Despite widespread efforts to caution pet owners about the hazards of exposure to lead, accidental poisoning with this heavy metal still occurs.

Fortunately, rapid and reliable testing, along with well-defined therapies, are available to the veterinary practitioner when lead poisoning is suspected. Forty-two (13%) of 325 dog and cat whole blood samples submitted to a California regional toxicology laboratory for lead testing between 1990-1994 had detectable levels of lead. Most of these positive samples (33, 10% of the total) had significant exposure (> 10 ug/dl). Over half of the significant exposures (20%, or 6% overall) were at toxic levels (>30 ug/dl).

All species of animals, including caged birds, can be affected. Ingestion is the usual route of exposure, and young animals are especially at risk because of their efficient absorption from the gut. Sources of lead include figurines and toys, solder, plumbing supplies, shot, sinkers, improperly glazed bowls, lead-based paint such as from building remodeling or artist's paint, car batteries, tile and linoleum, and foil from wine bottle tops. Cats will lick leaded paint dust that has settled on their haircoats during remodeling.

Lead affects thiol- and zinc-enzymes, GABA-mediated neurotransmission, hemoglobin synthesis, and red blood cell membranes. The nervous, hematopoietic, and gastrointestinal systems are thereby involved. Lead poisoning in dogs may cause blindness, ataxia, circling, muscle spasms, hysteria, convulsions, mental slowness, abdominal pain, vomition, diarrhea or constipation, and anemia. Poisoned cats may have nonspecific signs of lethargy and anorexia. Horses can suffer from peripheral nerve demyelination leading to the "roarer" syndrome. Psittacine birds have an acute onset of vague signs including depression, weakness, anorexia, diarrhea, ataxia, head tilt, blindness, circling, and convulsions.

Diagnosis of lead poisoning is based on a history of exposure to lead, typical signs, anemia with inappropriate numbers of nRBC and/or basophilic stippling of red blood cells, radiographic evidence of lead in the gut (not always present), and analytical evidence of lead in blood or tissue. Whole blood drawn into lavender top tubes (LTT) containing EDTA or green top tubes containing heparin is the sample of choice to test for lead levels in live animals. The minimum blood sample volume is 100ul. At postmortem, ingesta, liver, and kidney (frozen, not fixed) are tested for lead. A blood lead concentration > 10 ug/dl suggests significant exposure, and > 30 ug/dl with appropriate signs indicates poisoning. Lead poisoning may be confused with rabies, distemper, hepatitis, and other heavy metal poisonings, and in cats, with other causes of unexplained anorexia and depression.

Treatment of lead poisoning begins with decontamination so that exposure to the source of lead is ended. Lead objects in the GI tract can be removed surgically. Otherwise, oral sodium or magnesium sulfate (0.5 mg/kg, in a 10% solution in water) can be used to remove residual lead, which must be done before using chelating agents. Ca EDTA (Versenate®, 25 mg/kg PO q 6 hr in 5% dextrose/water for 5 days) chelates lead and hastens secretion. The parenteral regimen must be followed by 2 to 4 days of rest before giving another round of therapy (if needed), to minimize renal damage. Severe cases may require chelation with BAL (dimercaprol) to remove lead from the brain before EDTA can be used. New agents, for example DMSA (dimercaptosuccinic acid), are being developed that will chelate lead with the efficacy of BAL and relative safety of EDTA.

Treatment of lead poisoning in pets should be accompanied by a discussion about decontamination of the premises. Urge owners to test other animals, and to seek medical advice regarding testing of children and other people, who may have been exposed to t he toxic environment.