Toxicological Study of Arsenic and Lead Poisoning

Submitted By: Submitted To:

Kuhsla Neupane (13) Dr.Arjun Pandit
Lasta Shrestha (14)
Madhav Rawat (15)
Manjila Niraula (16)
 Arsenic Poisoning

Introduction:
Arsenic poisoning is one of the mean important causes of heavy metal
poisoning in domestic animals and commonly occurs in herbivores due to
accidental ingestion of herbicides, insectides, wood preservative etc.

Source:
 Excessive use or accidental ingestion of arsenical pesticides i.e
Insectides (copper acetoarsenites), herbicides/defoliants (sodium or
potassium arsenite), rodenticides (arsenical trioxide), wood
preservative (arsenic pentoxide) etc.
 indiscriminate use of arsenic as a ectoparasites (lead arsenate as dip)
 drinking water (especially well water) containing high arsenic
 arsenic - contaminated soil, which are often licked by animal with
mineral deficiency
 extended use of organic arsenical feed additives (arsanilic acid in
poultry and swine as growth promoter)

Toxic Dose:
 inorganic arsenic are more toxic than organic arsenicals
 toxic dose: 1-25mg/kg body weight
Toxicokinetics
 Soluble arsenicals (trivalent and pentavalent) are readily absorbed
from GIT and through skin
 It is distributed throughout the body - particularly in liver, kidney,
heart and lungs.
 Arsenic can be found in hair and nails where it stays for months.
 Because of being chemically similar to phosphorous, it is deposited in
bone and teeth and retained their for long period.
 It is party detoxified in liver and excreted in the urine, faeces, bile,
milk, saliva and sweat.
 Arsenic can cross placenta but passage through BBB is limited

Toxicodynamics:
Trivalent arsenic binds with the sulfhydryl groups of lipoic acid which is an
essential co-factor for the enzymatic decarboxylation or keto acids, such as
pyruvate, Ketoglutamata and ketobutyrate. Thus, arsenic acid inactivates
lipoic acid and inhibits formation of acetyl succinyl and propionyl co-
enzymes A. Other oxidative decarboxylation used by lipoic acid is also
inhibited. Thus, glycolysis or citrate cycle is inhibited.
Arsenic produces local corrosive action on gut. However, GI damage is seen
regardless of route of absorption. Liver, kidney and intestine is rich in
oxidative enzymes and arsenic has special affinity to them. Arsenic
increases capillary permeability and capillary endothelial cells of these
organs are very much susceptible. The wall of blood vessels and smooth
muscles are dilated.
Laboratory diagnosis:
 Urine:
 Proteinuria, cast and albuminuria are there.
 Arsenic poisoning is usually diagnosed with the urine test for
arsenic as arsenic ions are present very shortly after ingestion.
 A urinary excretion of arsenic >100mg/24 hours is regarded as
indicative of exposure to a potentially toxic amount of arsenic
 Monomethylarsine and dimethylarsine are present in the urine 24
hours after ingestion in acute poisoning.
 Blood: 0.9 ug/dl, monocytic hypochromic anaemia, leukocytosis and
mild eosinophilia.
 Liver function test: serum alkaline phosphatase and bilirubin is raised
and there is excretion of urobilinogen in the urine.
 Hair and nails samples containing >300 ppm or 100 mg of arsenic per
100 gm of specimen are diagnostic of arsenic poisoning
 Radiopaque sign on abdominal x-ray

Lead poisoning

Introduction:
Lead is one of the commonest caused of poisoning in farm, particularly
sheep and cattle.

Source:
  ingestion of paints ( licking of cans, freshly painted walls, or dry
pealing paints)
 Ingestion of greases, linoleum , leaded gasoline solid lead etc
 licking of discorded batteries , gunshot
 grazing near busy highway containing toxic amount of lead from auto
exhaust
 drinking water from lead plumbing
 milk secreted from lead poisoned animals can be dangerous to young
ones
Toxic dose:
I. Acute toxicity
 Calves : 50-600mg/kg body weight
 Cattle, horse, sheep, goat: 600-800 mg/kg
 Swine and dog:-25 gm
II. Chronic
 Cattles: 1-3gm/day
 Cattle, horse, Sheep, goat: 1-7gm/day

Toxicokinetics:
 Only a small portion (<10%) of lead is absorbed because of the
formation of insoluble lead complex with the which are excreted in
faces.
 Once the lead is absorbed, 85-95% binds to hemoglobin in
erythrocytes. The remaining binds to serum albumin.
 Only 21% of lead is free and available for to tissue and is responsible
for toxic effect. .
 Lead can pass through blood brain and placental barrier.
  High level of lead are excreted by kidney and some amount in bile
and milk.

Toxicodynamics:
Lead inhibits sulfhydryl group of enzymes of cellular metabolism. It
destroys the blood brain barrier and produces symptoms of
encephalopathy. It also causes damage to capillary endothelial cells and
produces cerebral oedema and haemorrhage. After reaching into neurons
and glia, it disturbs cellular membrane and molecular mechanism. Lead
decreases the concentrations of copper, iron and zinc and interferes with
these metals as prosthetic groups of enzymes in mitochondria. Therefore,
lead affects cellular respiration, oxidative phosphorylation and the ATP-
synthetase complex. It causes haemoglobin deficiency and leads to
deficiency of hemoproteins including mitochondrial respiratory
cytochromes and microsomal cytochrome. Hence, deficiency is obviously
due to the sulphydryl-containing enzymes because heme synthesis utilizes
sulphydryl enzymes.

Lab diagnosis:
 Cattle :
a) Ingesta, liver and kidney contains lead levels above 10 ppm.
b) In chronic poisoning the concentration of lead in bone may be
100 ppm or more.
 Dog :
a) Hair contains 88 ppm of lead.
b) The blood contains at least 0.35 ppm, liver-17.4 ppm and
urine-lead level increases markedly after Ca-EDTA therapy.
 Chickens :
 a) Blood and liver lead level more than 10 ppm.
b) Faeces 1-2910 ppm lead.
 Horse :
a) Liver, 0.0023-0.75, Kidney, 0.0013-1, Spleen, 0.1-0.25, muscle,
0.02-0.05 and bone, 3-12 ppm.

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