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Lead Toxicity Treatment & Management

  • 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

Approach Considerations

The most important step in treatment is to prevent further exposure to lead. Accurate assessment of environmental and occupational exposure is essential. Modifying children’s behavior to decrease hand-to-mouth activity is beneficial.

The US Occupational Safety and Health Administration (OSHA) has recommendations for occupational lead exposure. Under these guidelines, the permissible exposure limit is 50 µg/m3 for an 8-hour, time-weighted average. Workers with blood lead levels (BLLs) of 60 µg/dL or higher must be removed from the workplace. Additionally, employees should be removed from the workplace if the average of their last 3 BLLs is 50 µg/dL or higher. Individuals with BLLs of 40 µg/dL or higher must undergo medical evaluation.

Community-wide preventive actions are recommended when children are found to have BLLs of 10 µg/dL or higher. With BLLs of 15-19 µg/dL, nutritional and educational interventions are recommended. With BLLs of 20 µg/dL or higher, medical evaluations and environmental interventions are recommended.

Medical treatment (ie, chelation therapy) is but one element of a comprehensive treatment plan for exposure to lead; removal of the source of lead exposure is more important. The interventions described below relate to chelation therapy for the most severe cases of lead poisoning. Chelation is of only transient benefit in the patient whose source of lead exposure has not been identified and removed.


Chelation Therapy

Chelation therapy, especially in the setting of encephalopathy, can be complicated. If appropriate facilities for treatment are not available, consider transfer to an institution that is capable of managing an encephalopathic patient and also has a provider experienced in lead poisoning and chelation therapy. Ideally, children should be treated in specialized pediatric intensive care units.

Chelation agents

Succimer is a water-soluble, oral chelating agent that is appropriate for use with BLLs higher than 45 µg/dL.[21, 30]  In a retrospective study from Nigeria, chelation therapy using dimercaptosuccinic acid (DMSA) lowered blood lead levels in children with severe lead poisoning.[31]

D-penicillamine is a second-line oral chelating agent, although it is not approved by the US Food and Drug Administration (FDA) for use in lead poisoning.

Edetate (EDTA) calcium disodium (CaNa2 EDTA) is a parenteral chelating agent. It should never be used as the sole agent in patients manifesting with lead encephalopathy, because it does not cross the blood-brain barrier and can potentially lead to exacerbation of lead encephalopathy; dimercaprol, which does cross the blood-brain barrier, should be administered first. Life-threatening hypocalcemia has been reported when disodium EDTA was inadvertently substituted for CaNa2 EDTA.

Dimercaprol (also referred to as British antilewisite [BAL]) is another parenteral chelating agent recommended as an agent of first choice for patients with lead encephalopathy. With high BLLs (ie, > 100 µg/dL), it is used in conjunction with CaNa2 EDTA.

Acute lead poisoning and nephropathy

In the acute setting, if suggestive radiopacities are observed on a plain radiograph of the abdomen, gastric lavage, cathartics, or whole bowel irrigation may be used to limit lead absorption.

With acute lead poisoning, the indications for chelation therapy are well defined. Institute chelation therapy in children with BLLs of 45 µg/dL or higher. Treat children whose BLLs are 70 µg/dL or higher as medical emergencies.

Succimer and penicillamine may be given orally. Penicillamine may be used when blood lead levels are 25-40 µg/dL, especially with a negative CaNa2 EDTA mobilization test result. Succimer may be an alternative; its main indication is in persons whose BLLs are 45 µg/dL or higher.

Intravenous (IV) therapy is preferable for persons with BLLs of 70 µg/dL or higher. Use the combination of dimercaprol and CaNa2 EDTA with BLLs of 70 µg/dL or higher and in the presence of lead encephalopathy.

In adults, consider chelation therapy for patients with blood lead levels BLLs of 70 µg/dL or higher. Also consider chelation therapy in symptomatic adults with BLLs exceeding 50 µg/dL. Available chelation agents for adults are dimercaprol and CaNa2 EDTA; penicillamine and succimer do not have US Food and Drug Administration (FDA) approval for this application, although they are effective treatments.

Chelation therapy reverses Fanconi syndrome, transient hypertension, and tubular structural changes observed on histopathology findings.

Chronic lead nephropathy

Patients with chronic lead nephropathy, in the absence of marked interstitial fibrosis and with only minimal impairment in kidney function, may respond to chelation therapy.

Extremely limited data are available regarding the benefits of chelation therapy with documented lead nephropathy. In 1979, Wedeen et al treated patients with occupational lead nephropathy and found a 20% improvement in the GFR in 4 of 8 patients given EDTA 3 times a week for 6-50 months.[32] The reported improvements in kidney function could be from reversal of acute-on-chronic lead nephropathy.

Lin and coworkers from Taiwan performed 3 well-designed studies addressing populations of patients with high-normal BLLs and chronic kidney disease.[33, 34, 35]

The first of these studies included 32 subjects with chronic kidney disease (serum creatinine level [SCr] of 1.5-4 mg/dL) and mildly elevated body lead burden (lead excretion value of 150-600 µg with the 3-D CaNa2 EDTA lead mobilization test). Subjects were randomly assigned to receive EDTA chelation therapy or placebo weekly for 2 months and were followed for an additional 12 months. The reciprocal of serum creatinine (1/SCr) versus time data suggested that using chelation may slow the progression of renal disease.

The second study described the results of chelation therapy in 36 subjects (24 study group subjects and 12 controls) with serum creatinine values of 1.5-4 mg/dL and high-normal bone lead burden. This time, chelation therapy with CaNa2 EDTA was administered weekly for 3 months. In the treated group, creatinine clearance improved by as much as 10.2% at 1 year, whereas in the control group, kidney function declined by as much as 11%.

The third study included 202 subjects who were followed for 2 years. In this study, 64 patients with a high-normal body lead burden (urinary lead excretion > 80 µg and < 600 µg after 1 g of CaNa2 EDTA infusion) and SCr lower than 4.2 mg/dL were randomized to chelation or placebo.

In the initial 3 months, the chelation group received 1 g of CaNa2 EDTA every week, and the controls received placebo. In the ensuing 24 months, repeated chelation therapy was administered weekly to patients with a high-normal lead burden unless, on repeated testing, the body lead burden fell below 60 µg.

The glomerular filtration ate (GFR) increased by 11.9% (+3.4 mL/min) in the chelation group at the end of the initial 3 months, whereas it fell by 3.6% (-1 mL/min) in the control group. Thereafter, no further improvement in the GFR was observed in these patients. At the end of 27 months, the mean change in GFR was +2.1 mL/min in the chelation group and -6 mL/min in the control group over the 27-month study.

These studies suggest that in patients with an increased lead burden, chelation with small doses of CaNa2 EDTA at longer intervals might be safe for treating chronic kidney disease. However, repeated and chronic exposure to CaNa2 EDTA may create its own nephrotoxicity; therefore, use caution when deciding to institute chelation therapy. Exclude other causes of kidney disease, and define an endpoint of therapy, such as normalization of the CaNa2 EDTA test results or improvement in kidney function.

Supplementary measures

Closely monitor cardiovascular and mental status in patients with lead poisoning. Maintain an adequate urine output. Assess renal and hepatic functions.

Diphenhydramine may help alleviate the adverse effects of dimercaprol. Iron supplementation should be avoided in patients receiving dimercaprol chelation therapy because dimercaprol forms a complex with iron, leading to toxicity.


Dietary Measures

The diet should be adequate in energy (caloric) intake and replete in calcium, zinc, and iron. Data from the Normative Aging Study suggest that low dietary intake of vitamin D may increase accumulation of lead in bones, whereas low dietary intake of vitamin C and iron may increase lead levels in blood in subjects who range in age from middle-aged to elderly.

Similar data associate calcium and iron deficiency with lead absorption in children. Although no studies have specifically addressed treatment of lead exposure with calcium and iron supplementation, it is a logical therapy to help limit the absorption of lead.




The 2010 Healthy People objective to eliminate childhood lead poisoning can be achieved through primary prevention. Pediatricians and family practitioners provide a fundamental role with anticipatory guidance about potential sources of lead exposure and its hazards for the development of children.

A successful primary prevention should focus on the 2 main exposure sources for children in the United States: lead in housing and nonessential uses of lead in certain products, such as imported and domestically manufactured toys, eating and drinking utensils, cosmetics, and traditional medicines.

Environmental measures for prevention of lead toxicity include abatement of lead paint usage, removal of lead from gasoline, and removal of lead solder from cans. Lead abatement in dwellings must be performed by skilled and experienced workers.

For adults, occupational measures focus on engineering controls, such as isolation by containment and local exhaust systems, personal protective equipment (eg, respirators), and good work practices. Workers should be educated regarding the health risks of lead and sources that may cause poisoning.

OSHA standards should be followed in the workplace. These standards for permissible exposure limit lead in the workplace to a maximum of 50 µg/m3 of air averaged over an 8-hour period. Medical surveillance is indicated when workers are exposed to lead levels exceeding 30 µg/m3 for more than 30 days a year (regardless of respiratory protection).


Efforts to prevent lead poisoning have focused primarily on secondary prevention because the cost of primary prevention in the form of environmental inspection and abatement of all homes and other sources of lead is prohibitive. This focus does not reflect the true importance of primary prevention.

Secondary prevention focuses on the early detection of lead poisoning. The CDC has devised screening criteria to determine which children are at high risk for lead poisoning; screening of BLLs should be carried out according to these criteria (see Workup). Medical evaluation, treatment, and environmental and public health follow-up are essential in individuals with elevated BLLs.



Consultation with a toxicologist and a nephrologist is appropriate. Medical toxicology services can typically be located by contacting a local poison center.

All occupational exposures must be reported to OSHA. The local or county health departments responsible for monitoring children with lead toxicity, should be informed about patients with elevated lead levels or those undergoing medical treatment, so that they may initiate appropriate environmental evaluation and lead abatement.

Many local health departments have programs for appropriate lead screening of children, in cooperation with local pediatricians. Stressing the need for screening in any patient at risk (because of housing, industrial, ethnic, recreational concerns) is important. Repairs of older homes must be done carefully to avoid lead exposure. Proper lead abatement in older homes prevents future exposure to lead and, thus, prevents further lead poisoning.


Long-Term Monitoring

All patients treated for lead poisoning require extensive outpatient follow-up. The intent of such follow-up is to avoid further exposure to lead and to maintain lead levels in the acceptable range.

After chelation, the blood lead level should be rechecked in 7-21 days to determine whether repeat chelation therapy is required. Chelation therapy, either oral or intravenous, may be continued in an outpatient setting if indicated. Carefully monitor kidney and liver function during therapy.

Assess the source of lead. Involvement of the local health department can assist in this regard. Do not discharge patients from the hospital until they can go to a lead-free environment. Children in particular should not be allowed to return to a lead-contaminated environment; if they are exposed to more lead, their lead levels will rapidly rise again.

There is a general belief, probably incorrect, that once chelation is terminated, BLLs will rebound rapidly. Numerous publications have discussed the effect of lead stored in bone.[36, 37, 38, 39, 40, 17] In the light of the known kinetics of lead in the body and the reports of expected decreases in lead level over time, this would not appear to be expected, because the half-life of lead in bone is measured in years. Thus, significant elevations in BLL after termination of chelation should be considered probable reexposure.

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

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

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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