• The most common pediatric environmental health problem involves a systemic intoxication by the heavy metal, lead; most commonly this is with inorganic lead.
• Children in the U.S. are predominantly exposed to lead through ingestion of paint chips and contaminated housedust and soil from deterioration of pre-1980 housing and buildings.
• The Centers for Disease Control and Prevention (CDC) considers a blood lead level of 10 µg/dL or higher to represent undue lead exposure and absorption; a level of 20 µg/dL or higher is generally considered to constitute lead poisoning.

• Lead adversely effects many organ systems including the neurological (encephalopathy, peripheral neuropathy in adults, subtle neuropsychological effects), hematological (anemia due to several mechanisms), gastrointestinal (abdominal colic), renal (proximal renal tubular injury leading to Fanconi syndrome), and reproductive systems.
• Many of the toxic effects result from inhibition of enzymes involved in heme biosynthesis, as the electropositive metal binds to the negatively charged sulfhydryl groups on the active sites of delta-aminolevulinic acid dehydratase (ALA-D), ferrochelatase, porphobilinogen synthase, coproporphyrinogen oxidase, and other enzymes. Divalent lead also acts competitively with calcium in various biologic systems and lead affects nucleic acids.
• Children absorb lead more efficiently from the gastrointestinal tract and are more likely to ingest lead through hand-to-mouth activity as compared to adults.
• As the developing, immature central nervous system is susceptible to the toxic effects of lead, the neuropsychological effects of lead poisoning upon young children have been of particular concern.

• Prevalence of elevated lead levels and geometric mean blood lead level (BLLs) have decreased significantly in the last 20 years.
• Almost 1,000,000 American children aged 1 to 5 years (4.4% of a representative national sample) are estimated to have BLLs of 10µg/dL or higher.
• Higher prevalence occurs among children aged 1 to 3 years, African-American andMexican-American children, those from lower income families, those living in metropolitan areas with populations of one million or greater, and those living in older housing.
• Approximately 86% of American pre-1980 publicly owned housing units and 83% of privately owned units contain some lead-based paint.

• Acute encephalopathy
• Seizures
• Coma
• Death (predominantly due to cerebral edema)
• Mental retardation
• Cognitive, behavioral, attentional, and neurodevelopmental impairment
• Anemia
• Fanconi syndrome

• In general, there is an increased risk for long-term neuropsychological sequelae, which increases with lead exposure and absorption that is more intense, of longer duration, and begins at an early age when the central nervous system is still maturing.
• Recurrent episodes of symptomatic lead poisoning increase the risk for permanent sequelae.
• More subtle effects may not be detected until school entry.

• Most lead poisoning in children is asymptomatic.
• Head encephalopathy should be considered in the differential diagnosis of a child presenting with seizures, altered mental status, and/or coma.
• Lead poisoning should also be considered in the differential diagnosis of mental retardation, behavioral disorders, and anemia.

Question: Exposure to a source of lead?
Significance: The most common sources of lead include residence in or visitation of older, deteriorated housing, a parental occupation or hobby involving lead exposure, use of remedies or cosmetics containing lead, and ingestion of contaminated water, food, or beverages.

Question: Typical symptoms?
Significance: Although many of the clinical manifestations of symptomatic lead poisoning are non-specific, a cluster of complaints including anorexia, intermittent abdominal pain, constipation, sporadic vomiting, change in mental status (such as irritability or lethargy), decreased play activity, and change in developmental status (particularly with regression of developmental milestones) may herald this condition.

Question: Lead encephalopathy?
Significance: Can present with change in consciousness, ataxia, persistent vomiting, seizures, and coma; often this presents after a prodrome of the previous symptoms.

Question: Anemia or developmental delay?
Significance: Result of lead poisoning.

• Not generally helpful at lower lead levels. Symptomatic and/or encephalopathic patients may have acute gastrointestinal, neurological, hematological, and systemic manifestations.
• Assess for clinical evidence of developmental delay.
• Burton gum lead line: A blue-gray discoloration at the gum-tooth interface typically along the lower incisors rarely can be seen in the setting of chronic, fairly high lead exposure and poor dental hygiene.

Test: Blood lead test, either venous or capillary.
Significance: Compare result with CDC classification system. Results may be reportable to local health authorities. Is only a measure of recent lead exposure; does not indicate total body burden of lead.

Test: Complete blood count
Significance: To assess for anemia. Anemia is seen in lead poisoning starting at about 60 µg/dL from globin and heme synthesis inhibition and hemolysis. Iron deficiency anemia is often seen concomitantly. Anemia related to lead toxicity is typically normocytic and normochromic; a microcytic, hypochromic anemia may be seen with a mixed etiology. Basophilic stippling is sometimes seen on peripheral blood smear.

Test: Free erythrocyte protoporphyrin (FEP) and other blood and urine markers
Significance: Markers of lead-induced inhibition of heme synthesis. FEP can be useful clinically to follow the recovery from heme synthesis inhibition during management.

Test: Abdominal radiograph
Significance: Looking for radio-opaque foreign material suggestive of ingestion of lead paint chips or other lead-containing foreign body.

Test: Long bone x-rays
Significance: To look for “lead lines” or metaphysical sclerosis, characterized by increased density along transverse lines in the metaphyses of growing long bones representing increased mineralization due to interference with the metabolism of bone matrix.

Test: X-ray fluorescence for estimation of body lead burden
Significance: This has been used mainly in experimental settings.

• Environmental management, which includes removing children from the lead source(s), should occur when venous lead levels are recurrently 15 to 19 µg/dL (CDC Class IIB) and when levels are greater than or equal to 20 µg/dL (CDC Class III).
• Chelation therapy should complement environmental management in all children with venous levels of 45 µg/dL (CDC Class IV) or higher, using parenteral calcium disodium ethylenediamine tetraacetate (EDTA; also calcium disodium versenate) or oral agents such as meso 2,3-dimercaptosuccinic acid (DMSA, succimer, Chemet). Chelation of children with levels in the 25 to 45 µg/dL range may be considered in certain cases although it is not routinely recommended. Outpatient therapy can take place if a lead-safe environment has been identified and compliance is expected. Succimer is given at 10 mg/kg/dose (or 350 mg/m²/dose) every 8 hours for 5 days, then every 12 hours for 14 more days. Weekly monitoring for neutropenia, platelet abnormality, and increased liver enzymes is recommended. Succimer is more lead-specific than other chelators and causes less mineral depletion.
• Children with symptomatic lead poisoning or with levels of 70 µg/dL (CDC Class V) or higher should be admitted immediately to a hospital for parenteral chelation with both intramuscular dimercaprol (BAL or British anti-Lewisite) and intravenous or intramuscular calcium disodium EDTA. As there are many issues involved with administration of both chelating agents, consultation of appropriate guidelines and pharmacological information is recommended. Children with encephalopathy constitute a medical emergency and should receive the preceding treatment in an intensive care setting with attentive neurosurgical support. Consultation with a clinician experienced in lead toxicity treatment is advised for these patients.
• Ingested lead-containing foreign bodies should be evacuated with whole bowel irrigation using a high molecular weight glycol solution.
• Nutritional support with calcium and iron supplementation should be given if intake is inadequate; deficiencies of these increase lead absorption from the gastrointestinal tract. Iron supplementation should be withheld during chelation therapy.

• Prompt environmental follow-up of current lead exposure situations and vigilance for additional exposure (with family moves, visitation of new residences, etc.) should occur.
• Follow-up of elevated venous levels from 10 to 19 µg/dL (CDC Class IIA, IIB) approximately every 3 to 4 months.
• Follow-up of venous levels of 20 µg/dL or higher at 1 to 2 month intervals until no additional lead exposure is present and levels have decreased.

• Primary prevention: removal of potential environmental lead hazards.
• Secondary prevention: screening for elevated lead levels. Since 1997, CDC has recommended that state and local health departments make the determination for a universal versus targeted screening approach. Screening is recommended by use of a blood lead test for children at ages 1 and 2 and for those of 36 to 72 months of age without previous screening.
  • Universal screening for communities where the risk for lead exposure is widespread and where 12% or more of children aged 12 to 36 months have lead levels of 10 µg/dL or higher and/or 27% or greater of the housing stock was built prior to 1950.
  • Targeted screening for communities not meeting above criteria. Screening would be indicated for children meeting local criteria for screening such as residence in a specified geographic area, membership in a high-risk group, or a high risk status as determined by the use of a personal-risk questionnaire.
• Tertiary prevention: case management and environmental remediation for children with lead poisoning. Closer attention to the first 2 modes of prevention should obviate the need for this.

• Abatement of building-based (residential) lead hazards by removal or enclosure of lead-containing structures.
• Control of environmental lead dust exposure and ingestion by good housekeeping (wet dusting and mopping of household dust) and personal hygiene (cleaning of child’s hands, toys, personal items, etc.).
• Removal of any other known lead source from the child’s environment.

• Delay in checking a blood lead test in the presence of clinical signs or symptoms of lead poisoning or neuropsychological disorders.
• Failure to inquire about lead exposure possibilities, especially of non-urban children.

Q: What is lead abatement?
A: Lead abatement is removal of a lead hazard from the environment either by replacing it (e.g., installing a new window), enclosing the area with the lead source (e.g., installing paneling), removing the lead-based paint from a surface (burning or dry sanding methods should never be used), or encapusulating the area (placement of a specific coating over the lead-containing surface, which prevents access to the lead hazard).

Q: Is lead abatement permanent?
A: Often the lead paint that is chipping or peeling is removed from a home. Any areas with intact lead-based paint may become deteriorated with aging, leading to new lead hazards.

Q: Why didn’t my child’s brother or sister get lead poisoned at the same age, as he/she lived in the same house?
A: Children are different; some do much more hand-to-mouth activity than others, which is the main way that children get lead into their bodies. Also, your home may not have had the same lead dangers (hazards) when the sibling was younger.

American Academy of Pediatrics Committee on Drugs. Treatment guidelines for lead exposure in children. Pediatrics 1995;96:155–160.

American Academy of Pediatrics Committee on Environmental Health. Screening for elevated blood lead levels. Pediatrics 1998;101:1072–1077.

Centers for Disease Control and Prevention. Screening young children for lead poisoning: guidance for state and local public health officials. US Dept of HHS, 1997.

Centers for Disease Control and Prevention. Update: blood lead levels—United States, 1991–94. MMWR 1997;46:141–146.

Chisolm JJ, O’Hara DM, eds. Lead absorption in children: management, clinical, and environmental aspects, 1st ed. Urban & Schwarzenberg, Baltimore-Munich: 1982.

Pueschel SM, Linakis JG, Anderson AC, eds. Lead poisoning in childhood. Baltimore: Paul H. Brookes Publishing Co., 1996.