CHAPTER 38
Inorganic Metallic Irritants—Arsenic
Introduction
Physical properties: Metallic arsenic (black in color) is
not poisonous, as it is not absorbed from the GIT. It is
a normal constituent of all animal tissues, in minute
amounts.
Toxic Compounds and its Uses
i. Arsenious oxide or arsenic trioxide (Fig. 38.1A)
(sankhya, somalkhar, white arsenic or arsenic): Most
toxic form of arsenic. It has no taste or smell and
is sparingly soluble in water. It is used in fruit
sprays, sheep-dips, weed-killers, insecticides, rat
poisons, flypapers, calico-printing, wallpapers,
artificial flowers and as mordant in dyeing.
ii. Copper arsenite (Scheele’s green) and copper
acetoarsenite (Paris green or emerald green) (Fig.
38.1B): It is used as coloring agent for substances
including confectionary.
iii. Sodium and potassium arsenate.
iv. Arsenic sulfide: Yellow orpiment (hartal) or arsenic
trisulfide, and red realgar or arsenic disulfide
are used as depilatory, coloring pigment and in
flypaper.
v. Arseniuretted hydrogen or arsine is a colorless gas
with garlic-like odor.
vi. The natural sources of arsenic are soil, water and
some sea fish (mussels, prawns). High arsenic
content of soil and subsoil water of some places
is the cause of endemic toxicity (from shallow
tube-wells inserted for drinking water).
A B
Figs 38.1A and B: (A) Arsenious oxide, (B) Copper acetoarsenite
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vii. Tobacco smoke, particularly cigars also contain
arsenic, and in some beers as impurities.
Action
„ Arsenic interferes with cellular respiration by
„
uncoupling mitochondrial oxidative phosphorylation
by combining with the sulfhydryl groups of
mitochondrial enzymes, especially pyruvate dehydro
­­
genase and certain phosphatases. Consequently,
­
conversion of pyruvate to acetyl CoA is decreased,
citric acid cycle activity is decreased and production
of cellular ATP is decreased.
„ It inhibits cellular glucose uptake, gluconeogenesis,
„
fatty acid oxidation and further production of acetyl
CoA.
„ Locally, it causes irritation of the mucous membranes,
„
and remotely, depression of the nervous system.
„ Arsenic is a carcinogenic substance since lung, skin
„
and bladder (transitional cell) carcinoma has been
observed in populations with multiple exposures.1
Absorption and Excretion
It is absorbed orally through the GIT, skin and lungs
(arsine) or parenterally.
„ It is present in almost all tissues, and found in the
„
greatest quantity in the liver, followed by kidneys
and spleen.2
„ In cases, where the patient survives, it is found in
„
the muscles (for months), bones, hair, nails and skin
(sulfhydryl groups in keratin) for years. Normally,
the hair contains < 2 parts/million arsenic.
It is excreted mainly by the kidneys (urine), but some
part through feces, bile, sweat, milk, nails and hair.
„ The arsenic is excreted in the hair and nails within
„
few hours of ingestion, and in cases of intermittent
chronic poisoning there will be successive deposits
of arsenic in the hair and nails.
„ Arsenic is secreted into the stomach and intestines
„
after absorption, even when given by routes other
than mouth.
490 Review of Forensic Medicine and Toxicology

Signs and Symptoms (Acute Poisoning)
Symptoms usually appear by 10 minutes (min) to 1
hour (h) after ingestion, but may be delayed, if arsenic
is taken with food.
System Signs and symptoms
GIT Sweetish metallic taste, nausea, persistent vomiting,
burning in mouth and throat, and difficulty in swallowing,
garlic odor in breath, intense thirst, pain in esophagus and
abdomen, purging accompanied by tenesmus, pain and
irritation about the anus. Initially, defecation is frequent
and involuntary, dark-colored, but later it become
shaking chills, backache and anemia. The urine
appears black due to hemoglobinuria. Death may
be preceded by anuria and convulsions.
Fatal dose: 120–200 mg of arsenic trioxide (adults),
2 mg/kg (children).4
Fatal period: 1–2 days.
Laboratory Investigations
Urine, stool, blood, vomit, hair and nails from patients,
and in addition, stomach and intestinal contents, bone,
liver, bile and kidneys from dead bodies are tested.
„ Urine: Excretion of > 50 µg/l in 24 h urine is

„
colorless, odorless and watery resembling rice-water. indicative of poisoning. Metabolites of arsenic
Renal Oliguria, uremia, albuminuria, red cells and casts, pain
including methylarsonic acid and dimethylarsenic

during pulmonary edema, ARDS, micturition.
CVS Hypotension, pulmonary edema, ARDS, circulatory acid may be recovered in a urine specimen.
„ Blood (serum arsenic > 0.9 µg/dl), stool, liver, kidneys

collapse, ventricular tachycardia and fibrillation.

„
Hepatic Fatty infiltration. and bones show presence of arsenic. As with all heavy

MS Pain in limbs, weakness. metals, microcytic hypochromic anemia is common.

CNS Headache, vertigo, hyperthermia, tremors, convulsions, „ Hair: Arsenic > 75 µg% is suggestive of poisoning.

coma, general paralysis.
„
„ Nails: Presence of > 100 µg% of arsenic is suggestive
Skin Delayed loss of hair, skin eruptions.
„
of poisoning.

„ Radiopaque sign on abdominal X-ray.
„ Acute exposures generally manifest with the cholera-
„
„ ECG: QRS broadening, QT prolongation, ST
„
like gastrointestinal symptoms of nausea, vomiting,
„
abdominal pain and severe diarrhea (Diff. 38.1).3 depression and T-wave flattening.
5
„ Marsh, Reinsch and Gutzeit tests are obsolete.
„ In fulminant type, when large dose (> 3 g) is taken, the
„
„
GIT symptoms are absent and death occurs in 1–3 h Neutron activation analysis and atomic absorption
from shock and peripheral vascular failure. spectroscopy helps in estimating concentration of
„ In narcotic type, the GIT symptoms are less. There arsenic in hair, nails and bone.
„
is giddiness, formication, tenderness of the muscles,
delirium, coma and death. Rarely, there is complete Treatment
paralysis of the extremities. Hemodynamic stabilization is of primary importance,
„ Arsine gas exposure causes hemolysis, damages the and large amounts of crystalloid solutions may be
„
liver and kidneys (hemoglobinuria and renal failure) required because of significant GI losses (i.e. vomiting
and depresses the CNS. There is nausea, vomiting, and diarrhea).
Differentiation 38.1: Arsenic poisoning and cholera
S.No. Feature Arsenic poisoning Cholera
1. Pain in throat Before vomiting After vomiting
2. Vomiting and purging Purging follows vomiting Vomiting follows purging
3. Vomitus Contains mucus, bile and blood Watery, without mucus, bile or blood
4. Stools Rice-watery, may contain blood Rice-watery, no blood, and passed in
a continuous involuntary jet
5. Tenesmus and pain around anus Present Absent
6. Voice Not affected Rough and whistling
7. Conjunctiva Inflamed Not inflamed
8. Laboratory investigation Š Radiopaque shadow (X-ray abdomen) seen in arsenic trioxide Vibrio cholerae present
Š
Š Level of urinary coproporphyrin III may be increased
Š
Š Arsenic in chemical analysis
Š
9. Circumstantial evidence Poisoning may be present in an individual or a family or a group May occur is sporadic or epidemic
form in the locality
10. Motive Homicidal, rarely accidental No such thing

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 Inorganic Metallic Irritants—Arsenic
i. Gastric lavage is done repeatedly with large amount
of warm water and milk; activated charcoal does not
adsorb arsenic appreciably and is not recommended
in patients whom co-ingestants are not suspected.
ii. Demulcents (butter or greasy substances) prevent
absorption.
iii. Whole bowel irrigation with polyethylene glycol
may be effective to prevent GIT absorption of
arsenic.
iv. Antidote is BAL or dimercaprol, given in a dose of
3–5 mg/kg IM 4 hourly for 2 days, 6 hourly for 1
day and then 12 hourly for 10 days. Oral succimer
(DMSA), 10 mg/kg every 8 hourly for 10 days or
dimerval (DMPS, drug of choice for treating most heavy
metal poisonings), 200 mg IV 4 hourly until oral
product can be given in a dose of 100 mg TDS or
QID may be used instead of BAL.
v. Alkalis should not be given by mouth as they
increase the solubility of arsenic.
vi. Purgatives (castor oil/magnesium sulfate) are given
to remove unabsorbed poison from intestine.
vii. Glucose-saline with sodium bicarbonate is helpful
to combat shock and improve alkali reserve.
viii. Hemodialysis or exchange transfusion may be done.
Earlier, freshly precipitated ferric hydroxide (antidotum arsenici)
was used for stomach wash in the treatment of arsenic poisoning
which formed ferric arsenite, is no longer recommended.
Postmortem Findings
External
i. The body looks emaciated due to dehydration.
ii. Rigor mortis appears early.
iii. Putrefaction is delayed due to anti-bacterial action
of arsenic and partly due to dehydration.6
iv. The eyeballs are sunken and the skin is cyanosed.
v. Blood tinged vomitus and fecal matter may be
present on body and clothes.
Internal
i. The mucous membrane of the mouth, pharynx and
esophagus may show inflammation or ulceration.
ii. Hemorrhages may be found in the abdominal
organs and mesentery, and occasionally in the
larynx, trachea and lungs.
iii. Lungs: Congested, pulmonary edema with
subpleural ecchymoses.
iv. Heart: Subendocardial petechial hemorrhages of the
ventricle may be found, even when the stomach
shows little signs of irritation.
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491
v. Stomach: Mucosa is swollen, edematous,
desqua mated and red, either generally or in
­
patches, especially in the pyloric region. Usually,
groups of petechiae are seen scattered over the
mucosa, but sometimes large submucosal and
subperitoneal hemorrhages may be seen—red
velvety appearance.7 A mass of sticky mucus
covers the mucosa in which particles of arsenic
may be seen. Congestion is most marked along the
crest of the rugae. Inflammation is more marked
at the greater curvature, posterior part and the
cardiac end of the stomach.
vi. Small intestine: It contains large flakes of mucus
with very little fecal matter. The mucosa is pale-
violet and shows signs of inflammation with
submucous hemorrhages along its whole length.
vii. Cecum and rectum show slight inflammation.
viii. Liver, spleen and kidneys: Congested, enlarged
and show cloudy swelling, and occasionally fatty
degeneration. Nephritis, and scarring of renal
cortices are seen.
ix. Brain: Edema with patchy necrosis or hemorrhagic
encephalitis. The meninges are congested.
Chronic Arsenic Poisoning (Arsenicosis /
Arsenicism)
Chronic arsenic poisoning may occur due to:
„ Recovery from an acute poisoning.
„
„ Accidental ingestion of small doses repeatedly by
„
those working with the metal.
„ Intake of food/drink in which there are traces of
„
arsenic (may be homicidal in nature).
Tolerance: Some people take arsenic daily as a tonic or
as an aphrodisiac and they acquire tolerance to 250–300
mg or more in one dose. Such people are known as
arsenophagists.
Signs and Symptoms
It is divided into four stages (Table 38.1):
i. GIT disturbances
ii. Catarrhal changes
iii. Skin rashes
iv. Nervous disturbances.
„ A metallic taste, excessive salivation, and garlic odor
„
of breath and sweat may indicate chronic arsenic
poisoning.
„ Melanosis and leucomelanosis with or without
„
keratosis are the earliest symptoms of arsenicosis.
492 Review of Forensic Medicine and Toxicology

Table 38.1: Signs and symptoms in chronic arsenic poisoning ii. Small intestine: Reddish with thickened mucosa.

1 iii. Liver: Hepatomegaly, fatty degeneration or even
System Signs and symptoms

necrosis with non-cirrhotic portal fibrosis.13
GIT Nausea, vomiting, abdominal cramps, loss of
appetite, constipation or diarrhea, salivation. iv. Kidneys: Tubular necrosis.

Ocular Congestion, watering of the eyes, photophobia. v. Heart: Myocardial necrosis may be seen.

„ Bone marrow histopathology will show hypoplasia.
RS Cough, hoarseness of voice, bronchial catarrh,

„
hemoptysis, dyspnea. „ If arsenic poisoning is suspected, hair or tissue

Skin and There may be a rash resembling fading measles rash.
nails Speckled brown pigmentation, mostly on the skin
flexures, temples, shoulders, eyelids and neck (raindrop
pigmentation). Macular areas of depigmentation
may appear on normal/hyperpigmented skin—
leucomelanosis. Hyperkeratosis of the palms and
soles with irregular thickening of the nails and
„
samples should be obtained for confirmation.
Medico-legal Aspects
Arsenic poisoning can be homicidal, suicidal, accidental,
occupational or unintentional.
i. Homicide: Arsenic was a popular homicidal poison

development of white bands of opacity in the nails of because:
fingers and toes (called Aldrich-Mees lines). Brittle
nails and alopecia are also seen.8-11 � Onset of symptoms is gradual � Cheap

CNS Peripheral neuropathy with tingling, numbness of � Symptoms simulate those of � Colorless

hands and feet, polyneuritis, anesthesia, paraesthesia cholera � Tasteless



with painful swelling (erythromelalgia), encephalopathy. � Small quantity is required to � Odorless



Neuritis resembles chronic alcoholism. cause death � Easily obtainable



CVS Hypertension, ischemic heart disease, cardiac failure, � Can be administered easily with

dependent edema. food, drink or betel leaf (paan)

Renal Chronic nephritis, urine may be red or green in color, � Chronic cases causing debility

dysuria and anuria may develop from renal tubular resemble certain diseases

necrosis.
Hepatic Hepatomegaly, jaundice, cirrhosis of the liver. Disadvantages of arsenic as homicidal poison:


Hematologic Bone marrow suppression, hypoplasia, anemia, z It retards putrefaction.
z
thrombocytopenia and leukemia. z It can be detected in decomposed/buried bodies.
z
z Arsenic can be found in bones, hair and nails
„ Chronic exposure also causes diabetes, vasospasm
z
for several years.14
„
and peripheral vascular insufficiency (blackfoot
z It can be detected in charred bones or ashes.
disease—peripheral vascular disease characterized
z
ii. Suicide is rare, because it causes too much of pain.
by systemic arteriosclerosis resulting in dry


iii. Accidental death may be due to admixture with
gangrene and spontaneous amputations of affected


articles of food or from its improper medicinal
extremities).12
use. Chronic poisoning results from drinking well
Treatment water containing arsenic.
iv. Arsenic exposure can be occupational in those
i. Remove the patient from the source of exposure


working in metal foundry, mining, glass production


and administer BAL in usual doses.
ii. Vitamin B complex and IV sodium thiosulfate are or in the semiconductor industry.
v. It is sometimes ingested or applied locally in the


useful.


iii. Symptomatic treatment. form of a paste or ointment on abortion sticks to
procure abortion.


Postmortem Findings vi. It may be used as cattle poison.


External: Emaciation, pigmentation, keratosis, alopecia, Postmortem Imbibition of Arsenic
white streaks on nails, jaundice, wasting of muscles,
and ulceration of nasal septum. „ Arsenic is the 12th most abundant element on earth.
„
This makes it obvious that in postmortems and
Internal exhumations, the possibility of imbibition from the
i. Stomach: It may be normal or may show a chronic surrounding earth should be considered. Adequate


gastritis. Some rugae may show patchy inflam- controls should be taken from surrounding and
matory redness or focal ulceration. distant soil and ground water, as any arsenic found

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 Inorganic Metallic Irritants—Arsenic 493

in the body may found its way by percolation from contaminated is likely to be much greater than the
natural sources. concentration of arsenic in the contaminating fluid.
„ Keratin tissues absorb arsenic by contamination from „ In poisoning cases, the concentration of arsenic

„
„
outside. The concentration in hair and nails thus should be more than in the soil/ground water.

MULTIPLE CHOICE QUESTIONS

1. Chronic arsenic poisoning does not cause: 8. Arsenic causes all, except: WB 09





NEET 13,15 A. Raindrop pigmentation

A. Mixed sensory and motor neuropathy B. Alopecia

B. Mesothelioma C. Palmar hyperkeratosis

C. Hyperkeratosis of skin D. Blue line in gums

D. Anemia 9. A middle aged man presented with paraesthesia of




2. In arsenic poisoning, greatest amount is found in: hands and feet. Examination revealed presence of




PGI 06 ‘Mees’ lines in the nails and raindrop pigmentation

A. Muscle B. Kidney in the hands. The most likely diagnosis is:

C. Liver D. Brain AIIMS 08, 09, 11





3. Cholera presents with symptoms mimicking: TN 10 A. Lead poisoning





A. Arsenic poisoning B. Arsenic poisoning


C. Thallium poisoning


B. Dhatura poisoning


D. Mercury poisoning


C. Barbiturate poisoning


10. Raindrop pigmentation is seen in:


D. Morphine poisoning



Kerala 07; BHU 10; NEET 13


4. Fatal dose of arsenic trioxide in adults: AIIMS 14
A. Arsenic poisoning B. Phosphorous poisoning



A. 20–30 mg B. 50–60 mg




C. Mercury poisoning D. Thallium poisoning




C. 60–80 mg D. 120–200 mg




11. Mees’s lines are characteristic of:




5. Reinsch test is used in diagnosis of poisoning due




PGI 09; CMC (Ludhiana) 10,13; NEET 14


to: UP 11; COMEDK 12

A. Mercury poisoning B. Arsenic poisoning

A. Arsenic B. Lead




C. Lead poisoning D. Copper poisoning




C. Iron D. Copper sulphate




12. Blackfoot disease is caused by: NEET 14




6. In a suspected case of death due to poisoning where



A. Arsenic B. Cadmium


cadaveric rigidity is lasting longer than usual, it may




C. Lead D. Mercury
be a case of poisoning due to: DNB 10; Bihar 10




13. Fatty yellow liver is seen in poisoning with: AI 08

A. Lead B. Arsenic



A. Arsenic B. Aconite








C. Mercury D. Copper C. Oxalic acid D. Mercury








7. ‘Red velvety’ stomach mucosa is seen in poisoning 14. The poison that can be detected in hair/bones long




with: Gujarat 07; JIPMER 14 after death is: Gujarat 07; COMEDK 08; FMGE 08


A. Mercury B. Arsenic A. Lead B. Mercury








C. Lead D. Copper C. Arsenic D. Cannabis








1. B 2. C 3. A 4. D 5. A 6. B 7. B 8. D 9. B 10. A











11. B 12. A 13. A 14. C




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