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ARSENIC POISONING
Click to edit Master subtitle style Amir Sadaula (01) Arjun Pandit (02) Bikas Puri (03) Bishwo Bandhu Pokharel (04)

Abstract
Arsenic poisoning being a common heavy metal poisoning affects large number of animal as well as human population. The common sources of arsenic poisoning are pasture near smelters, baits, weedicides, paints, drinking water containing arsenic etc. If the level of arsenic is more than 0.25 ppm in drinking water, then poisoning can occur in animals. Arsenic is rapidly excreted in urine, feces and milk. As the chemical is found in milk, it can be of serious public health concern. The important manifestations of the poisoning includes blood tinged diarrhea, cold extremities, hind limb paralysis, colic and brick red mucus membrane. The treatment of arsenic poisoning includes use of specific antidote, Dimercaprol (BAL). The present context of arsenic toxicity in Nepal is dreadful especially in Terai district where the level of arsenic in drinking water is much higher than the recommended level, 0.01ml/l. So, it is important for the farmers as well as other people around the risk areas to be aware about arsenic poisoning. Keywords: Arsenic, Poisoniong, Dimercaprol, Nepal, Terai.

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ARSENIC

Cumulative poison, stored particularly in liver, skin and hair. SOURCES -Pasture near smelters,
-Paints, -Weedicides, -Rodenticides, -Baits, -Milk from arsenic poisoned cattle, -Water containing arsenic, -Strong solution of lead arsenate during dipping etc.
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ORAL LETHAL DOSE OF ARSENIC

Animals Horse Cow Sheep and goat Swine dog fowl Arsenic trioxide 10-45gm 15-45 gm 3-10gm 500-1000mg 100-150mg 50-300mg Sodium arsenite 1-3gm 1-4 gm 200-500mg 50-100mg 50-150mg 10-100mg
Source: B. K. Roy (2008)
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FACTORS INFLUENCING TOXICITY

Species

Herbivores are more commonly poisoned. Cats and dogs are maliciously poisoned. Swine and fowl are rarely poisoned. Inorganic trivalent arsenic is more potent than inorganic pentavalent. Organic arsenicals are less toxic than inorganic arsenicals. Soluble arsenicals are more toxic than less soluble. Slow excretion rate increases toxicity. Constant exposure produces tolerance.

Oxidation state

Solubility

Rate of excretion

Tolerance

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TOXICOKINETICS

Distributed to all biological fluid. Higher concentration in liver, kidney and spleen. Rapidly excreted in urine, feces, bile, milk and saliva. Half life = 1.5 days. Doesnt cross blood brain barrier but readily cross placental barrier.

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MECHANISM OF ACTION

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Clinical signs

Peracute Acute Subacute and chronic

Fig: Arsenic treated goat

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SYMPTOMS

Peracute cases

Death without showing any symptoms

colic

Acute cases

Colic Staggering Weakness Trembling Vomition Fast and weak pulse

Salivaion Projectile watery diarrhoea Bood tinged faeces Hind limb paralysis Normal or subnormal temperature Death in 1-3 days

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Subacute

Anorexia Blood mixed diarrhoea or mucoid diarrhoea Cold extremities Hematuria and convulsion

Chronic

Poor condition Thirst Break red mucus membrane Normal temperature Weak irregular pulse

Skin lesions in man

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POST MORTEM LESIONS

Cattle

Reddend abomasal or duodenal mucosa. Submucosal edama and haemorrhage in the abomasum and duodenum. Intestinal content having foul smell. Liver soft and yellow. Lung edematous and congested. Faces inflammed and edematous. Larynx edematous and congested.

Swine

Fowl

Proventiculus and gizzard inflammed. Gelatinous exudate beneath horny line of gizzard. Sloughing of horny lines of gizzard. 1212

Fig: Congested lungs

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Fig: Intracytoplasmic oedema, and hyperkeratosis in the skin of arsenic-treated goats.

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LAB DIAGNOSIS

In clinical determination of arsenic is tissue (liver or kidney), toxicity is associated with concentration greater than 3 ppm. Drinking water containing greater than 0.25 ppm arsenic is potentially toxic to large animals.

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DIFFERENTIAL DIAGNOSIS

Haemorrhagic gastroenteritis Lead poisoning Caustics, irritant plants, urea, chlorate, and pesticide poisoning.

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TREATMENT

Recent exposure and no clinical signs.

Animal showing clinical signs.

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RECENT EXPOSURE AND NO CLINICAL SIGNS

Induce emesis followed by activated charcoal orally.

small animals :- 25-100 grams.

Dose : large animals :- 500-1000 grams.

Followed by oral administration of GI protectants such as kaolin, pectin one to two hours after charcoal therapy. Excessive fluid therapy.
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ANIMALS SHOWING CLINICAL SIGNS

Excessive fluid therapy. Specific antidote. Dimercaprol (BAL)

Dose : 4-7 mg/kg bwt I/M tid for 2-3 days or until recovery.

Water soluble analogue of BAL i.e. DMSA ( Dimercaprosuccinic acid ) is also effective.
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In large animals, thioctic acid (lipoic acid) alone or in combination with BAL is effective.

If alone dose is 50 mg/ kg bwt I/M tid as 20% solution. With BAL dose is 3 mg/kg bwt I/M every 4 hours for 2 days, every eight hours on third day and every 12 hours for next 10 days. Cattle, horse : 20-30 gm in 300 ml of water. Sheep, goat : 5-8 gm in 300 ml of water. Pig : 0.5-3 gm in 300 ml of water. Effective against arsenic chlorate. Wide safety margin. 10-50 mg/kg bwt orally 3-4 times a day for 3-4 days.
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Sodium thiosulphate (orally).

D-penicillamine.

SUPPORTIVE THERAPY

Good nourishing, care Warm room

Besides, symptomatic and suppotive treatment with analgesics , antibiotics, cardiac stimulants and fluid therapy should be done.

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CONTEXT IN NEPAL

Eleven terai districts are more at risk. Nawalparasi is the district with highest level of arsenic in drinking water. So, animal as well as people of these area are at risk.
(UNICEF).

-1.4 million people at risk -world Health Standard of 0.01 ml/l. - The level is more than 0.05 ml/l.
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CONCLUSION

Arsenic poisoning is common heavy metal poisoning. It can cause heavy losses in the livestock economy if care is not taken. As arsenic is rapidly excreted in milk of the affected animal, it can cause serious chronic health problem in humans also. So, farmers as well as pet owners should be aware about this serious problem and it is the need of today.
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REFERENCES
Buck, W. B. Osweiler, G.D. and Van Gelder, G.A. (1976). Clinical Diagnosis, Veterinary Toxicology, Dubuane, Iowa : Kendall/Hunt. Peoples, S.A. (1964). Arsenic Toxicity in Cattle, Ann. Newyork Acad Sci., Vol.122,2,644. Roy, B.K.(2008). Veterinary Pharmacology and Toxicology. Kalyani Publishers, Ludhiana. http://www.unicef.org/infobycountry/nepal_35975.html

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Thank you for your patience

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