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Lead Toxicity Medication

  • Author: Pranay Kathuria, MD; Chief Editor: Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS  more...
Updated: Feb 08, 2016

Medication Summary

The mainstay of treatment is chelation therapy. Chelation agents contain sulfhydryl groups that bind or chelate lead, and the resulting complex is excreted either renally or hepatically. The chelation agents succimer and penicillamine are given orally, whereas dimercaprol and edetate (EDTA) calcium disodium (CaNa2 EDTA) are administered parenterally.

These agents reduce body stores of lead. Reducing blood lead levels also may mobilize skeletal stores of lead. Therefore, caution must be exercised in using chelation agents, both because of their adverse effects and because of their ability to mobilize lead.



Class Summary

Antidotes are used to prevent intoxication resulting from lead poisoning. These agents bind lead in the vascular compartment and prevent it from reaching the end organs of toxicity. Chelators promote the excretion of lead.

Succimer (Chemet)


Succimer, or meso 2,3-dimercaptosuccinic acid (DMSA), is an analogue of dimercaprol used in lead poisoning. It has high sensitivity for lead, but its ability to chelate essential trace metals is low. It is available as capsules of 100 mg. Succimer is generally well tolerated after oral (PO) administration and produces a linear dose-dependent reduction in serum lead concentration. It forms a water-soluble chelate with heavy metals and is excreted in urine. It produces plumburesis approaching that achieved with the combination of CaNa2EDTA and dimercaprol.

In January 1991, succimer became the only drug approved by the US Food and Drug Administration (FDA) specifically for lead chelation in children and the only drug approved to treat a specific laboratory test—namely, a blood lead level (BLL) higher than 45 µg/dL (2.17 mmol/L). It has been shown to be an effective oral chelator.

Although never a substitute for careful environmental controls, succimer produces a rapid decline in lead level and reverses many of the biochemical indicators of toxicity. It is not currently licensed for use in adults. Although experience suggests that this agent is safe and effective, its use must be considered carefully. Adults exposed from an occupational source must be carefully excluded from further exposure.

Patients with extremely high lead levels may experience abnormalities in gastrointestinal (GI) motility; thus, the absorption of succimer may be unpredictable or erratic. Use of this agent in patients with lead levels higher than 60 µg/dL has not been carefully studied. Therefore, consideration should be given to the use of parenteral therapy until lead levels drop below this value.

Edetate calcium disodium (Versenate)


CaNa2EDTA is nearly the perfect chelator. It is water-soluble, can be administered either intravenously (IV) or intramuscularly (IM), allows lead to be renally eliminated, is not metabolized, and has few toxic effects. Its main limitation is that it removes lead from extracellular spaces only.

CaNa2EDTA should generally be given IV, diluted to a concentration of less than 0.5% in 5% dextrose in water (D5W) or isotonic saline. In patient with acute lead encephalopathy and increased intracranial pressure, dilution to concentration of less than 3.0% may be necessary, or the IM route may be preferred to limit fluids. Ideally, the first dose of dimercaprol should be given at least 4 hours before CaNa2EDTA. Note that CaNa2EDTA initially may aggravate symptoms of lead toxicity because of its mobilization of stored lead.

CaNa2EDTA may induce central nervous system (CNS) toxicity if BAL therapy is not initiated first when blood lead levels are higher than 70 µg/dL in children or 100 µg/dL in adults and in encephalopathy. To prevent hypocalcemia, only CaNa2EDTA should be used for chelation in heavy metal toxicity.

When CaNa2EDTA is given IM, the same daily dose is used, divided into 2-6 doses. IM preparations of CaNa2EDTA are extremely irritating to muscle and intensely painful. Lidocaine or procaine with the IM preparation lessens the pain.

Dimercaprol (BAL in Oil)


Dimercaprol (British antilewisite [BAL], or 2,3-dimercapto-1-propanol) was the first chelator used in encephalopathic individuals and is the drug of choice for treatment of lead toxicity. It is a chelating agent for intracellular and extracellular lead that and diffuses into red blood cells (RBCs) and rapidly crosses the blood-brain barrier. Sulfhydryl groups combine with ions of heavy metals to form soluble, nontoxic complexes that are excreted renally. Dimercaprol is excreted primarily in bile, making it an agent that can be used in patients with renal failure.

Combination therapy with dimercaprol and CaNa2EDTA is recommended in all cases of severe, acute intoxication (eg, BLL > 100 µg/dL), particularly when encephalopathy is present. Dimercaprol is administered IM every 4 hours, mixed in a peanut oil base; therefore, it should not be used in patients allergic to peanuts. In very severely poisoned patients, the dose is increased to 7 mg/kg, with great caution.

Adverse effects are fever, pain at the injection site, nausea, vomiting, headache, and sterile abscess formation.

D-penicillamine (Cuprimine, Depen)


D-penicillamine (3-mercapto-D-valine), a second-line oral chelating agent, is a hydrolysis product of penicillin that is FDA-approved for the treatment of Wilson disease and cystinosis. It has been used as an oral chelator of lead for 30 years but has never been licensed for this indication by the FDA.

Penicillamine is effective orally and has few adverse effects. It can be administered over an extended period (weeks to months) for children with lead levels below 45 µg/dL. Penicillamine is available as capsules of 125 mg and 250 mg. Pyridoxine supplementation is required. Adjust the dose for patients with compromised renal function.

Dimercaptopropanesulfonic acid (Dimerval)


Dimercaptopropanesulfonic acid (DPMS) has received much attention worldwide, but it is not yet available in the United States, except under special FDA Investigational New Drug (IND) permits. In Europe and Asia, DPMS has become the drug of choice for most heavy metal intoxications. It is available both in an oral form and in a water-based parenteral form.

Contributor Information and Disclosures

Pranay Kathuria, MD FACP, FASN, FNKF, Professor of Medicine, Director, Division of Nephrology and Hypertension, University of Oklahoma School of Community Medicine

Pranay Kathuria, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Heart Association, American Society of Hypertension, American Society of Nephrology, National Kidney Foundation

Disclosure: Nothing to disclose.


Adam K Rowden, DO Assistant Professor of Emergency Medicine, Jefferson Medical College of Thomas Jefferson University; Director, Division of Toxicology, Department of Emergency Medicine, Albert Einstein Medical Center; Consulting Toxicologist, Children's Hospital of Philadelphia

Adam K Rowden, DO is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, American College of Osteopathic Emergency Physicians, American Osteopathic Association, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Rika Nagakuni O'Malley, MD Instructor, Department of Emergency Medicine, Thomas Jefferson University Hospital

Disclosure: Nothing to disclose.

Chief Editor

Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS Professor Emeritus of Neurology and Psychiatry, Clinical Professor of Medicine, Clinical Professor of Family Medicine, Clinical Professor of Neurosurgery, State University of New York Upstate Medical University; Neuroscience Director, Department of Neurology, Crouse Irving Memorial Hospital

Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS is a member of the following medical societies: American College of International Physicians, American Heart Association, American Stroke Association, American Academy of Neurology, American Academy of Pain Medicine, American College of Forensic Examiners Institute, National Association of Managed Care Physicians, American College of Physicians, Royal College of Physicians, Royal College of Physicians and Surgeons of Canada, Royal College of Surgeons of England, Royal Society of Medicine

Disclosure: Nothing to disclose.


David A Griesemer, MD, Professor, Departments of Neuroscience and Pediatrics, Medical University of South Carolina

David A Griesemer, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine, American Academy of Neurology, American Epilepsy Society, Child Neurology Society, and Society for Neuroscience

Disclosure: Nothing to disclose.

Christopher P Holstege, MD Associate Professor of Emergency Medicine and Pediatrics, University of Virginia School of Medicine; Director, Division of Medical Toxicology, Center of Clinical Toxicology; Medical Director, Blue Ridge Poison Center; Associate Medical Toxicology Fellowship Director, Veterans Affairs Department of Health

Christopher P Holstege, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, European Association of Poisons Centres and Clinical Toxicologists, Medical Society of Virginia, Society for Academic Emergency Medicine, Society of Toxicology, and Wilderness Medical Society

Disclosure: Nothing to disclose.

J Stephen Huff, MD Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine

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Jonathan S Rutchik, MD, MPH Assistant Professor, Department of Occupational and Environmental Medicine, University of California at San Francisco

Jonathan S Rutchik, MD, MPH is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Occupational and Environmental Medicine, and Society of Toxicology

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Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

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Peripheral smear taken from 8-year-old Pakistani girl who presented with acute hemolytic anemia and lead level of 125 µg/dL.
Growth arrest lines, also known as lead lines, in bones of child who recovered from lead poisoning.
Lead line on gingival border of adult with lead poisoning.
Wrist drop in adult with lead poisoning and renal failure.
Abdominal flat plate showing multiple radiopaque foreign bodies, including paint chips and earring.
Kidney biopsy results from patient with chronic lead nephropathy show nonspecific tubular atrophy and interstitial fibrosis. Note absence of interstitial infiltrate. Single glomerulus included in section is normal. Image courtesy of Vecihi Batuman, MD, FACP.
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