Chapter 29 - Lead

Abstract

Lead is a toxic element and has not been shown to be an essential trace element for nutrition. Common sources of lead include lead-acid storage batteries, lead weights, small lead trinkets and toys, lead shot and bullets for weapons, lead arsenate pesticides, and environmental contamination from mining, smelting and recycling operations. Although the use of lead has been restricted in many products (such as gasoline, paints, etc.), lead poisoning in animals is encountered with greatest frequency compared to any other metal. Following absorption, lead is widely distributed in the body, including the brain. Lead is slowly excreted via the bile and slightly in the urine. Lead interferes with several biochemical processes in the body by binding to sulfhydryl and other nucleophilic functional groups causing inhibition of several enzymes and changes in calcium/vitamin D metabolism. Lead also contributes to oxidative stress in the body. Many of the neurotoxic effects of lead appear related to the ability of lead to mimic or in some cases inhibit the action of calcium as a regulator of cell function. Mammals, birds and reptiles have all been found to develop lead poisoning. Clinical signs of lead toxicosis vary with the species involved, duration of exposure, and amount of lead absorbed. The major systems affected by lead poisoning are the gastrointestinal tract, central nervous system and hematological system. Neurological signs include seizures, blindness, and death. The treatment of lead poisoning includes supportive therapy and chelating agents such as calcium ethylenediaminetetraacetic acid. This chapter describes the toxicity, toxicokinetics, mechanism of action, and antidotal treatment of lead in animals.