HI ,,,

GOOD
AFTERNO

ARSENIC
Arsenic is a chemical element with
symbol As and atomic number 33.
Arsenic is a metalloid.
Symbol : As
Electronic configuration : [Ar] 4s2 3d10
4p3
Atomic number : 33
Discovered in : 2500 BC
Atomic mass : 74.9216 0.00002 u

CONTIN.

It is a metalloid , belongs to group V of

periodic table of elements.
It exists in 3 forms - elemental
trivalent
( arsenite)
pentavalent
(arsenate )
Trivalent are more toxic than
pentavalent bec of more solubility .

Conti..

Inorganic forms of Asarsenic trioxide and pentavalent

and
trivalent forms of Na, K , Ca salts.
Organic forms
MSMA
( monosodium methanearsonate)
DSMA ( disodium methanearsonate ) etc
arsine gas is most toxic compound of As . It
comes from charging of storage batteries or
action of water on pyritic ores .

Arsenic trioxide
powder

HISTORY OF ARSENIC
> 2400 Years ago as a therapeutic
agent and poison in
GREECE and ROME .
PARACELSUS
mentioned arsenic
preparations in his
writing ( 1520 AD )

History Of Arsenic
its name has become synonymous with poison.

the Italian family of Borgias used arsenic as

their favorite poison for political
assassinations.
It is believed that Napoleon was poisoned
by arsenic-tainted wine served to him while8

Telugu Doctors.co.in

The Arsenic Disaster

The largest mass poisoning in history
"Bangladesh is grappling with the largest mass poisoning of a population
in history because groundwater used for drinking has been contaminated
with naturally occurring inorganic arsenic

it is said that between 33 and 77 million of Bangladesh's 125 million

population was at risk.

"The scale of this environmental disaster is greater than any seen before",
wrote Smith.

"It is beyond the accidents at Bhopal, India, in 1984 and Chernobyl,

Ukraine, in 1986."

INDIA

KARNATAKA

SOURSES OF ARSENIC TOXICITY

Arsenic was a common
poison used for
homicidal and suicidal
purposes in ancient
times .
Accidental poisoning
also recorded since
used in ant and roach
baits .

Various sources:-

1. Drinking water esply well

water is the major source of
As
2. Pesticides
( copper aceto arsenite /
paris green )
3. Rodenticide arsenic trioxide
4. Wood preservatives arsenic
pentoxide
5 . Ant baits Na / K arsenite

Well water

Is our well water also contain arsenic

Yes . Well
water is
the major
source of

 In 1814 Paris Green was

invented
One grain could kill a
man but that didn't stop
the production of this
brilliant and beautiful
colour
Used as a dye for
clothing, and wallpaper.
It was also used in glass
manufacture, leather
tanning, as a colour in
cosmetics and soaps,
inks, food colouring,
candles, sheep dip,
artist's pigments, paint
for children's toys .
it was sold as a highly
effective rat poison.

Contin.
6. contaminated soils and burn piles .
7.Arsenic as a drug
( ruminotorics , skin tonics , lead
arsenite dip , sodium thiacetarsamide )
8. over usage of arsenical feed additives
in poultry or swine - as growth promoter .
9. burning of wood products treated
with arsenical preservatives .

Burning of wood treated with arsenic preservative also

release arsenic

Conti.

10. Smelting of Cu ,Zn , Pb ores

release As as a
by-product
11. Arsenic gas & arsenic trioxide
used in computer chips
12. Dyes and paint containing arsenic .
13. malicious poisoning with arsenic
trioxide is very common.

FACTORS AFFECTING TOXICITY

Species - herbivores affected more

cats and dogs less poisoned
swine and fowls are rarely
affected

FACTORS AFFECTING TOXICITY

Oxidation status - order of toxicity

inorganic trivalent As > inorganic
pentavalent
> organic As

Solubility finely divided As is more

toxic than coarse and poorly soluble .

Herbivores are affected more, since they

eat pasture contaminated with Arsenic

Conti.
Health of the animal dehydrated ,
ill and
poor conditioned animals
are more susceptible to toxicity bec
renal excretion is slow in these
animals.
tolerance constant exposure will
provide some degree of tolerance
to As.

TOXICITY
Most commonly seen in bovines
followed by horses and sheep .
Dogs are less ,while swine and fowls
are rarely affected .
LD-50 :- 1-25 mg/kg BW for sodium
arsenite .
but arsenic trioxide is 3-10 times
less toxic than sodium arsenite.

Conti.

Average lethal dose for arsenic is

Species

Arsenic
trioxide

sodium
arsenate

Cattle

15-45g

1-4g

horses

10-45g

1-3g

Dogs

100-150g

50-150g

Sheep and goat

3-10g

200-500g

Fowls

50-300g

10-100g

TOXICOKINETICS
Soluble arsenicals are absorbed
readily from GI tract and skin.
After absorption it is distributed
throughout the body but highest
concentration seen in hair and nails .
Arsenic also deposits in bone and
teeth because of similarity with
phosphorous.
In domestic animal As doesn't stay
for long in the body . It is rapidly
excreted in urine, faeces ,bile , milk ,

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Arsenic Poisoning Characteristic

Mees' lines of chronic arsenic
poisoning. Note the transverse
white lines on all the nails of both
hands.

Conti.
Arsenic mainly
metabolised in
liver by
methylation .
Within the body
pentavalent As
converted into
trivalent As .

Contin..
Conversion of pentavalent to
trivalent will accounts for
nephrotoxicity.
As readily crosses placental barrier ,
but limited transport seen across
BBB.
Excretion is rapid . Nearly completed
within a few days .

MECHANISM OF ACTION
Major effects of arsenic are mainly
attributed to trivalent arsenic .
Trivalent arsenic
1. It binds to SH groups of lipoic acid and
inactivates it . Lipoic acid mainly act as
cofactor for enzymatic decarboxylation of
keto acids such as pyruvate ,
ketoglutarate and ketobutyrate . So this
will inhibits TCA cycle and glycolysis. It
leads to impairment in tissue respiration
which attributes to cellular toxicity .

Conti..

2. It affects integrity of vascular

endothelium , mainly in GI tract .

Pentavalent inorganic arsenic It acts as a UNCOPLER of mitochondrial

OXIDATIVE PHOSPHORYLATION .
( it competes with phosphate in
formation ATP . It forms unstable ester that
is rapidly hydrolysed . This process is
called arsenolysis )

pentavalent organic arsenic They interfere with vit B complex

required for maintenance of nervous
tissue .lt leads to demyelination and
axonal degeneration .

Arsine gas It is the gaseous hydride of trivalent

arsenic .
It causes haemolysis and pulmonary
oedema by unknown mechanism.
Rapid haemolysis is bec of binding of
arsine with haemoglobin and reacting
with oxygen
This effect does not depend on
sulphydral inhibition . Hence
DIMERCAPROL has no effect on
haemolysis .

Clinical signs

I. Trivalent inorganic / organic arsenic :4 types 1. Acute toxicity

2. Per acute toxicity
3. sub acute toxicity
4. chronic toxicity

Peracute toxicity
Here no clinical signs are observed
and animal is found dead

Acute toxicity
Signs seen are
severe gastroenteritis
Colic
Staggering gait
Salivation
Vomiting in dog and cat .
Increased thirst & watery diarrhoea with blood
Fast and weak pulse , hypotension
Oliguria/ anuria , ruminal atony
Hind limb paralysis , prostration
Normal to subnormal temperature , coma &
death

Contin.

Severity of clinical signs correlates

with haemoconcentration indicated
by PCV .
Animals inadvertently sprayed with
soluble arsenites may exhibit
vesicles , pustules , ulcer and skin
necrosis .

Sub acute toxicity

Here animals will live several days
with same clinical signs as
mentioned for acute toxicity but they
are less pronounced .
Percutaneous absorption of arsenic
may cause oedema of skin , skin
eruptions , and secondary skin
infections .

Chronic toxicity
Rarely seen in animals but well
documented in man .
Chronic poisonioning is characterised by
wasting , poor condition
thirst
brick red discoloration of visible
mucous membrane
Weak irregular pulse .
Swelling of joints , joint pain with
stiffness and paralysis.

Conti
Disorders of reproduction ( sterility & abortion )
also noticed in chronic arsenic exposure .
Chronic As poisoning is in animals is generally
encountered in industrial regions following
ingestion of contaminated forage and water .
Malicious poisoniong is rare in veterinary
practice but noticed in case of human medicine .

II. Pentavalent organic arsenical

toxicity
Mainly found in arsenical feed additives .
Signs are seen after 2-4 days of feeding .
Signs seen are
1. ataxia , incoordination, and blindness
2. affected animals become week and assume
dog sitting posture , eventually become
paralysed in lateral recumbency
3. appetite remains normal and animal is alert
blindness is characteristic of arsinilic acid
poisoning which is not seen with other
arsenicals

Post mortem findings

In per acute no lesions seen .
In acute poisoning there will be
inflammation of GI tract , Oedema, rupture
of blood vessels and necrosis of epithelial
and sub epithelial tissues .
Necrosis may progress to perforation of
gastric or intestinal wall .
Contents of gut are fowl smelling and blood
tinged and may contain shreds of epithelial
tissues .

Contin
There may be diffused inflammation of liver
and other abdominal viscera
Occasionally haemorrhages occur on
surface of heart
Skin is dry , leathery and peeling following
cutaneous exposure
In sub acute cases there will be pale ,
swollen kidneys, pale liver , petechial
haemorrhages of intestinal serosa and
mucosa .

Microscopic lesions
In GI tract :intestinal capillary dilatation
,mucosal and sub mucosal oedema , necrosis
and sloughing of mucosa
in kidney :- glomerular necrosis and severe
renal tubular necrosis
In liver :- fatty degeneration and necrosis of
liver .
Capillary degeneration is observed in
various organs including gut skin , lungs
and kidneys

Diagnosis
Based on 1. history
2. circumstantial evidences
3. clinical signs and lesions
A suden onset of severe colic , bloody /
watery diarrhoea containing mucoisal shreds
and post mortem findings of haemorrhagic
gastro-enterits and degenerative changes in
liver and kidneys should always be
interpreted as possible arsenic poisoning .
Further chemical determination of arsenic in
tissues and ingesta provides confirmation .

Conti..
Samples to be analysed are
Antimortem samples :- urine , vomitus , faeces &
hair .
post mortem samples :- liver , kidney and
nervous tiddues
Analysis of feed , plant , soil , water should be
done also
Liver and kidney of healthy animal rarely contain
< 1 ppm of As but in toxic condition >3ppm
arsenic
Urinalysis reveals high As content for many days ,
proteinuria , increased specific gravity and casts .

Contin
Arsenic poisoning has to be
differentiated from following
a. lead poisoning :
b. caustics , irritants , urea
posoning .

Arsenic poisoning in
humans

Treatment and management

Specific therapy

Dimercaprol
Thioctic acid
Sodium thiosulphate
Mesodimercatosuccinic acid

Supportive therapy

Dimercaprol / British anti-lewisite

Dithiol containing cheliatging
agent
It forms non toxic and easily
excretable complex with arsenic
Dose:large animals 3 mg / kg bw
( 5% sol. in 10 %
sol.of benzoate in arachis oil)
small animals 2.5-5 mg /kg
bw
( 10 % sol. in oil )

Contin.
Dimercaprol has to be given before the
onset of signs of poisoning , otherwise
it cannot regenerate the enzymes that
have been inhibited .
Dimercaprol also has some of side
effects . Such as vomiting , tremors and
convulsion .
If it is given a at higher concentration
or at too frequent intervals animal may
die of dimercaprol poisoning.

Thioctic acid
It is considered as
most effective than
dimercapropl for
arsenic poisoning
in cattle .
Thioctic acid is
used alone or with
combination of
dimercaprol .
Dose :- 50 mg / kg
BW , IM , t.i.d as
20% sol.

Sodium thiosulphate
It is a safe antidote to arsenic poisoning .
the sulphur of thiosulphate reacts with
arsenic and immobilise it .
Dose :- 1. horses and cattle
8-10 mg (total dose ) IV
as
10 20 % solution
2. sheep and goat one fourth
of above dose

Sodium thiosulphate

Mesodimercaptosuccinic acid
(MDSA)
and Dimercaptosuccinic acid
(DMSA)

These are water soluble derivatives

of dimercaprol and said to be
superior to dimercaprol , but efficacy
is not well tested against arsenic
poisoning .

Supportive and maintenance

therapy
Emetics , gastric lavage and activated
charcoal
- given only if ingestion is recent .
They will prevent the further absorption of As
- contraindicated once the signs have
started
Fluid therapy for correction of shock ,
dehydration and acidosis . Blood may be
given if necessary .
Renal function monitored and urinary flow
promoted using 10 % dextrose solution.

Conti .
Animal should be kept warm and
comfortable
Sufficient vitamins , antibiotics , , analgesics
and other symptomatic care may be
instituted
High portion of protein diet is recommended
during post exposure period .

Prognosis
Grave if not treated properly or if there
is extensive organ damage and animal is
prostrate .
Mortality is high in case of acute poisoning
with inorganic trivalent arsenicals .
With organic pentavalent arsenicals , the
mortality is low but morbidity is high and
recovery may take 2-4 weeks with good
nursing and supportive care .

Public health concerns

All arsenicals should be treated
as poison .
Their containers must bear a
warning label
poison
They must be kept out of general
reach . And only trained workers
should be allowed to use
Milk from poisoned cow is toxic to
humans but flesh of surviving
animals is safe for human
consumption .