Lead Toxicosis in Small Animals

Chapter 37


Lead Toxicosis in Small Animals



Lead contamination of residential environments has decreased through removal of lead from residential paints, gasoline, and other household items. Accordingly, the incidence of lead poisoning in small animals has decreased over the last 30 years, and lead now accounts for less than 1% of reported accidental poisonings in pets. Nevertheless, lead intoxication in pets does occur, and the vagueness of clinical signs that frequently accompany lead poisoning can create diagnostic challenges.



Pathogenesis of Lead Toxicosis



Sources of Lead


Lead may be found in a wide variety of products, including paints, linoleum, caulking and putty compounds, solders, wire shielding, old metal tubing, certain weights (e.g., fishing sinkers, curtain weights), roofing felt, golf balls, ammunition, computer equipment, wine cork covers, pottery glazing, lead-containing toys, and lead arsenate pesticides. In addition, contaminated soil and water can be potential sources of lead. Exposure to organolead from various leaded petroleum products has decreased considerably following legislation restricting the use of leaded gasoline and oil in the United States.


The most common source of lead in cases of small animal poisoning is leaded paints from buildings erected before passage of the 1977 legislation requiring that residential paints contain no more than 0.06% (600 ppm) lead. In many cases older leaded paints have been painted over with unleaded paints, and it is estimated that 74% of privately owned homes built before 1980 still contain hazardous amounts of leaded paint. Renovation of these homes results in the generation of paint chips or dust that, if ingested by pets, can result in clinical lead intoxication. Cats may be at increased risk for toxicosis during these situations because of their grooming habits, which can result in significant ingestion of lead-containing particulates that collect in their fur.



Kinetics


The degree to which ingested lead is absorbed depends on variables such as the physical form of lead, particle size, and matrix association. In addition, patient variables that influence the degree of lead absorption from the gastrointestinal (GI) tract include age, diet, and preexisting disease. The acidic environment of the stomach favors ionization of the lead, which is then absorbed from the duodenum. Lead shot embedded in soft tissues such as skeletal muscle is not appreciably absorbed and is not an important source of lead toxicosis. Conversely, lead shot that enters areas capable of active inflammation (e.g., joint cavities) may become solubilized by the enzymatic activity of the inflammatory reaction and could subsequently be absorbed.


Once absorbed, lead is carried primarily on the red blood cells, with less than 1% to 2% bound to albumin or free in the plasma. Unbound lead distributes widely through tissues, with the highest concentrations found in bone, teeth, liver, lung, kidney, brain, and spleen. Bone serves as a storage depot for lead, which substitutes for calcium in the bone matrix. During times of increased activity of bone remodeling such as fracture repair stored lead may be released from the bone, resulting in toxicosis. Lead crosses the blood-brain barrier and concentrates in the gray matter of the brain. This passage of lead into the brain occurs to a greater extent in young animals. Unbound lead crosses the placenta and is passed through the milk in lactating animals.


Most ingested lead is excreted in the feces unabsorbed. Lead in the blood passes through the glomerulus and accumulates in the renal tubular epithelium. During the natural process of sloughing of tubular epithelial cells, the lead is slowly eliminated from the body. Chelation therapy can greatly increase the rate of urinary excretion of lead by allowing the chelated lead to be passed in the urine without entering the tubular epithelium. Lead has a multiphasic half-life because of its distribution into depot areas such as bone and brain. In dogs intravenously administered lead, it has triphasic elimination half-lives of 12 days, 184 days, and 4,591 days.



Mechanism of Action


Lead has a wide variety of effects within the body, including interfering and competing with calcium ions, binding to cellular and enzymatic sulfhydryl groups, altering vitamin D metabolism, and inhibiting membrane-associated enzymes. Inactivation of the enzymes ferrochelatase and δ-aminolevulinic acid dehydratase causes impairment in heme synthesis, resulting in red blood cell abnormalities. Anemia can develop with chronic exposure to lead. GI signs in lead-intoxicated patients may be caused in part by alteration of smooth muscle contractility as a result of interference of lead on intracellular calcium-dependent mechanisms. Lead can disrupt the blood-brain barrier of immature animals by interfering with normal endothelial cell function. Lead decreases cerebral blood flow and alters neuronal energy metabolism and neurotransmission within the central nervous system (CNS). Recently, the propensity of lead to induce oxidative damage through the production of reactive oxygen species has been the subject of much study. Lead-induced inhibition of endogenous antioxidant enzymes such as superoxide dismutase and catalase can lead to injury of cell macromolecules through a variety of oxidative pathways including lipid peroxidation of cellular membranes.


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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Lead Toxicosis in Small Animals

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