Arsenic poisoning in Cows (Bovis) | Vetlexicon
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Arsenic poisoning

ISSN 2398-2993

Synonym(s): Arsenical toxicity


  • Cause: cattle may ingest arsenicals through accidental access to:
    • Old commercial products containing arsenicals.
    • Buildings used for storing old products containing arsenicals.
    • Arsenic contaminated land (eg contaminated vegetation, soil or water).
    • Ash from burnt wood treated with arsenical containing wood preservatives.
  • Signs: inorganic and aliphatic arsenicals: 
    • Peracute - sudden death.
    • Acute - severe, watery diarrhea, acute severe abdominal pain, weakness, oliguria, death.
    • Subacute - watery diarrhea, possibly melena, dehydration, ataxia, convulsion.
    • Chronic - localized skin lesions, weight loss, inappetence, decreased milk yield.    
  • Diagnosis: history of exposure, clinical effects and clinical pathology. Exclusion of other differentials.
  • Treatment: inorganic and aliphatic arsenicals: supportive care, aggressive hydration, antidotal therapy and removal from the source.
  • Prognosis: poor in acute cases of inorganic and aliphatic organic arsenical toxicity.

Geographic incidence

  • Arsenic toxicity in cattle can occur anywhere in the world, but there is much regional variation.
    • Occurrence is generally less common than in the past due to a reduction in the use of arsenical compounds in veterinary medicine and agriculture.
  • Arsenicals may be found in some veterinary medicines and were historically found in a variety of commercial products, for example:
    • Insecticides (eg dips, sprays, powders).
    • Herbicides.
    • Fungicides.
    • Some paints.
    • Some wood preservatives.
  • Acute arsenic toxicity in domestic animals is uncommon, although in certain regions (eg around mining sites) the risk of exposure may be greater.
  • There is a greater risk of toxicity in cattle in regions where there has been contamination of the environment:
    • Arsenic does not degrade and so persists in the soil for a long time.
    • Industries such as mining and smelting, eg may result in an increase in inorganic arsenic levels in the soil and in nearby water sources. Root uptake of arsenic by plants can result in vegetation contamination.
    • Land around old livestock dipping sites may also be a potential source of arsenic.

Age predisposition

  • Elderly animals may be more susceptible to poisoning, possibly due to decreased renal excretion.

Breed/Species predisposition

  • None.

Public health considerations

Arsenic is toxic to humans.
  • Potential food safety implications: 
    • Arsenic ingestion may have implications for meat and milk in both acute cases and subclinical exposure. 
    • Meat and other products will be unfit for human consumption.  
    • Seek current specialist advice on the assessment and management of potential food safety issues regarding meat and milk from exposed animals and appropriate withdrawal times:
      • The author has found no specific withdrawal times or residue limits stated in the literature. Each case must be assessed on an individual basis and specialist advice sought. Advisors will account for the arsenic compound involved and the circumstances, including extent of exposure, number of animals effected etc.
  • Potential public health concern regarding environmental contamination if manure from clinically or sub-clinically affected cattle is used as fertilizer, as arsenic can be excreted in the animal’s urine and feces.
    • Seek specialist advice.  Advisors will consider the type of arsenic compound involved and the circumstances (e.g. the extent of arsenic exposure, number of animals involved, proximity of nearby by water courses, etc.).  For example, manure used from one affected animal used as fertiliser will have different implications than from 15 cattle.
    • Arsenic contaminated carcases must be disposed of safely. Seek specialist advice.  Factors to be considered regarding carcase disposal include the extent of exposure, proximity of nearby water courses, etc.

Cost considerations

  • Animals requiring veterinary attention will result in increased veterinary fees for the farmer. 
  • There are obvious production losses associated with fatalities and in cases of subclinical toxicity. 
  • There may also be cost implications associated with the management of food safety issues.

Special risks

  • Pre-existing debilitation or dehydration.
  • Cattle will graze arsenic contaminated land and vegetation as they do not find arsenic distasteful and seem attracted to contaminated vegetation and soil, displaying pica behavior. It has been suggested that the apparent attraction may be because at least some arsenic compounds reportedly have a salty taste (including CCA, a pentavalent inorganic arsenical).



  • Commercially arsenic may be found in products in organic and inorganic forms of either trivalent or pentavalent states:
    • Organic arsenicals could be either aliphatic or aromatic.
    • Toxicity due to inorganic or aliphatic organic arsenicals results in a similar clinical picture.
    • Of the inorganic (trivalent or pentavalent) and aliphatic organic arsenicals, the trivalent inorganic forms are the most toxic forms of arsenic.
    • Phenylarsenicals (ie aromatic organic pentavalent arsenicals) may be used typically in pig and poultry production as feed additive growth promoters and can result in arsenic toxicosis in pigs with dosing errors for example, but are the least toxic form. However, such organic pentavalent phenylorganic arsenical pig and poultry supplements have now been banned in the European Union and North America.
  • Most cattle poisoning cases are acute and are due to the ingestion of inorganic or aliphatic organic arsenicals.
  • Possible sources of oral arsenic exposure in cattle include:
    • Old arsenical product containers discarded onto cattle pasture.
    • Accidental access to old arsenical product containers.
    • Access to arsenic contaminated land and/or water.
    • Access to land that was used historically for the insecticidal dipping of livestock.
    • Ash from burnt wood treated with arsenical containing wood preservatives.
  • Dermal and percutaneous absorption of arsenicals can occur and may result in systemic toxicity:
    • Through non-intact or inflamed skin.
    • From exposure to insecticidal dips.

Predisposing factors

  • Weak, elderly, dehydrated or debilitated animals are more susceptible to toxicity, possibly due to decreased renal excretion.
  • Subclinical arsenical toxicity can occur in cattle in regions where there is environmental contamination (either natural or anthropogenic) and the animals are chronically exposed to arsenic contaminated water and/or vegetation.


  • The concentration of arsenic, its chemical form and its solubility determine its toxicity.
  • Soluble arsenic salts are more toxic. Soluble arsenicals are quickly absorbed from the gastrointestinal tract (GIT).
  • Arsenicals cause vascular changes that can result in increased permeability. Fluid will leak from the capillaries into the intestinal mucosa and GI lumen, causing fluid loss and hypovolemia, hypotension and eventual circulatory collapse. Thrombosis may also occur.
  • Trivalent, inorganic arsenicals and aliphatic organic arsenicals disrupt cellular energy metabolism by reacting with sulfhydryl groups in cells and inhibiting sulfhydryl enzyme systems required for oxidative phosphorylation and the production of adenosine triphosphate (ATP):
    • Actively dividing cells and tissues with high oxidative systems and energy requirements such as the mucosa of the gastrointestinal tract, liver, kidney, spleen and lung, are the organs most vulnerable.
    • Inorganic arsenical and aliphatic arsenicals toxicity causes a typical enteric clinical picture (eg gastroenteritis, diarrhea, dehydration).    
  • The pentavalent form of arsenic is substituted for phosphate resulting in uncoupling of oxidative phosphorylation. This leads to axonal degeneration and demyelination and neurological effects.
  • Nervous system signs seen with organic arsenicals such as the pentavalent phenylorganic arsenicals are due to the inhibition of dehydrogenase enzymes resulting in peripheral nerve degeneration and demyelination:
    • Aromatic organic pentavalent arsenicals typically used as pig and poultry growth promoters (eg phenylarsonicals) are reportedly less toxic, but quickly absorbed following ingestion.
  • Arsenicals can be excreted in various ways, via the urine or feces: 
    • Arsenic is generally quickly excreted in livestock.
    • With phenylarsenicals and pentavalent forms of arsenicals, renal excretion typically occurs in many species with approx. 40-70% of the absorbed quantity being excreted quickly, within a couple of days. 
    • The excretion rate for trivalent, inorganic arsenicals is slower and they are largely excreted via the bile into the feces.   
  • Chronic exposure may result in the build-up of arsenic in the skin, hair and hooves.
  • If the skin is exposed to high levels of arsenic or the skin circulation is reduced, local dermal necrosis may occur in the absence of systemic effects. However, dermal absorption can be rapid when there is good skin circulation resulting in systemic effects in the absence of damage to the skin.
  • Lesions occur due to capillary damage:
    • Gastrointestinal tract:
      • Marked inflammation, submucosal edema, congestion and vesicle development. There may be GIT mucosal and submucosal necrosis and associated sloughing. Necrosis may result in perforation.
    • Kidneys:
      • Capillaries within the glomeruli dilate, swell and undergo degeneration. Tubular necrosis and renal fibrosis may develop. Hypotension and dehydration occur which leads to proteinuria and oliguria.
    • Skin:
      • Dermal exposure to arsenicals leads to hyperemia, blistering and edema.


  • Inorganic arsenicals and aliphatic organic arsenicals:
    • Peracute cases:
      • Depression and sudden death is typical. 
      • Death may occur within 3-4 hours. 
    • Acute cases:
      • Most common form in cattle.
      • Associated with a high morbidity and high mortality which can occur over 1-3 days. 
      • Clinical effects may occur from 12-50 hours following oral exposure, the timing of which is also influenced by the amount of ingesta present in the forestomachs.
      • Death can occur within 24-48 hours of onset of clinical effects.
    • Subacute cases:
      • Clinical signs are like those seen in acute cases, but the clinical course is more prolonged; affected cattle could survive for several days (eg 2-7 days). 
      • Deaths may be seen several days following the removal of cattle from the source of arsenic exposure.
    • Chronic cases:
      • Can occur in cattle, but are uncommon as arsenic is quickly excreted.
      • These cases may be sub-clinically affected and so harder to diagnose.
      • Chronic cases are seen with those animals in which exposure is continuous or regularly repeated. An example would be in some regions of India, where there are high levels of arsenic in water, soil and vegetation.
  • Clinical signs associated with organic pentavalent phenylarsenical feed supplement toxicity are generally neurological and may occur 2-4 days after a large dose, or following chronic exposure.


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Further Reading


Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Gonçalves M A, da Cruz R A S, Reis M O, Pavarini S P, Sonne L & Driemeier D (2017) Vascular injury in spontaneous subacute toxicosis caused by organic arsenic in cattle Pesq Vet Bras 37 (7), 676-680. DOI: 10.1590/S0100-736X2017000700004.
  • Rana T, Bera A K, Das S, Bhattacharya D, Pan D, Das S K (2014) Subclinical arsenicosis in cattle in arsenic endemic area of West Bengal, India. Toxicol Ind Health 30 ( 4), 328-335 PubMed.
  • Bertin F R, Baseler L J, Wilson C R, Kritchevsky J E, Taylor S D (2013) Arsenic toxicosis in cattle: meta-analysis of 156 cases.  J Vet Intern Med 27 (4), 977-981 PubMed.
  • Dash J R, Datta B K, Sarkar S, Mandal T K (2013) Chronic arsenicosis in cattle: possible mitigation with Zn and Se.  Ecotoxicology and Environmental Safety 92, 119-122