MSPCA-Angell Headquarters

350 South Huntington Avenue, Boston, MA 02130
(617) 522-7400
Email Us

Angell Animal Medical Centers – Boston

350 South Huntington Avenue, Boston, MA 02130
(617) 522-7282
More Info

Angell West

293 Second Avenue, Waltham, MA 02451
(781) 902-8400
More Info

Angell at Nashoba – Low-Cost Wellness Care

100 Littleton Road, Westford, MA 01886
(978) 577-5992
More Info

Animal Care and Adoption Centers – Boston

350 South Huntington Avenue, Boston, MA 02130
(617) 522-5055
More Info

Animal Care and Adoption Centers – Cape Cod

1577 Falmouth Road, Centerville, MA 02632
(508) 775-0940
More Info

Animal Care and Adoption Centers – Nevins Farm

400 Broadway, Methuen, MA 01844
(978) 687-7453
More Info

Donate Now

More Ways to Donate

From an online gift to a charitable gift annuity, your contribution will have a significant impact in the lives of thousands of animals.

A Technician’s Guide to Lead Toxicosis

By Kate Dorsey, DVM


Lead toxicosis, also known as lead poisoning or plumbism, is a clinical syndrome that occurs secondary to exposure to toxic amounts of lead. Clinical signs typically involve the gastrointestinal and nervous systems. Hematologic and radiographic abnormalities may be seen, but diagnostic confirmation is usually obtained via whole blood lead level.

To assess whole blood lead level, blood samples may be collected in a heparin-containing/green-top tube or an EDTA-containing/purple-top tube. Normal blood lead level is less than 0.1 ppm (10 mcg/dl). A blood lead level of greater than 0.35-0.4 ppm (35-40 mcg/dl) is diagnostic of lead toxicosis, in conjunction with appropriate clinical signs. A blood lead level between 0.1-0.35 ppm (10-35 mcg/dl) suggests significant exposure; with appropriate clinical signs, it is suggestive of lead toxicosis. Blood lead concentration does not necessarily correlate with severity of clinical signs, as it does not reflect total body lead burden. In fact, in cases of chronic lead toxicosis, blood lead level may be lower than expected, due to distribution of lead into different body compartments such as bone.

Lead toxicosis may arise secondary to acute or chronic exposure. The acute toxic dose in dogs is between 200-1000 mg/kg (dependent on lead form). Acute clinical signs include acute onset of vomiting and neurologic signs (e.g. mental dullness, depression, hyperexcitability, abnormal behavior, ataxia, tremors, opisthotonus, seizures, blindness, central vestibular abnormalities, polyneuropathy, paralysis). Acute toxicosis can be fatal within several days. Chronic lead toxicosis occurs after repeated exposures over time, with a cumulative dose in dogs of 1.8-2.6 mg/kg/day. Chronic signs include gradual onset of vomiting, regurgitation (secondary to megaesophagus), diarrhea, anorexia, abdominal discomfort, lethargy, weight loss, anemia, and sometimes neurologic signs (e.g. behavior changes, intermittent seizures).

Lead exposure mainly occurs via the gastrointestinal tract. Examples of possible sources of lead include lead paint, paint residues/dust from sanding, old wallpaper, foodstuffs stored in containers with lead base, vegetables grown in lead-saturated soils, car batteries, linoleum, solder, plumbing materials/supplies, lubricating compounds, putty, tar paper, lead foil, golf balls, lead objects (shot, fishing sinkers, drapery weights), leaded glass, older painted toys, and improperly glazed ceramic food/water bowls. The most common source of lead for dogs and cats is lead paint or lead-contaminated dust/soil. Dogs are more likely to directly ingest paint or objects, while cats are more likely to be exposed to dusts via grooming. Risk factors for exposure include housing in older, non-renovated buildings where lead-based paint was used (e.g. painted prior to 1977) and housing in older buildings undergoing renovation.

Figure 1: Basophilic stippling in a red blood cell

Lead exerts its toxic effects by substituting for physiologically active metal ions (e.g. calcium, zinc) which are important for cell homeostasis. In doing so, lead has the potential to affect many biological processes, including metal transport, energy metabolism, apoptosis, ion conduction, cell adhesion, intercellular and intracellular cell signaling, enzymatic processes, protein maturation, and genetic regulation. Bioavailability of lead is enhanced in young animals, fasting animals, and animals deficient in calcium, zinc, iron, and/or Vitamin D. Conversely, high dietary levels of zinc and calcium decrease lead bioavailability. More than 90% of absorbed lead is bound to red blood cells; unbound lead is widely distributed in tissues, with bone being a long-term storage site for lead.

In red blood cells, lead interferes with hemoglobin synthesis by inhibiting the incorporation of iron into heme. Lead increases red blood cell fragility and the rate of red blood cell destruction. Lead can cause a regenerative iron deficiency (microcytic/hypochromic) anemia (present in 8% of dogs with lead intoxication), as well as poikilocytosis, echinocytosis, neutrophilic leukocytosis, and the presence of target cells. The most common documented hematologic finding in cases of lead toxicosis (more common in cases of chronic toxicosis) is the disproportionate presence of nucleated red blood cells (nRBCs). nRBCs are present in approximately 54% of dogs with lead intoxication. Five-40 nRBCs per 100 white blood cells, in the absence of anemia, is highly suggestive of lead intoxication. However, the absence of nRBCs does not rule out lead toxicosis. Basophilic stippling of red blood cells may also be seen, due to lead’s inhibition of a specific enzyme, resulting in accumulation of RNA degradation products and aggregation of ribosomes inside red blood cells. Basophilic stippling is present in approximately 25% of dogs with lead intoxication.

Figure 2: Nucleated red blood cell (nRBC)

In addition to complete blood count (CBC) and blood smear evaluation, radiographs may also be useful in evaluation for possible lead toxicosis. Radiopaque gastrointestinal material is noted in approximately 20% of dogs with lead intoxication. Lead lines, due to precipitation of lead salts within the epiphyseal plate of long bones, is an uncommon finding. Postmortem histopathologic findings include cerebrocortical lesions (spongiosis, gliosis, neuronal necrosis, demyelination, vascular hypertrophy,) and intranuclear inclusion bodies (the intracellular storage form of lead) in hepatocytes or renal tubular epithelial cells). Inclusion bodies are pathognomonic for lead toxicosis.

Treatment of lead toxicosis consists first of symptomatic treatment (e.g. medical management of gastrointestinal signs and seizures) and evacuation of the gastrointestinal tract (via emesis, cathartics, enemas, endoscopic/surgical removal of lead objects). Antioxidants and thiol-containing drugs (e.g. Vitamin C, Vitamin E, alpha-lipoic acid, n-acetylcysteine), as well as B vitamins such as thiamine, may provide some supplemental benefit. Magnesium sulfate (2-25 g orally in dogs, 2-5 g orally in cats, as a 20% solution or less) may be useful as a cathartic and may also precipitate lead in the gastrointestinal tract to lead sulfate, which is less bioavailable, thereby reducing systemic lead absorption. Activated charcoal does not bind to lead and is not recommended as a treatment in cases of lead ingestion or intoxication.

Ultimately, chelation (i.e., binding) therapy is necessary in most cases of lead toxicosis. Removal of macroscopic amounts of lead from the gastrointestinal tract should be performed before commencement of chelation, as older chelating agents will enhance absorption of lead from the gastrointestinal tract. In addition, older chelating agents, such as calcium disodium versenate (CaNa2EDTA), are nephrotoxic, can cause zinc/iron/manganese depletion with long-term therapy, and can cause discomfort at the injection site. However, because they are given parenterally, they can be used in patients with severe gastrointestinal signs of illness. CaNa2EDTA can be diluted to a 1% solution with D5W or 0.9% saline, and given 25-50 mg/kg SQ/IM/IV every 6 hours for 2-5 days. Multiple treatment courses may be needed, with a 5-day rest period between courses.

Succimer (meso-2,3-dimercaptosuccinic acid or DMSA) is currently the chelating agent of choice and can be dosed at 10 mg/kg orally (or rectally) every 8 hours for 10-15 days. Multiple treatment courses may be needed, with a 14-day rest period between courses. This drug is preferred because it is not nephrotoxic, it does not significantly chelate essential minerals, and it does not increase lead absorption from the gastrointestinal tract and can therefore be administered while lead is still in the gastrointestinal tract.

Clinical signs should dramatically improve within 1-2 days of instituting chelation therapy, while a decrease in blood lead level is first expected around day 5 of treatment. Generally, one round of chelation therapy is sufficient. Additional round(s) of therapy should be considered if the blood lead level is still increased and clinical signs are still present. Rebound toxicosis can occur within 14 days post-chelation, as lead stores are redistributed from bone and tissue in animals with chronic lead poisoning. If clinical signs recur, another round of chelation therapy is recommended. If clinical signs do not recur, monitoring of the blood lead level every 14 days is suggested to ensure that levels continue to decrease. Overall, prognosis for patients with mild-moderate clinical signs is good. However, it is important to identify the source(s) of exposure and eliminate access in order to prevent continued or recurrent toxic effects.

RN5 lightbox


Important Updates