Lead poisoning in animals and people is a major concern
worldwide. Poisoning in animal populations may serve as a sentinel to assess the
extent of environmental contamination and human health problems related to lead. In
veterinary medicine, lead poisoning is most common in dogs and cattle. Lead
poisoning in other species is limited by reduced accessibility, more selective
eating habits, or lower susceptibility. In cattle, many cases are associated with
seeding and harvesting activities when used oil and battery disposal from machinery
is handled improperly. With the elimination of tetraethyl lead from gasoline in many
countries, the number of lead poisoning cases attributed to oil consumption has
declined in recent years. Other sources of lead include paint, linoleum, grease,
lead weights, lead shot, and contaminated foliage growing near smelters or along
roadsides. To prevent future occurrences of lead poisoning, it is crucial to
identify the source. Lead poisoning is also encountered in urban environments and
during the renovation of old houses that have been painted with lead-based paint,
leading to exposure of small animals and children. The consumption, through
grooming, of dust containing lead has been reported in cats. Improper disposal of
lead-poisoned animal carcasses may result in toxicoses in nontarget scavenger
animals. Scavenging by endangered species such as the condor raises unique
Absorbed lead enters the blood and soft tissues and
eventually redistributes to the bone. The degree of absorption and retention is
influenced by dietary factors such as calcium or iron levels. In ruminants,
particulate lead lodged in the reticulum slowly dissolves and releases
significant quantities of lead. Lead has a profound effect on
sulfhydryl-containing enzymes, the thiol content of erythrocytes, antioxidant
defenses, and tissues rich in mitochondria, which is reflected in the clinical
syndrome. In addition to the cerebellar hemorrhage and edema associated with
capillary damage, lead is also irritating, immunosuppressive, gametotoxic,
teratogenic, nephrotoxic, and toxic to the hematopoietic system.
Acute lead poisoning is more common in young animals. The
prominent clinical signs are associated with the GI and nervous systems. In
cattle, signs that appear within 24–48 hr of exposure include ataxia, blindness,
salivation, spastic twitching of eyelids, jaw champing, bruxism, muscle tremors,
Subacute lead poisoning, usually seen in sheep or older
cattle, is characterized by anorexia, rumen stasis, colic, dullness, and
transient constipation, frequently followed by diarrhea, blindness, head
pressing, bruxism, hyperesthesia, and incoordination.
Chronic lead poisoning, occasionally seen in cattle, may
produce a syndrome that has many features in common with acute or subacute lead
poisoning. Impairment of the swallowing reflexes frequently contributes to the
development of aspiration pneumonia. Embryotoxicity and poor semen quality may
contribute to infertility.
GI abnormalities, including anorexia, colic, emesis, and
diarrhea or constipation are predominant manifestations in dogs. Anxiety,
hysterical barking, jaw champing, salivation, blindness, ataxia, muscle spasms,
opisthotonos, and convulsions may develop. CNS depression rather than CNS
excitation may be evident in some dogs. In horses, lead poisoning usually
produces a chronic syndrome characterized by weight loss, depression, weakness,
colic, diarrhea, laryngeal or pharyngeal paralysis (roaring), and dysphagia that
frequently results in aspiration pneumonia.
In birds, anorexia, ataxia, loss of condition, wing and
leg weakness, and anemia are the most notable signs.
Animals that die from acute lead poisoning may have
few observable gross lesions. Oil or flakes of paint or battery may be
evident in the GI tract. The caustic action of lead salts causes
gastroenteritis. In the nervous system, edema, congestion of the cerebral
cortex, and flattening of the cortical gyri are present. Histologically,
endothelial swelling, laminar cortical necrosis, and edema of the white
matter may be evident. Tubular necrosis and degeneration and intranuclear
acid-fast inclusion bodies may be seen in the kidneys. Osteoporosis has been
described in lambs. Placentitis and accumulation of lead in the fetus may
result in abortion.
Lead concentrations in various tissues may be useful to
evaluate excessive accumulation and to reflect the level or duration of
exposure, severity, and prognosis and the success of treatment. Concentrations
of lead in the blood at 0.35 ppm, liver at 10 ppm, or kidney cortex at 10 ppm
are consistent with a diagnosis of lead poisoning in most species. Many
countries have deemed blood lead concentrations >0.05–0.10 ppm to be a
notifiable disease in food-producing animals. Inspection or clearance by a
regulatory veterinary officer or biosecurity inspector is mandatory before
shipment for food consumption is permitted.
Hematologic abnormalities, which may be indicative but not
confirmatory of lead poisoning, include anemia, anisocytosis, poikilocytosis,
polychromasia, basophilic stippling, metarubricytosis, and hypochromia. Blood or
urinary δ-aminolevulinic acid and free erythrocyte protoporphyrin levels are
sensitive indicators of lead exposure but may not be reliable indicators of
clinical disease. Radiologic examination may be useful to determine the
magnitude of lead exposure.
Lead poisoning may be confused with other diseases that
cause nervous or GI abnormalities. In cattle, such diseases may include
polioencephalomalacia, nervous coccidiosis, tetanus, hypovitaminosis A,
hypomagnesemic tetany, nervous acetonemia, organochlorine insecticide poisoning,
arsenic or mercury poisoning, brain abscess or neoplasia, rabies, listeriosis,
In dogs, rabies, distemper, and hepatitis may appear
similar to lead poisoning.
If tissue damage is extensive, particularly to the nervous
system, treatment may not be successful. In livestock, calcium disodium edetate
(Ca-EDTA) is given IV or SC (110 mg/kg/day) divided bid for 3 days; this
treatment should be repeated 2 days later. In dogs, a similar dose divided qid
is administered SC in 5% dextrose for 2–5 days. After a 1-wk rest period, an
additional 5-day treatment may be required if clinical signs persist. No
approved veterinary product containing Ca-EDTA is currently commercially
Thiamine (2–4 mg/kg/day, SC) alleviates clinical
manifestations and reduces tissue deposition of lead. Combined Ca-EDTA and
thiamine treatment appears to produce the most beneficial response.
d-Penicillamine can be administered PO to dogs (110
mg/kg/day) for 2 wk. However, undesirable adverse effects such as emesis and
anorexia have been associated with this treatment.
d-Penicillamine is not recommended for livestock.
Succimer (meso 2,3-dimercaptosuccinic acid, DMSA) is a chelating agent that has
proved to be effective in dogs (10 mg/kg, PO, tid for 10 days) and is also
useful in birds. Fewer adverse effects have been associated with DMSA than with
Cathartics such as magnesium sulfate (400 mg/kg, PO) or a
rumenotomy may be useful to remove lead from the GI tract. In cattle, surgery to
remove particulate lead material from the reticulum after the ingestion of
batteries is rarely successful. Barbiturates or tranquilizers may be indicated
to control convulsions. Chelation therapy, in combination with antioxidant
treatment, may limit oxidative damage associated with acute lead poisoning.
Antioxidants such as n-acetylcysteine (50 mg/kg/day, PO) have been used in
combination with DMSA.
Mobilization of lead at parturition, excretion of lead
into milk, and lengthy withdrawal times in food-producing animals raise
considerable controversy regarding the rationale for treatment from both public
health and animal management perspectives. The half-life of lead in the blood of
cattle ingesting particulate lead is usually >9 wk. Withdrawal times, which
may be >1 yr, should be estimated by periodic monitoring of blood lead
concentrations. In a herd of cattle with confirmed cases of lead poisoning, all
potentially exposed cattle should be evaluated. A small but significant portion
of the asymptomatic cattle may have concentrations of lead in tissues that
exceed recognized food safety standards.
Last full review/revision September 2013 by Barry R. Blakley, DVM, PhD