines with the globin portion of haemoglobin and
therefore localizes in the blood. There is minimal
penetration of the blood-brain barrier and within
24 hours arsenic redistributes itself to the liver,
kidney, spleen, lung and GI tract, with lesser accu-
mulation in muscle and nervous tissue. Once in
the tissues, arsenic exerts its toxic effect through
several mechanisms, the most significant of which
is the reversible combination with sulphydryl
groups. Arsenic blocks the Krebs cycle and inter-
rupt oxidative phosphorylation thus resulting in a
marked depletion of cellular ATP and eventually
death of the metabolizing cell. Arsenic also inhibits
the transformation of thiamine in to acetyl CoA
and succinyl-CoA resulting in the features of thia-
mine deficiency. Arsenolysis is a major form of
toxicity in which the arsenic anions can substitute
for phosphate in many reactions. Arsenic is
capable of inhibiting oxidative phosphorylation
through two different mechanisms 2-4 weeks after
ingestion, arsenic is incorporated into hair, nails
and skin as it binds to the sulphydryl groups of
keratin. Four weeks after ingestion, arsenic begins
to localize in the bone where it substitutes for
phosphate.
Organic Arsenicals are more rapidly excreted
than the inorganic form. Pentavalent forms are
cleared faster than trivalent form. The toxicity is
related to:
i. How fast it is excreted from the system?
The inorganic forms are more toxic than the
organic forms and the trivalent forms are
more toxic than the pentavalent forms depen-
ding on their rapidity of excretion.
ii. To what degree it may accumulate in the
tissues? Pentavalent forms are accumulated
more rapidly than the trivalent forms which
is approximately the reverse order of excre-
tion.
556 Textbook of Forensic Medicine and Toxicology
Arsine gas (AsH3) causes rapid haemolysis
and renal damage may persist for years following
single acute poisoning. Arsenite is absorbed from
GIT and retained in high levels in the tissues.
The poisoning due to Arsenic compounds can
be acute, subacute and chronic.
Acute Arsenic Poisoning
The acute arsenic poisoning results from the: (i)
Oral ingestion (ii) Inhalation of arsenic gas (iii)
Rubbing in to the skin (iv) Introduction in to rectum
or vagina.
Arsenic poisoning is usually the result of
accidental or suicidal ingestion of insecticides;
(Paris green) that is copper arsenite or calcium or
lead arsenate. Pesticide containing arsenic is
freshest source of poisoning
The toxic symptoms of acute arsenic poisoning
depends upon individual susceptibility. Orchar-
dists can ingest 6.8 mg /day without any signs
and symptoms but arsenic trioxide as low as 30
mg has been found fatal. This extraordinary degree
of tolerance to ingestion of arsenic could be due
to blockage of absorption, alteration in its distribu-
tion to tissues, enhanced or accelerated transfor-
mation of arsenite to less toxic arsenate, and
decreased reduction of arsenate to arsenite by
peripheral tissues.
Fatal dose→The fatal dose of arsenic trioxide
is 180 mg but the dose depends on the compound
ingested, its physical form and the inherent
tolerance of the patient to arsenic
Fatal period→Fatal period for arsenic poi-
soning is 12-48 hours but can be fatal even within
2-3 hours.
Mechanism or Action
The mechanism of toxicity of all arsenic com-
pounds is the same. Once in the tissues, arsenic
exerts its toxic effect through several mechanisms
such as: (i) Reversible combination with sulphydryl
groups (ii) Reacts with SH group in tissue proteins
(iii) Interferes with number of enzyme system
essential for cellular metabolism (iv) Capillary poi-
son, dilates capillary (v) Fatty degeneration of liver
(vi) Hyperemia and haemorrhages in the intestine
(vii) Renal tubular necrosis (viii) Peripheral nerves
show disintegration of axis cylinder (axonal neuro-
pathy) with fragmentation and resorption of myelin.
Signs and Symptoms
Acute Poisoning
The symptoms of acute intoxication usually occur
within 30 minutes of exposure:
1. Initially the patient experiences a metallic
taste in the mouth and slight garlicky odour
in the breath along with xerostomia (dry
mouth) and dysphagia.
2. This is followed abruptly by severe nausea
and vomiting, colicky abdominal pain and
profuse diarrhoea (bloody in some cases)
with rice water stools, due to vasodilation
with transudation of fluid into the bowel
lumen in addition to mucosal vesicle forma-
tion and sloughing leading to increased
peristalsis.
3. Generalised vasodilation caused by capillary
damage results in transudation of plasma
and severe hypovolemia.
4. If the dose of arsenic ingested is large,
cyanosis, cold clammy extremities, hypoxic
encephalopathy, convulsions and acute
tubular necrosis may occur following shock.
5. Hyperpyrexia and acute haemolysis may
also occur.
6. If the ingested dose is smaller, the patient
will have severe headache, vertigo, periorbital
oedema, skeletal muscle cramping and
evidence of renal damage manifested as
oliguria, proteinuria, and haematuria.
7. If death does not occur in the first few hours
from shock, the patient may die a few days
later from acute hepatic or renal failure.
9. Cardiac manifestations include acute cardio-
myopathy, subendocardial haemorrhages,
and ECG changes (prolonged QT interval and
non-specific ST-T changes). The cardiac
symptoms are due to decreased cardiac out-
put due to hypovolaemia and direct toxic
effect on the cardiac muscle.
 Metallic Poisons 557

10. Arsenic has a predilection for keratin that is Table 37.1: Differential diagnosis of acute
why the concentration is higher in hair and arsenic poisoning
nails. Findings Arsenic poisoning Cholera
11. Death from acute arsenic poisoning is Pain in throat Present before Present after
usually caused by irreversible circulatory vomiting vomiting
insufficiency. Purging Follows vomiting Precedes vomiting
Vomitus Consists of mucous Watery
When the dose is not large enough to kill the
bile and blood
patient, a number of secondary effects can be Stools High coloured, Rice water and
seen 2-4 weeks after ingestion of the poison. discharged with involuntary
These include hair loss, Mee’s lines (white trans- straining and
verse lines seen on the nail plate up to a year tenesmus
Voice con- Not affected Peculiar and rough
after arsenic intoxication), sensorimotor periphe- junctivitis Inflamed Not inflamed
ral neuropathy (may develop within a few hours of
ingestion but usually seen 2-8 weeks after expo-
sure), skin changes (as in chronic poisoning) and Narcotic form produces mainly CNS symptoms
possible chronic renal failure. such as: (i) Giddiness (ii) Precordial distress (iii)
The signs and symptoms start within half an Tenderness of muscles (iv) Delirium (v) Dilated
hour but may be delayed for several hours when pupils and complete paralysis of muscles at times.
it is given in rectum, vagina or skin. The dilatation Unusual symptoms such as (i) Convulsions (ii)
Lockjaw (iii) Raised temperature (iv) Loss of
of capillaries is responsible for most of the symp-
speech and memory (v) Joint pains can also be
tom: (i) Burning pain and throat constriction (ii)
produced.
Stomach pain which may increase on pressure
(iii) Increased salivation (iv) Intense thirst (v) Arsine Gas
Vomiting that is projectile, dark brown or yellow
Arsine gas acts as a poison to haemoglobin of
in colour and contains stomach contents, blood
red blood cells and causes haemolysis. It most
and mucus (vi) Purging, tenesmus, pain and irri- commonly produces haemoglobinurea and
tation about anus. The stools are dark coloured anaemia. The other symptoms produced as a
and bloody and later on are colourless, odourless result of poisoning due to arsine gas Jaundice,
and watery resembling rice water (vii) Due to dark red urine, heart failure, delirium and coma.
capillary transudation of plasma following rupture
of vesicles under intestinal mucosa (viii) Cramps Subacute Poisoning
in the calf muscles (ix) Restlessness (x) The Subacute poisoning results when the compounds
patient is dehydrated (xi) Skin is cold and clammy of arsenic are given in small doses at repeated
(xii) Face is pale and anxious (xiii) Eyes are intervals. The signs and symptoms that are pro-
shrunken (xiv) Pulse is irregular and quick (xv) duced are dysphagia, cough, foul smelling tongue
Respiration is laboured (xvi) Hypoxia, convulsions that is dry and congested, the motions are bloody.
and coma precede death (xvii) Cirrhosis and
ascites results from the therapeutic doses of Chronic Arsenic Poisoning
Flower’s solution (1% Arsenious trioxide) (xviii) This is much more insidious and the diagnosis is
Due to direct action on the myocardium the ECG often difficult to establish. The earliest cutaneous
shows T-wave inversion and persistent prolon- manifestation is persistent erythematous flushing
gation of QT interval (xix) Arsine dust: When arsine caused by cutaneous capillary dilation. Hyper-
dust is inhaled, it causes cough with frothy spu- keratosis then occurs with desquamation of the
tum, pulmonary oedema, cyanosis, breath- palms and soles, brittle nails with Mee’s lines,
lessness, corneal ulcer and conjunctivitis. patchy of diffuse alopecia (hair loss) and oedema
558 Textbook of Forensic Medicine and Toxicology
of the face, periorbital region, or ankles from loca-
lised transudation of intravascular fluid. Bowen’s
disease is a long-term complication of chronic
arsenic intake and often indicates that systemic
neoplastic processes are occurring. Haemato-
logic abnormalities include normochromic and
normocytic anaemia caused partly by haemolysis,
leukopenia and thrombocytopenia and mild
eosinophilia. Karyorrhexis is normally seen and
manifested by bizarre nuclear forms seen on bone
marrow examination. Interference with folate
metabolism may lead to a megaloblastic picture.
Neuropathy is the hallmark of arsenic poison-
ing. It is usually a symmetrical sensorimotor poly-
neuropathy, often resembling Guillain-Barre syn-
drome. The predominant clinical features of neuro-
pathy are paresthesia, numbness, and pain, parti-
cularly of the soles of the feet. Eventually, mus-
cular atrophy (possibly even paralysis) and ataxia
are seen. Encephalopathy may be seen in some
cases, presenting as severe headache, perso-
nality disturbance, convulsions or coma. Other
features of chronic arsenic poisoning are nausea,
vomiting, diarrhoea and irritability.
Patients who recover from the acute form of
poisoning develop (i) Skin and mucosal changes
(ii) Peripheral neuropathy (iii) Linear pigmentation
in the fingers (iv) Cutaneous manifestations appear
within 1-4 weeks and consist of dry, diffuse and
scaly desquamation with hyperpigmentation over
the trunk and extremities and hyperkeratosis of
palm and soles (v) Mucosal surfaces also show
signs of irritation like conjunctivitis, photophobia
and pharyngitis (vi) After 5 weeks, transverse white
streaks 1-2mm width appears above base of each
fingernail called Mees line. Those who have more
than one exposure may show double line, several
millimeters apart (vii) After 1-3 weeks, features of
peripheral neuropathy like decreased sensations
of touch, pain and temperature appear in a sym-
metrical fashion. There is ‘glove and stocking’ dis-
tribution. There is distal weakness resulting in wrist
drop, unable to walk, distal reflexes are decreased
and atrophy of muscles.
Laboratory Findings
Diagnosis
Definitive diagnosis of arsenic poisoning is difficult
because of the natural presence of trace amounts
of arsenic in the body and because, due to the
multi systemic toxicity of arsenic, the clinical
manifestations vary widely so both acute and
chronic poisoning simulate many other diseases
and be overlooked in the differential diagnosis.
Diagnosis is often particularly difficult in homicidal
poisoning attempts because the patient will not
usually know that he/she has ingested arsenic.
Arsenic poisoning is usually diagnosed with a
urine test for arsenic since monomethylarsine and
dimethylarsine are present in the urine 24 hours
after ingestion and arsenic ions are present very
shortly after ingestion (useful for diagnosis of acute
poisoning). A urinary excretion of arsenic >200
mg/24 hr is regarded as indicative of exposure to
a potentially toxic amount of arsenic. The gastric
contents can also be screened for arsenic and, if
it is very soon after ingestion a blood test will also
reveal arsenic. Analysis of body tissues, nails
and hair is important in diagnosis of chronic arsenic
ingestion. Colorimetry, polarography, atomic
absorption spectroscopy and neutron activation
analysis are effective methods for arsenic
detection. Hair and nail samples containing
>3ppm or 100mg or arsenic per 100g of specimen
are diagnostic of arsenic poisoning. Analysis of
hair is often used many years after death to
determine the cause of death. This is how the
true cause of death (chronic arsenic poisoning) of
Napoleon Bonaparte was determined 140 years
after he died (Weider, 1999).
i. Urine: Normal value of arsenic is 0.01-
0.06mg/litre of urine and it may be even upto
0.2 mg/litre. Most patients with exposure
having more than 0.1 mg/litre, upto 1mg/litre
of urine. Proteinuria, casts and albuminuria
are there.
ii. Blood: The normal blood level is 100mg/litre.
There is moderate anaemia and leucopenia
2000-5000 mm3 except Arsine poisoning
causes leukocytosis and mild eosinophilia.
iii. Liver function tests: There is failure to
excrete bilirubin, decreased metabolism of
protein, serum alkaline phosphatase and
bilirubin is raised, urobilinogen in the urine
iv. CSF is normal.

v. Hair: In normal persons, average concen-
tration is 0.05/100 gm of hair but more than
1mg/100 gm indicates poisoning.
As arsenic is widely distributed in nature, their
presence may not always indicate of the poison-
ing.
Treatment
1. Empty stomach by emetics, tartar emetics
should not be used; copper sulphate also
should not be used as it leads to the
formation of copper arsenite.
2. Stomach wash should be done with freshly
prepared solution of ferric oxide in table
spoonful doses suspended in water; with
arsenious acid it forms ferric arsenite that is
a harmless and insoluble salt. Ferric chloride
(45 ml) and sodium carbonate or magnesium
oxide (15 gm) in half glass of water, strained
through muslin is used for the lavage. The
following reaction occurs FeCl3 + MgOFe2O3
+ MgCl2
3. For gastric lavage, 1% sodium thiosulphate
in water is helpful.
4. Dialysed iron may be used as a substitute.
5. 10% solution of sodium thiosulphate as 7½
gm I.V. injection but it is of doubtful value.
6. British Anti Lewsite (B.A.L.) is administered
4 hrly for 2 days, 6 hrly for 1 day and total
dose 12 hrly afterwards; total dose is 2.5-
3mg/kg body wt. The duration of B.A.L.
depends upon (i) Clinical state and (ii) Res-
ponse of the patient. B.A.L. is to be stopped
if side effects like nausea, vomiting, burning
sensation in the mouth, tachycardia, hypo-
tension, constriction in the throat appear.
7. To know when the chelation is to be stop-
ped, 24 hr urine sample is to be collected
and if Arsenic levels fall below 50 mg/24 hrs,
it should be stopped for 5 days and then
started again so that the tissue arsenic is
mobilized and ready for chelation.
8. Oral Penicillamine 100 mg/kg body wt in four
divided doses is given in 24 hrs for 4-8 days
after initial 12-48 hrs of B.A.L. therapy.
9. Demulcents such as ghee and barley water
are given.
Metallic Poisons 559
10. Castor oil or magnesium sulphate is adminis-
tered to diminish intestinal absorption of
arsenic.
11. Morphine is given to relieve pain.
12. Saline is administered intravenously for
dehydration and enuresis.
13. To relieve cramps, massage is employed.
14. Body temperature is to be maintained.
Treatment of Poisoning by Arsine Gas
(i) Patient to be taken to fresh air (ii) Oxygen inhala-
tion to be started (iii) Exchange transfusion should
be undertaken (iv) Haemodialysis (v) Alkaline
drinks. All of the above methods help to eliminate
arsine from the blood. B.A.L. is not effective in
arsenic gas poisoning.
Autopsy Findings
1. Rigor mortis lasts longer.
2. General shrunken appearance due to
dehydration.
3. Eyeballs are shrunken.
4. Cyanosis of hands and feet is there.
5. Jaundice is also present.
6. Mucous membrane of mouth and pharynx
is inflamed and ulcerated.
7. Stomach is the main organ to be inflamed;
food particles are mixed with arsenic embe-
dded in the mucous. The inner wall of the
stomach is swollen, congested and tinged
with streaks of blood and arsenic. On scrap-
ing the mucous membrane is congested and
inflamed and is brownish red or scarlet in
colour. There is petechial haemorrhages.
The inflammation is more marked in the
greater curvature and the cardiac end. Ulce-
ration, gangrene and perforation have been
rarely reported.
8. Small intestine is flabby and contains large
flakes of mucous with little faecal matter,
submucosal haemorrhages are present and
the epithelium is flabby and oedematous.
9. Large intestine contains seromucous and
the intestinal glands are swollen and enlar-
ged.
10. Lungs are congested, oedematous and show
subpleural ecchymosis.
560 Textbook of Forensic Medicine and Toxicology
11. Caecum and rectum are inflamed and the
mucous membrane is flabby.
12. Liver, spleen and kidney is enlarged and
congested and shows fatty infiltration and
degeneration.
13. Heart contains coagulated blood and ecchy-
mosis of the endocardium and muscles of
the left ventricle is there.
14. Brain is congested and ventricles are full of
serum.
Autopsy Findings in Arsine Gas Poisoning
(i) Skin is dirty yellow in colour (ii) Mucous mem-
brane of stomach and intestine is yellow and
inflamed (iii) Liver is small or enlarged and shows
fatty degeneration (iv) Spleen shows evidence of
destruction of blood and deposition of blood pig-
ment throughout the organ (vi) Kidney is enlarged,
congested and shows tubular necrosis (vii) Lungs
are congested and oedematous.
Chronic Arsenic Poisoning
Chronic arsenic poisoning results from: (i) Chronic
repetitive inhalation of arsine gas (ii) Chronic
repetitive ingestion. Chronic poisoning usually
results from the:
1. Persons engaged in the occupation of: (i)
Smeltering that is extraction of metals from ore
by melting (ii) Refining of ores (iii) Manufacture
of weed killers, insecticides, paints, dyes and
cosmetics.
2. Persons who ingest it as medicine for long
periods.
3. May follow the acute poisoning after recovery.
Chronic poisoning consists of the following
stages:
First stage: The following symptoms are produced
in the first stage: (i) Loss of weight (ii) Loss of
appetite and salivation (iii) Colicky pain and
constipation (iv) Vomiting and diarrhoea (v) Gums
are red and soft (vi) Tongue is coated, is thin white
silvery and furred (vii) Oedema of eyelids and
ankles (vii) Temperature and pulse is raised.
Second stage: In the second stage of chronic
poisoning following symptoms are produced: (i)
Cutaneous eruptions (ii) Catarrh of larynx and
bronchial tube (iii) Dryness and itching of skin (iv)
Voice is hoarse and husky (v) Photophobia and
conjunctivitis (vi) Running nose and coryza (vii)
Cough with bloody expectoration (viii) Liver is
enlarged and cirrhotic (ix) Kidneys are damaged
(x) Prominent changes are produced in the skin:
• Generalized or localized, rain drop type of
pigmentation of the skin involving the covered
parts of the body such as flexors, nipples, lower
abdomen, temples and eyelids. This can be
differentiated from Addison’s disease as
mucous membrane of the mouth is spared.
• Epithelial hyperplasia, discrete multiple wart
like keratosis on the palm, soles, head and
trunk (Basal cell carcinoma—Bowen’s disease)
• Epitheliomata are present in 20% of the cases.
• Nails are brittle with linear pigmentation.
• Hairs are dry and fall off.
• Painless perforation of the nasal septum.
Third stage: (i) Sensory symptoms are
predominantly present such as headache, tingling,
numbness and hyperaesthesia of the skin (ii)
Tenderness and muscle cramps (iii) Circumscribed
oedema of eyelids and ankles (iv) Knee jerk is
usually lost (v) Impotence is commonly present
(vi) There is evidence of bone marrow depression
and aplastic oedema.
Fourth stage: (i) Peripheral neuritis with glove
and stocking type of anaesthesia; there is
decreased pain, temperature and touch sensation
(ii) Muscular atrophy of extensor muscles resulting
in wrist drop and foot drop (iii) Muscular weakness
(vi) Ataxia (v) Cramps (vi) Tremors and general
emaciation (vii) Anaemia and dysuria (viii) Death
is due to failure of heart muscles.
Differential diagnosis: Chronic arsenic poisoning
is to be differentiated from alcoholic neuritis. In
the former the symptoms and signs are produced
more rapidly. Are widespread and there is no
glycosuria whereas in alcoholic neuritis glycosuria
is positive.
Treatment
1. Remove the patient from source of poison.
2. B.A.L. is to be given 6 hourly for 2-3 days and
then once daily.

3. Vitamin B1 injection for peripheral neuritis.
4. Improve general health.
Medicolegal Aspects
1. It is an ideal homicidal poisoning, used for
frequently in India; can be mixed with sweets,
bread, cooked vegetable, drinks, milk, pan and
cigarettes. Mass homicidal poisoning simulates
cholera. It is tasteless, odourless, easily avail-
able and small doses are required for homicide.
In western countries, small doses are given for
a prolonged period that simulates gastroenteritis
to conceal the crime. The disadvantages of
being used as a homicidal poison are: (i) Can
be detected even in the charred bodies (ii) It
delays putrefaction (iii) Can be detected in
decomposed bodies (iv) Can be found in bones,
hair even years after the poisoning.
2. It is used on abortion sticks as paste or
ointment.
3. It is used as a cattle poison, is mixed with
water in the well.
4. Is used for suicidal purposes.
5. The poisoning can result accidentally due to
its improper medicinal use when it is applied
locally as a cure for impotence, poisoning can
result from its application on the abraded skin,
when it is accidentally mixed with food or
drinks, when used as vaginal pessaries, and
when it is mistaken for baking powder or soda.
Beer drinkers in Lanceshire country in 1900
developed chronic arsenic poisoning and
peripheral neuritis was produced.
Arsenophagists: Arsenophagists use the drug
as a habit for impotency
6. By dividing hair in small successive lengths
from the root upwards and analyzing them
separately, one may get the important infor-
mation regarding the time that has elapsed
since the administration of arsenic. Arsenic
starts depositing in the hair after 15 days. If
the length of hair is 1 cm that is equal to 25
days. By neutron activation analysis, the rela-
tion between ingested arsenic and arsenic
content of the hair can be known.
7. Arsenic is excreted in the stomach and intes-
tine after absorption, even when administered
by routes other than mouth.
Metallic Poisons 561
8. It has the power of retarding decomposition and
it does not disappear with decomposition.
Postmortem imbibitions of arsenic: When there
is a criminal charge of arsenic poisoning, the
defence may take the plea that Arsenic was intro-
duced after death and postmortem imbibition
occurred in the tissues. The doctor can defend it
by replying that it takes an anatomical course,
more on the left side. Signs of inflammation and
ulceration of stomach will be absent in case of
postmortem imbibition of arsenic.
Exhumed body: Arsenic cannot percolate in the
cadaver from the soil, as it is an insoluble form of
salt. The nails and hair will have a higher concen-
tration from the soil. The soil is to be kept for
chemical analysis.
MERCURY
Mercury is known as quick silver, a liquid metal
with bright silvery luster that is volatile at room
temperature. We ingest some amount of mercury
along with our diet; 5-20 mg is taken along with
the foodstuffs daily.
The tolerable weekly intake of mercury per
person is 300 mg out of which not more than 200
mg should be methyl mercury. It is not a normal
constituent of the human body. Normal levels in
unexposed individuals:
• 0-8mg/100ml of blood.
• 0.6-1.6μg per 100ml of urine.
• 5-150μg per 100gm may be found in liver and
kidney.
Deadening of mercury: Mercury is converted in
to a dull gray powder (contains 33% of mercury):
(i) When it is shaken with oil (ii) Triturated with
sugar, chalk (iii) Used for ointment purposes.
Uses of Compounds of Mercury
Have a wide range of use:
1. Inorganic salts: (i) Calomel cathartic—Mer-
curous chloride, used as purgative (ii) Mercurial
ointment (iii) Vaginal creams (iv) Fingerprint
powders (v) Amalgam (dental filling) (vi)
Vermilion (Mercury sulphate).