Managing Elevated Lead Levels
When Parents Turn to You For Help
A PARENT ASKS:
My child’s previous pediatrician told me that my 4-year-old daughter has a high lead level. She was tested 3 times in the last year. The lead values were 7, 12, and most recently 10 µg/dL. She is otherwise healthy and does not eat paint chips. Why is her lead level high, and what can I do about this?
THE PARENT COACH ADVISES:
Lead exposure in children has seen a significant decline over recent years in the United States, mainly due to federal regulation of lead-based paint and leaded gasoline. Despite improvements, many children nevertheless remain at risk, and lead exposure still is common. From 1999 to 2004, 1.4% of U.S. children had blood lead levels (BLLs) greater than 10 µg/dL, and the large majority had some source of low-level exposure.1
The dangers of exposure.
An increasing number of studies highlight the continued risk of lead exposure in children, and it is now believed that no BLL can be considered safe. At levels of 60 to 100 µg/dL, lethargy is seen with vomiting, anorexia, and decreased consciousness.2 However, children are asymptomatic at lower lead levels, and the subclinical effect on childhood intelligence continues to be a great concern. In 1994, a systematic review of 26 studies3 examined the variability in intelligence quotient (IQ) scores compared against blood lead concentration in children. The authors reported that increases in lead levels were associated with a decrease in IQ by 5 years of age. Moreover, a decrease in IQ score of 1 to 2 points was seen for each doubling in serum lead concentration. Additional studies have revealed cognitive impairment at BLLs below 10 µg/dL, even in children as young as 3 years of age.4 Lead exposure also has neurologic effects as evidenced by changes in childhood behavior: Children younger than 5 years with BLLs of 15 µg/dL or greater had a significant increase in maternal-reported maladaptive behavior.5 Elevated bone lead levels in older children were associated with greater aggression and antisocial behavior as judged by parents and teachers in one retrospective cohort study.6
How are children exposed?
While lead-based paint was banned in the United States in 1977, it is still present in approximately 38 million homes.2 Lead paint can easily contaminate dust and soil as it chips off or is removed during remodeling and repainting. Children are exposed either by eating paint chips or by dust through hand-to-mouth contact and putting toys or other objects in the mouth. Lead-containing dust is the most common source for exposure in children with BLLs between 10 and 25 µg/dL.7 Other sources of exposure include lead pipes and plumbing in older buildings, which create elevated lead concentrations in drinking water.2 No regulations are in place for monitoring the content in drinking water from private wells, which also presents a potential source. Prevention programs funded by the Centers for Disease Control and Prevention (CDC) have found that lead in traditional medicines,8 imported toys,9 and the clothes of working parents9 also are responsible for elevated BLLs in some children. Other possible sources include imported cosmetics and cookware.9 Vinyl mini-blinds also may break down and create lead dust after extended time in the sunlight.9
Who is at greatest risk?
Data from the Third National Health and Nutrition Examination Survey have identified several groups at high risk for lead exposure. These include persons living in homes built before 1946, persons living in urban areas, African American children, and families with low income.10 Additionally, children enrolled in Medicaid accounted for approximately 60% of those with elevated BLLs from 1991 to 1994,1 emphasizing the importance of screening in this population.
What can be done to avoid exposure?
If a home was built before 1978 and houses children younger than 6 years, families should consider having it tested through their state or local health department. Home test kits are available for purchase, but the federal government does not recommend them.11 Lead-based paint is dangerous when it is flaking from walls or other surfaces. It is very important to ensure that children in the home do not have access to paint chips and are unable to reach or chew on painted surfaces such as windowsills. It is also important to wash hands and toys regularly to decrease the ingestion of lead-containing dust. Because the soil outside of homes may be a source of exposure, children should play in grassy or mulched areas and avoid activity directly on the soil.9 A well-balanced diet that is high in calcium and iron is recommended to decrease lead absorption from the gastrointestinal tract.2
Approach to the patient with elevated lead levels.
BLLs usually decline when children reach about 2 years of age, corresponding to a decrease in normal mouthing behaviors. A persistently elevated BLL in a child older than 2 years is unusual; in this scenario, a detailed history of the child’s exposure is recommended, and environmental investigation by the state or local health department is warranted. Parents should be counseled to evaluate the sites where the child spends significant time, and they should be educated about common lead sources, the health risks of exposure, and changes in nutrition. BLLs should be tested again 3 months after the intervention. CDC guidelines now use a reference level of 5 µg/dL to identify children with elevated BLLs, a decrease from 10 µg/dL used in previous years. If serum lead levels remain elevated, less-common sources of exposure should be considered. The CDC recommends an environmental investigation of exposure sources be among the first steps in management when lead levels range from 20 to 44 µg/dL.9 The serum lead level then should be retested within 1 to 3 months. At levels 15 µg/dL or above, contacting lead poisoning prevention programs can help the family with home inspections and other services.9 When BLLs are 45 µg/dL or above, chelation with succimer is recommended within 48 hours, along with a complete neurologic examination. The use of chelation therapy in children with lead levels less than 45 µg/dL has not been shown to be beneficial to cognitive function and is not recommended.2,9
1. Jones RL, Homa DM, Meyer PA, et al. Trends in blood lead levels and blood lead among US children aged 1 to 5 years, 1988-2004. Pediatrics. 2009;123(3):e376-e385.
2. Chandran L, Cataldo R. Lead poisoning: basics and new developments. Pediatr Rev 2010;31(10):399-406.
3. Pocock SJ, Smith M, Baghurst P. Environmental lead and children’s intelligence: a systematic review of the epidemiological evidence. BMJ. 1994;309(6963):1189-1197.
4. Canfield RL, Henderson CR Jr, Cory-Slechta DA, Cox C, Jusko TA, Lanphear BP. Intellectual impairment in children with blood lead concentrations below 10 µg per deciliter. N Engl J Med. 2003;348(16):1517-1526.
5. Sciarillo WG, Alexander G, Farrell KP. Lead exposure and child behavior. Am J Public Health. 1992;82(10):1356-1360.
6. Needleman HL, Riess JA, Tobin MJ, Biesecker GE, Greenhouse JB. Bone lead levels and delinquent behavior. JAMA. 1996;275(5):363-369.
7. Lanphear BP, Matte TD, Rogers J, et al. The contribution of lead-contaminated house dust and residential soil to children’s blood lead levels: a pooled analysis of 12 epidemiologic studies. Environ Res. 1998;79(1):51-68.
8. Centers for Disease Control and Prevention. Childhood lead poisoning associated with tamarind candy and folk remedies—California, 1999-2000. MMWR Morb Mortal Wkly Rep. 2002;51(31):684-686.
9. Centers for Disease Control and Prevention. Managing Elevated Blood Lead Levels Among Young Children: Recommendations From the Advisory Committee on Childhood Lead Poisoning Prevention. Atlanta, GA: Centers for Disease Control and Prevention, US Dept of Health and Human Services; 2002.
10. Pirkle JL, Kaufmann RB, Brody DJ, Hickman T, Gunter EW, Paschal DC. Exposure of the U.S. population to lead, 1991-1994. Environ Health Perspect. 1998;106(11):745-750.
11. US Environmental Protection Agency. Testing Your Home for Lead in Paint, Dust, and Soil. Washington, DC: US Environmental Protection Agency; 2000. EPA publication 747-K-00-001.