Equis ISSN 2398-2977

Toxicity: lead

Contributor(s): Rachael Conwell, Wilson Rumbeiha, Prof Alan Seawright

Introduction

  • Chronic/acute (rare) ingestion of lead   →   various neuropathies, anemia, gastrointestinal disturbances.
  • Cause: ingestion of lead from old paint, used engine oil, sprays or herbicides, industrial pollution of feed sources. Lead shot residing along synovial membranes is also a possible cause of chronic lead toxicity.
  • Signs: dysfunction of cranial nerves IX and X followed by other peripheral neuropathies, dyspnea, non-specific weight loss and weakness, anemia.
  • Diagnosis: clinical signs, history of access, lead assays in blood, liver, kidneys.
  • Treatment: chelating lead with calcium versenate.
  • Prognosis: guarded to poor.

Pathogenesis

Etiology

  • Lead acetate found in lead paint, used engine oil, old batteries, pesticides, solder, ceramics, etc.
  • Industrial contamination by metal mining or smelting sites   →   aerial fallout onto pasture or hay, resulting in contaminated forage.
  • Lead oxide or lead sheeting.
  • Accidental feeding, ie boiled linseed oil.

Predisposing factors

General
  • Grazing of contaminated areas or feeding of contaminated forage.

Specific

  • Duration of exposure.

Pathophysiology

  • Following absorption, the majority of the lead is found within red blood cells, with the remaining bound to albumin and other proteins. Less than 1% is unbound. Lead is then redistributed into soft and mineralizing tissue and excreted very slowly via the bile.
  • Chronic ingestion of low levels of lead (acute rare)   →   toxicity   →   peripheral neuropathy particularly affecting cranial nerves IX and X; anorexia; increased fragility of erythrocytes and depressed production of red cells   →   anemia and basophilic stippling.
  • Lead interferes with heme synthesis, leading to ischemic damage in tissues, with nervous tissue the most susceptible. There is also a direct toxic effect of lead on mitochondria and disturbance of intracellular calcium regulation as well, and oxidative damage to proteins. Toxicity appears to affect peripheral nerves preferentially, probably due to slowing of nerve conduction due to segmented demyelination.
  • Young horses are particularly susceptible to nervous tissue damage because lead attacks developing nerves   →   peripheral nerve damage.
  • Other organs can be affected by lead toxicity, including the gastrointestinal tract, renal, cardiovascular and musculoskeletal systems.

Timecourse

  • Acute poisoning - uncommon.
  • Chronic poisoning requires regular intake over several months.
  • Horses ingest lots of contaminated soil as well as pasture - this is the important factor of lead exposure in the horse   →   intoxication.
  • Horses are far more resistant to lead poisoning than cattle.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Allen K J (2010)Laryngeal paralysis secondary to lead toxicosis.Equine Vet Educ22(4), 182-186 VetMedResource.
  • Puschner B & Aleman M (2010)Lead toxicosis in the horse: A review.Equine Vet Educ22(10), 526-530 VetMedResource.
  • Saulez M N (2010)Lead poisoning: Any more lurking around?Equine Vet Educ22(4), 187-189 VetMedResource.
  • Sojka J E, Hope W & Pearson D (1996)Lead toxicosis in 2 horses, similarity to equine degenerative lower motor neurone disease.J Vet Intern Med10(6), 420-423 PubMed.
  • Kowalczyk D Fet al(1981)The value of zinc protoporphyrin in equine lead poisoning - a case report.Vet Human Toxicol23, 12-15 PubMed.
  • Dollahite J W, Younger R L, Crookshank H R, Jones L P & Petersen H D (1978)Chronic lead poisoning in horses.Am J Vet Res39(6), 961-964 PubMed.
  • Willoughby R A, MacDonald E, McSherry B J & Brown G (1972)Lead and zinc poisoning and the interaction betweed Pb and Zn poisoning in the foal.Can J Comp Med36(4), 348-359 PubMed.

Other sources of information

  • Seawright A Aet al(1983)Heavy metal intoxications in horses.In:Veterinary Pharmacology and Toxicology. Eds: Y Ruchebuschet al. M T P Press Ltd, Lancaster, UK. pp 697-714.


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