AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Childhood lead poisoning is a worldwide problem. Although recent data continue to demonstrate a decline in the prevalence of elevated blood lead levels (BLL) in children in the industrialized world, lead remains a common, preventable, environmental health threat.

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.

In 1904, Gibson concluded that lead paint in the home was responsible for poisoning children. Despite this, lead was not banned from American household paints until 1978. 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. Toddlers often place objects in their mouths, resulting in ingestion of dust and soil and, possibly, an increased intake of lead. The 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, which renders them more susceptible to the effects of lead.

Lead poisoning in children has been the focus of many researchers. The American Academy of Pediatrics (APP) currently defines lead poisoning as a venous BLL equal to or higher than 10 mcg/dL (0.50 µmol/L). This level, which was originally intended to trigger community-wide prevention strategies, has often been misinterpreted as a definitive toxicologic threshold. Recent studies have indicated intellectual impairment in children with BLLs of less than 10 µg/dL. However, the lack of a specific BLL cutoff for adverse effects, the rather small sample size of these studies, and the absence of effective clinical or public health interventions that reliably and consistently lower BLLs that are already less than 10 µg/dL have made the Centers for Disease Control's (CDC's) Advisory Committee on Childhood Lead Poisoning Prevention keep the current level of concern at BLLs equal to or higher than 10 µg/dl.

Pathophysiology

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 (eg, 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 found in leaded gasoline, 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 adds little lead burden to the body in children. Lead particles are frequently large and coughed up. However, because children do not expectorate well, these particles are likely to travel up the mucociliary system and be swallowed, allowing for some absorption. Lead toxicity may also develop in adolescents who sniff leaded gasoline recreationally.

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.

Frequency

United States

According to the National Health and Nutrition Examination Survey (NHANES), from 1999-2002, the overall prevalence of elevated BLLs for the US population aged 1 year or older was 0.7%, a decrease of 68% from 2.2% in the 1991-1994 survey. In addition, the prevalence of elevated BLLs in children aged 1-5 years of age, who had the highest prevalence, was 1.6%, a decrease of 64% from 4.4% in the 1991-1994 survey. Children in minority populations, from low-income families, and who live in older homes are particularly at risk.

International

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

Mortality/Morbidity

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.

Race

Overall, from 1999-2002, non-Hispanic blacks and Mexican Americans had higher percentages of elevated BLLs (1.4% and 1.5%, respectively) than non-Hispanic whites (0.5%).

Age

Lead poisoning chiefly affects children younger than 6 years and adults in lead-risk occupations.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

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 symptoms
• • Anorexia
  • Vomiting
  • Constipation
  • Abdominal pain
• Neurobehavioral changes
• • Inattentiveness
  • Distractibility
  • Impulsiveness
  • Learning problems
• Peripheral nervous system effects (rare in children)
• • Weakness
  • Peripheral palsies

Physical

No specific physical signs exist for lead poisoning.

• Pallor (due to associated anemia)
• Hyperactivity
• Signs of increased intracranial pressure
• • Impaired consciousness
  • Bradycardia
  • Hypertension
  • Respiratory depression
  • Papilledema
  • Coma

Causes

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, and welding. Workers should be instructed to change their working clothes at work.
• Inadequate nutrition, such as a diet deficient in iron, may promote lead absorption.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Heavy metals poisoning

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• 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 that may be present in co-ingestions.
• A complete blood count may reveal hypochromic microcytic anemia. Basophilic stippling of the erythrocytes, which is characteristic of lead poisoning, is uncommon in children.
• Perform a urinalysis. Children may appear mildly dehydrated with concentrated urine and poor appetite. This can be the beginning for the development of inappropriate secretion of antidiuretic hormone.
• Whole BLL is the criterion standard for confirming the diagnosis of lead poisoning. A BLL of 10 mcg/dL or higher denotes 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.
• Erythrocyte protoporphyrin (EP) may be obtained in selected patients: Lead toxicity affects heme synthesis at several steps, including 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.
• In Russia, hair sample is the standard for lead poisoning screening. However, recent 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 often is helpful.
• Computerized tomography: Head CT may be needed in patients who present with altered mental status to exclude cerebral edema and structural lesions.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

Treatment of lead toxicity follows several parameters: prevention of further lead exposure, decontamination, chelation, and supportive therapy.

• Prevention of further lead exposure
• • 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.
  • 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.
• Decontamination
• • 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. This procedure 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.
• Chelation
• • The AAP does not recommend the use of chelating agents for venous lead levels of less than 45 mcg/dL.
  • Further information on the use of chelating agents is available in Medication.
• 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 (ICP) and pursue measures to decrease the ICP (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.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

The use of chelating agents is not recommended for BLL less than 45 mcg/dL. In 2005, the AAP Committee on Environmental Health issued the following guidelines for screening and treatment of elevated BLL:

• BLL <10 mcg/dL: No action is required.
• BLL 10-14 mcg/dL: Obtain a confirmatory venous lead level within 1 month. If the BLL is still within this range, patient education about lead exposure is needed, and the BLL test should be repeated in 3 months.
• BLL 15-19 mcg/dL: Same as #2, but repeat the BLL in 2 months.
• BLL 20-44 mcg/dL: Obtain a confirmatory venous BLL in 1 week. If the BLL is still within this range, assess complete medical, nutritional, and environmental hazards. Environmental evaluation by the local health department is also needed. A 2001 large-scale study reported no improvement in neurologic and behavioral test scores after succimer chelation of children with BLL in this range.
• BLL 45-69 mcg/dL: Obtain a confirmatory BLL within 2 days. If still within this range, undergo complete evaluation as in #4. At this level, chelation therapy is recommended. Treatment should be in a lead-free environment. If this is not possible, hospitalization is necessary. 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 CBC, electrolytes, and LFTs is necessary.
• BLL >70 mcg/dL: Hospitalize, obtain a confirmatory venous BLL, and initiate chelation with dimercaprol and calcium 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 CNS. Pretreatment with dimercaprol (which crosses the blood-brain barrier) is recommended.

Drug Category: Chelating agents

Chelating agents are the criterion standards for the treatment of patients with lead poisoning according to the BLL mentioned above. These agents bind to lead and promote its excretion. Patients receiving chelation therapy must be closely monitored because of the agents' potential toxicities.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Closely monitor cardiovascular and mental status.
• Maintain an adequate urine output.
• Assess renal and hepatic functions.
• Diphenhydramine may help alleviate the adverse effects of British antilewisite (BAL).
• Iron supplementation should be avoided in patients receiving BAL chelation therapy because BAL forms a complex with iron, leading to toxicity.

Further Outpatient Care

• All children being treated for lead poisoning need close follow-up care. Monitoring their BLL is important.

In/Out Patient Meds

• Outpatient treatment seems a good option for asymptomatic children with blood levels in the range of 45-69 mcg/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.

Transfer

• 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.

Deterrence/Prevention

• Primary prevention: 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.
• Secondary prevention: The CDC and AAP have issued recommendations regarding screening for lead poisoning as follows:
• • Universal screening - In areas where at least 27% of houses were built before 1950 and places where the prevalence of elevated blood levels in children aged 1-2 years is 12%
  • Targeted screening - In all other areas when 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 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?

Complications

• Lead-related deaths have become extremely rare since the advent of lead screening measures and decreased use of lead.
• Sequelae of lead intoxication include retardation and growth failure.

Prognosis

• Prognosis depends on the 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. Recent research has demonstrated that cognitive defects may occur at levels below the currently accepted BLL of 10 mcg/dL.
  • 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 mcg/dL.

Patient Education

• For excellent patient education resources, visit eMedicine's Poisoning Center. Also, see eMedicine's patient education article Poisoning.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to recognize lead poisoning in a symptomatic patient
• Inadequate screening measures, with the treating physicians not targeting the high-risk population
• Failure to secure the airway before the initiation of gastric lavage in an obtunded child with acute lead ingestion

Special Concerns

• Significant intravascular hemolysis may occur in patients with G-6-PD deficiency who are receiving BAL as a chelating agent.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• American Academy of Pediatrics Committee on Environmental Health. Lead exposure in children: prevention, detection, and management. Pediatrics. Oct 2005;116(4):1036-46. [Medline]. [Full Text].
• American Academy of Pediatrics Committee on Environmental Health. Lead. In: Handbook of Pediatric Environmental Health. American Academy of Pediatrics. Elk Grove Village, Ill. 1999:131-143.
• CDC. Preventing Lead Poisoning in Young Children. Atlanta, Ga:. CDC, United States Department of Health and Human Services;1991. [Full Text].
• CDC. Screening Young Children for Lead Poisoning. Guidance for State and Local Public Health Officials. Atlanta, Ga:. CDC, United States Department of Health and Human Services;1997. [Full Text].
• Canfield RL, Henderson CR, Cory-Slechta DA, et al. Intellectual impairment in children with blood lead concentrations below 10microg per deciliter. N Engl J Med. Apr 17 2003;348(16):1517-26. [Medline].
• Florin TA, Brent RL, Weitzman M. The need for vigilance: the persistence of lead poisoning in children. Pediatrics. Jun 2005;115(6):1767-8. [Medline].
• Graeme KA, Pollack CV. Heavy metal toxicity, part II: lead and metal fume fever. J Emerg Med. Mar-Apr 1998;16, No.2:171-177. [Medline].
• Koller K, Brown T, Spurgeon A, Levy L. Recent developments in low-level lead exposure and intellectual impairmentin children. Environ Health Perspect. Jun 2004;112(9):987-94. [Medline].
• Lanphear BP, Winter NL, Apetz L, et al. A randomized trial of the effect of dust control on children''s blood lead levels. Pediatrics. Jul 1996;98(1):35-40. [Medline].
• Lanphear BP, Hornung R, Ho M. Screening housing to prevent lead toxicity in children. Public Health Rep. May-Jun 2005;120(3):305-10. [Medline].
• Markowitz M. Lead poisoning. Pediatr Rev. Oct 2000;21(10):327-35. [Medline].
• Moss ME, Lanphear BP, Auinger P. Association of dental caries and blood lead levels. JAMA. Jun 23-30 1999;281(24):2294-8. [Medline].
• Rogan WJ, Dietrich KN, Ware JH, et al. The effect of chelation therapy with succimer on neuropsychological development in children exposed to lead. N Engl J Med. May 10 2001;344(19):1421-6. [Medline].
• Schaffer SJ, Campbell JR. The new CDC and AAP lead poisoning prevention recommendations: consensus versus controversy. Pediatr Ann. Nov 1994;23(11):592-9. [Medline].
• Tong S, von Schirnding YE, Prapamontol T. Environmental lead exposure: a public health problem of global dimensions. Bull World Health Organ. 2000;78(9):1068-77. [Medline].

Article Last Updated: Apr 20, 2006