Pediatric Lead Toxicity 

Updated: Jun 22, 2016
Author: Mohamed K Badawy, MD, FAAP; Chief Editor: Timothy E Corden, MD 



Lead toxicity is a worldwide pediatric problem. Although data continue to demonstrate a decline in the prevalence of elevated blood lead levels (BLLs) in children in the industrialized world, lead remains a common, preventable, environmental health threat. Sequelae of lead intoxication include mental retardation and growth failure. (See Epidemiology and Prognosis.)

Lead is a ubiquitous and versatile metal. It has been extensively used since ancient times, and the history of public exposure to lead in food and drink is extensive. Lead poisoning was common in Roman times because of the use of lead in water pipes and in wine containers.

Lead poisoning became common among industrial workers in the 19th and 20th centuries, when workers were exposed to lead in smelting, painting, plumbing, printing, and many other industrial activities. Following the advent of motor vehicles at the beginning of the 20th century and the introduction of leaded gasoline, environmental lead contamination substantially increased. (See Etiology.)

In 1904, the Australian physician J. Lockhart Gibson concluded that lead paint in the home was responsible for poisoning children.[1] Despite Gibson's work, and subsequent confirmation of it in the US medical literature, lead was not banned from US household paints until 1978.

Deteriorating lead paint in pre-1979 housing remains the most common source of lead exposure in children, accounting for up to 70% of elevated levels.[2] Other common sources of lead exposure include batteries, putty, cement, imported canned food, cosmetics, jewelry, leaded glass artwork, farm equipment, and illicit intravenous drugs.

Children are more susceptible than adults to the adverse effects of lead exposure.[3] Toddlers often place objects in their mouth, resulting in ingestion of dust and soil and, possibly, an increased intake of lead. The physiologic uptake rates of lead in children are higher than those in adults. In addition, children are rapidly growing, and their systems are not fully developed, which renders them more susceptible to the effects of lead. (See Etiology.)

Lead poisoning in children has been the focus of many researchers. In 1991, the Centers for Disease Control and Prevention (CDC) defined blood lead levels (BLLs) ≥10 µg/dL as the "level of concern" for children aged 1–5 years.[4] This level, which was originally intended to trigger community-wide prevention strategies, has often been misinterpreted as a definitive toxicologic threshold. In fact, no safe BLL threshold has been identified. Studies have indicated intellectual impairment in children with BLLs of less than 10 µg/dL.[5, 6]

In May 2012, the CDC replaced the term "level of concern" with an upper reference interval value defined as the 97.5th percentile of BLLs in US children aged 1–5 years from two consecutive cycles of the National Health and Nutrition Examination Survey (NHANES). By this method, the BLL upper reference value was calculated as 5 µg/dL.[4]

Patient education

For patient education information, see Poisoning. Because the effects of lead poisoning in children can be irreversible, primary prevention is critical; see the CDC's Prevention Tips.


Lead toxicity may be caused by inorganic or organic lead. Most cases of lead poisoning are caused by inorganic lead. Lead may enter the body through ingestion, inhalation, or transdermal absorption. Ingestion is the most common source of lead poisoning in children because of their normal hand-to-mouth activities. Inorganic lead absorption occurs via the mechanisms involved in absorption of essential elements, such as calcium and iron, and depends on the following factors:

  • Solubility - Lead salts are more soluble in acidic media

  • Particle size - Large particles (eg, paint chips) are poorly absorbed, whereas fine dust particles licked from the fingers or other objects may contribute to an increased lead load

  • Nutritional deficiencies -Iron, calcium, zinc, copper, and protein deficiencies result in greater lead absorption

  • Dietary fats and oils - Excess intake results in increased lead absorption

  • Other dietary components - Dietary components such as phytates, found in leafy green vegetables, bind lead particles and increase their elimination

Transcutaneous absorption of inorganic lead is minimal. However, organic lead, such as tetraethyl lead, may enter through the skin. Tetraethyl lead, the main organic compound in leaded gasoline, is converted in the body to triethyl lead and inorganic lead.

Inhalation of lead can occur with exposure to tobacco smoke. Blood lead levels high enough to suggest possible adverse cognitive outcomes have been measured in youths with secondhand smoke exposure.[7]

Absorbed lead is attracted to sulfur, nitrogen, and oxides. Its toxicity is elicited by inhibiting sulfhydryl-dependent enzymes. Most of the lead is sequestered in the bone, and the rest is distributed in the blood and soft tissues. Lead interferes with hematopoiesis at several steps. This results in less heme synthesis and the accumulation of toxic products (eg, aminolevulinic acid, protoporphyrin). The half-life of lead in the soft tissues and blood is approximately 30-70 days. Conversely, lead deposits in the bones for several years. Lead is primarily excreted by glomerular filtration.

As previously stated, children are more susceptible than adults to the adverse effects of lead exposure. Toddlers often place objects in their mouths, resulting in dust and soil being ingested and, possibly, an increased intake of lead. Physiological uptake rates of lead in children are higher than those in adults. In addition, children are rapidly growing, and their systems are not fully developed, rendering them more susceptible to the effects of lead.

Several environmental factors expose children to lead hazards, among which are dust, soil, paint chips, folk remedies, and the use of old ceramic cookware. Several parental occupations place children at risk, including lead mining, glass making, printing, welding, and electronic scrap recycling.[2] Workers should be instructed to change their working clothes at work.


Occurrence in the United States

According to the Centers for Disease Control and Prevention (CDC), the percentage of confirmed blood lead levels (BLLs) ≥10 µg/dL in US children younger than 72 months fell from 7.61% in 1997 to 0.56% in 2013. Nevertheless, the CDC estimates that at least 4 million US households have children living in them that are being exposed to high levels of lead, and approximately half a million US children age 1-5 years have blood lead levels above 5 µg/dL, the reference level at which CDC recommends public health actions be initiated.[8] Children who belong to minority populations or low-income families or who live in older homes are particularly at risk.

International occurrence

Lead continues to be a significant public health problem in developing countries. In general, children with heavy exposure to automobile exhaust (in countries where leaded gasoline is still sold), lead-based paint, or home-industry manufacture of batteries, ceramics, or painted artifacts have high lead burdens.[9, 10] Children living in rural areas who are not engaged in manufacturing pursuits do not usually have high lead burdens.

Race- and age-related demographics

Overall, from 1999-2002, non-Hispanic blacks and Mexican Americans had higher percentages of elevated BLLs (1.4% and 1.5%, respectively) than did non-Hispanic whites (0.5%). Lead poisoning chiefly affects children younger than age 6 years and adults in lead-risk occupations.


Prognosis depends on the blood lead level (BLL) and whether the patient was symptomatic on presentation. Asymptomatic patients tend to have a better prognosis, and studies demonstrate some improvement in intellectual functions following lowering of the BLL. Severe neurologic damage may follow lead encephalopathy.

Research has demonstrated that cognitive defects may occur at levels below the currently accepted BLL of 10 μg/dL.[5] Lanphear et al found an inverse relationship between blood-lead concentration and all cognitive function scores; this result was observed in math and reading scores for concentrations as low as 2.5 μg/dL.[11]

Lead-related deaths have become extremely rare since the advent of lead screening measures and decreased use of lead. Presently, death from lead encephalopathy is rarely encountered because of the aggressive approach to using chelating agents. However, complications may arise from the chelated lead complex. Therefore, careful monitoring of mental status, cardiovascular function, and renal and hepatic functions are essential parts of the ongoing evaluation.




The clinical picture associated with lead poisoning is vague. Symptoms are not specific enough to alarm the physician about lead toxicity. Most cases are currently identified through effective screening of the population at risk. However, patients with lead poisoning frequently have constipation, abdominal pain, and/or anorexia.

Gastrointestinal (GI) symptoms of lead poisoning include the following:

  • Anorexia

  • Vomiting

  • Constipation

  • Abdominal pain

Neurobehavioral changes observed in lead poisoning include the following:

  • Inattentiveness

  • Distractibility

  • Impulsiveness

  • Learning problems

Peripheral nervous system effects (rare in children) associated with lead poisoning include the following:

  • Weakness

  • Peripheral palsies

Physical Examination

No specific physical signs for lead poisoning are recognized, but patients may exhibit pallor (due to associated anemia) and hyperactivity.

Signs of increased intracranial pressure can include the following:

  • Impaired consciousness

  • Bradycardia

  • Hypertension

  • Respiratory depression

  • Papilledema

  • Coma





Approach Considerations

In the early 1990s, both the Centers for Disease Control and Prevention (CDC) and the American Academy of Pediatrics (AAP) recommended universal screening for lead toxicity in children at 1 and 2 years of age. With the subsequent decline in median blood lead concentrations, those organizations currently recommend performing environmental assessments to identify children at risk for lead exposure before screening.[8, 12]

Perform a rapid bedside glucose determination in children who present with altered mental status. Obtain serum pH and electrolyte levels, including calcium, magnesium, and phosphorus. Check for anion gap acidosis (see the Anion Gap calculator) that may be present in co-ingestions. A complete blood count (CBC) may reveal hypochromic microcytic anemia. Basophilic stippling of the erythrocytes, which is characteristic of lead poisoning, is uncommon in children.

Perform urinalysis. Children may appear mildly dehydrated, with concentrated urine and poor appetite. This can signal the beginning of the development of inappropriate secretion of antidiuretic hormone.

Whole blood lead level

Whole blood lead level (BLL) is the criterion standard for confirming the diagnosis of lead poisoning. For convenience, a fingerstick capillary lead level has been used for screening. Properly collected capillary samples have a 10% false-positive rate. Once an elevated lead level is detected, a venous lead level is assessed for confirmation.

Until recently, a BLL of 10 μg/dL or higher was considered to denote poisoning. Currently, the CDC recommends 5 μg/dL as a threshold for identifying children who have been exposed to lead and prompting measures to reduce the child’s future exposure to lead. That level corresponds to the 97.5th percentile of BLLs in US children aged 1–5 years from two consecutive cycles of the National Health and Nutrition Examination Survey (NHANES), which will be recalculated every 4 years. A BLL of 45 μg/dL remains the threshold for consideration of chelation therapy.[8]

Erythrocyte protoporphyrin

Erythrocyte protoporphyrin (EP) may be obtained in selected patients. Lead toxicity affects heme synthesis at several steps; this includes interference with the enzyme ferrochelatase, leading to the accumulation of EP. EP is easily detected because it fluoresces easily. EP is an adjunct for the diagnosis in the presence of elevated lead levels of 55 mcg and higher. At lead levels below that, EP is not a very sensitive measure, and its positivity declines. Therefore, EP is not used as a primary screening tool.

Hair samples

In Russia, hair sample is the standard for lead poisoning screening. However, studies have demonstrated that blood lead specimens are more sensitive than hair samples in detecting lead exposure.

Imaging Studies

Abdominal radiography

Presence of radiopaque flakes is a clear indicator of pica.

Long-bone radiography

Radiodensity may be detected at the distal metaphyseal area. These indications, known as lead lines, are true growth arrest lines and, although not pathognomonic, are associated with chronic lead exposure.

Chest radiography

This study is indicated in patients with lead encephalopathy to confirm the position of the endotracheal tube. Although radiographic findings of suspected aspirations may be initially absent, an initial radiograph is often helpful.

CT scanning

Head computed tomography (CT) scanning may be needed in patients who present with altered mental status to exclude cerebral edema and structural lesions.



Approach Considerations

Treatment of lead toxicity involves the prevention of further lead exposure, decontamination, chelation, and supportive therapy.

Outpatient treatment seems to be a good option for asymptomatic children with blood lead levels (BLLs) in the range of 45-69 μg/dL. However, be absolutely sure that the environment in which the child is placed is safe and lead free. If this is impossible to ensure, inpatient treatment is needed until the environmental situation is investigated in collaboration with social services and the local health department.

For patients with a BLL 70 μg/dL or higher, hospitalize the patient, obtain a confirmatory venous BLL, and initiate chelation with dimercaprol and calcium disodium edetate (EDTA). Because calcium EDTA does not cross the blood-brain barrier, its use as the only agent in this situation is not recommended because of the possibility of lead redistribution from the soft tissues to the central nervous system (CNS). Pretreatment with dimercaprol (which crosses the blood-brain barrier) is recommended.

When children have lead encephalopathy, the best approach is to transfer them to a children's hospital where pediatric intensivists and other resources are available.

All children being treated for lead poisoning need close follow-up care. Monitoring their BLLs is important. Closely monitor cardiovascular and mental status in patients with lead poisoning, maintain an adequate urine output, and assess renal and hepatic functions.


Decontamination may be performed in patients with acute lead ingestion in whom lead paint chips are identified on plain abdominal radiographs.

Gastric lavage may be performed. Secure the airway before the initiation of gastric lavage in an obtunded child with acute lead ingestion. The use of gastric lavage is controversial because lead paint chips, being large in size, are believed to be poorly absorbed and mainly excreted in stools. In 1997, the American Academy of Clinical Toxicology (AACT) stated that no evidence indicates that gastric lavage use improves clinical outcomes.

Although whole-bowel irrigation (WBI) may be performed to decrease the bioavailability of paint chips, it remains a theoretical option for lead ingestion because insufficient data support or exclude its use. Charcoal binds poorly to lead, and no evidence supports its use in acute lead ingestion.


Use of chelating agents is recommended for children with venous lead levels of 45 μg/dL or higher. These include oral succimer and parenteral  calcium disodium edetate (calcium EDTA) and British antilewisite (BAL; dimercaprol).

Significant intravascular hemolysis may occur in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency who are receiving BAL as a chelating agent. Iron supplementation should be avoided in patients receiving BAL chelation therapy because BAL forms a complex with iron, leading to toxicity. Diphenhydramine may help to alleviate the adverse effects of British antilewisite (BAL).

Supportive Therapy

Most children with lead poisoning are asymptomatic and are identified by screening. However, certain children may develop acute lead encephalopathy. In such circumstances, protection of the airway via endotracheal intubation may be necessary.

In the event of seizures, benzodiazepines are indicated. Maintenance of seizure control with phenobarbital may be needed. If seizures are difficult to control, presume the presence of increased intracranial pressure and pursue measures to decrease it (eg, hyperventilation, mannitol, steroids).

Maintain an adequate urinary flow to promote excretion of the lead-chelated complex. Once urinary flow is established, restrict fluids to maintenance and losses to prevent cerebral edema.

Deterrence and Prevention

Primary prevention

The 2020 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 plan should focus on the two main exposure sources for children in the United States: (1) lead in housing and (2) nonessential uses of lead in certain products, such as imported and domestically manufactured toys, eating and drinking utensils, cosmetics, and traditional medicines.

Parents should be educated about sources of lead, the common behavior involved (ie, pica), and the hazards associated with lead exposure on children's development.[8, 13]

Nutritional assessment is of particular importance because lead absorption is enhanced by improper dietary intake, especially in the presence of high fat intake and/or deficiency of certain elements, such as calcium and iron.

Secondary prevention

The Centers for Disease Control and Prevention (CDC) and AAP have issued recommendations regarding screening for lead poisoning. They recommend universal screening in areas where at least 27% of houses were built before 1950 and in places where the prevalence of elevated blood levels in children aged 1-2 years is 12%.

The CDC and AAP recommend targeted screening in all other areas in which a positive response is received to one or more of the following screening questionnaire items issued by the CDC:

  • Does your child live in or regularly visit a house that was built before 1950?

  • Does your child live in or regularly visit a house that was built before 1978 with recent or ongoing renovations or remodeling (within the past 6 mo)?

  • Does your child have a sibling or a playmate that has or did have lead poisoning?



Medication Summary

In patients with lead toxicity, the use of chelating agents is recommended for blood lead levels (BLLs) of 45 μg/dL or higher. Chelation can be started with oral succimer, or, if the patient is hospitalized, calcium disodium edetate (calcium EDTA) can be used. These agents have potential toxicities, and monitoring of the complete blood cell count, electrolytes, and liver function test results is necessary.

Chelating Agents

Class Summary

Chelating agents are the criterion standard for the treatment of patients with lead poisoning according to the blood lead levels (BLLs) discussed above. These agents bind to lead and promote its excretion. Patients receiving chelation therapy must be closely monitored because of the agents' potential toxicities.

Dimercaprol (BAL in oil)

Dimercaprol was first developed as an antidote for lewisite toxicity. It is water soluble and rapidly crosses the blood-brain barrier. Dimercaprol forms a nonpolar compound with lead that is excreted in bile and urine. It is the drug of choice in patients with acute lead encephalopathy, in whom the first dose is given and then the second dose is given combined with calcium EDTA after a 4-hour interval.

Edetate calcium disodium (Calcium Disodium Versenate)

This agent decreases blood lead concentration, reverses the hematologic effects of lead, and enhances the excretion of lead in urine.

Succimer (Chemet)

Dimercaptosuccinic acid (DMSA) is a water-soluble analog of dimercaprol. It causes a rapid decline in lead level and replenishes many of the sulfhydryl-dependent enzymes. In the absence of encephalopathy, patients may be treated with DMSA.

D-penicillamine (Cuprimine, Depen)

D-penicillamine is also known as D-dimethyl cysteine. It offers an alternative for oral treatment of lead poisoning. This agent is not approved by the US Food and Drug Administration (FDA) for use in lead poisoning, but has nonetheless been in use for more than 20 years.