The New England Journal of Medicine -- May 10, 2001 -- Vol. 344, No. 19, pgs 1470-71

Primary Prevention of Childhood Lead Poisoning -- The Only Solution

Lead poisoning in children was first recognized in its severe acute form, known as lead encephalopathy. ( 1 ) This condition is characterized by seizures, coma, and -- not infrequently -- death, and it is associated with severe neurologic sequelae in survivors. Although lead encephalopathy has become rare in the past 15 to 20 years, the dangers of clinically asymptomatic lead poisoning in children have become increasingly clear. Longitudinal studies of development from birth to adolescence show that irreversible cognitive damage can occur with blood lead levels considerably lower than those typically associated with overt symptoms. ( 2 , 3 ) Recognition of this problem has led to routine screening programs and clear guidelines for the management of severe lead poisoning (defined by whole-blood lead levels of 45 g per deciliter or more). In contrast, the appropriate management of moderate lead poisoning (defined by whole-blood lead levels of 20 to 44 g per deciliter) remains uncertain.

In this issue of the Journal, Rogan et al. ( 4 ) report the results of a multicenter, randomized trial of an oral lead-chelating agent, succimer, in children whose blood lead levels were 20 to 44 g per deciliter. The performance of these children on several cognitive assessments was below average -- an observation consistent with previous reports of deficits in academic achievement, abstract thinking, attention span, conceptual reasoning, and visuospatial perception in children with moderately high blood lead levels. ( 5 ) Although chelation therapy lowered blood lead levels, it had no effect on any of the several neurobehavioral and cognitive measures used in the study. The study suggests that even with succimer therapy, the neurocognitive effects of chronically elevated blood lead levels and total-body lead burden are irreversible. Such irreversibility of developmental deficits due to neurotoxicity has been documented previously in children who did not receive chelation therapy. ( 6 , 7 )

Chelation therapy was initially introduced to manage severe, and frequently acute, lead poisoning that would most likely result in death or severe, overt neurologic sequelae in survivors. ( 1 ) In affected children, whose blood lead levels were often greater than 100 g per deciliter, chelating agents rapidly lowered blood lead levels by brisk diuresis and stopped the progression of lead poisoning to the point of frank encephalopathy. ( 8 , 9 ) This treatment saved lives but did not eliminate the neurologic consequences, which were permanent. Very rarely, if ever, does chelation therapy for such severe lead poisoning reverse or prevent the signs and symptoms of lead-induced neurotoxicity. Rather, the benefit of chelation therapy for children with severe acute or chronic lead poisoning is defined in relation to the terrible prognosis for children who are not so treated.

Chelation therapy is now used routinely in children who have blood lead levels of 45 g per deciliter or more, with the goal of preventing neurologic deterioration, lead encephalopathy, and death. However, there have been no clear guidelines from the Centers for Disease Control and Prevention or other advisory bodies regarding therapy for children with blood lead levels of 20 to 44 g per deciliter, ( 6 , 7 ) who were represented by the participants in the present study. ( 4 )

The study by Rogan et al. used the most promising chelating agent, succimer, and what was considered to be a highly effective dosing regimen. We believe it unlikely that any other study design, study population, chelating agent, or dosing regimen would produce a materially different result. Neurocognitive tests assessed measures characteristically affected by lead toxicity. The study population accurately reflected, both demographically and socioeconomically, the children at highest risk in urban communities in the United States.

The lack of efficacy of succimer for the prevention of neurotoxic harm due to moderate blood lead levels in the children in the study by Rogan et al. and the limited efficacy of chelation therapy in cases of severe lead poisoning clearly cast doubt on the value of public health programs that rely primarily on treatment after lead poisoning has occurred. Rogan et al. emphasize the importance of the primary prevention of lead poisoning, which is the only satisfactory solution to this devastating problem. The predominant source of toxic exposure to lead for children in urban areas is lead paint, ( 10 ) although some incremental but far less substantial toxicity may be due to other sources, such as tap water contaminated by lead pipes.

For the primary prevention of lead poisoning from paint, we recommend permanent abatement -- that is, the complete removal or replacement of lead paint before a child lives in a home. ( 11 , 12 ) In contrast, "interim" measures, which were introduced for the short-term reduction of hazards associated with lead paint ( 11 , 13 ) and which involve scraping and painting over deteriorated surfaces and controlling household dust, have been claimed by some to save substantial cost; however, there is no evidence of savings in terms of net benefit over cost in the long-term prevention of childhood lead poisoning. Lead-painted surfaces in good condition rarely remain so. What was once intact lead-based paint is the source of all lead-bearing dust and paint chips. Therefore, it is the presence of lead paint on surfaces that defines the hazard, not the condition of surfaces containing lead paint.

Although succimer therapy resulted in lower blood lead levels, its failure to reverse neurocognitive deficits in the study by Rogan et al. confirms the need for collective and concerted efforts to prevent lead poisoning in children.

John F. Rosen, M.D.
Paul Mushak, Ph.D.
Children's Hospital at Montefiore
Bronx, NY 10467


1. Chisolm JJ Jr. The use of chelating agents in the treatment of acute and chronic lead intoxication in childhood. J Pediatr 1968;73:1-38.

2. Bellinger DC, Stiles KM, Needleman HL. Low-level lead exposure, intelligence and academic achievement: a long-term follow-up study. Pediatrics 1992;90:855-61.

3. Burns JM, Baghurst PA, Sawyer MG, McMichael AJ, Tong SL. Lifetime low-level exposure to environmental lead and children's emotional and behavioral development at ages 11-13 years. Am J Epidemiol 1999;149:740-9.

4. 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 2001;344:1421-6.

5. Dietrich KN. Environmental neurotoxicants and psychological development. In: Yeates KO, Ris MD, Taylor HG, eds. Pediatric neuropsychology: research, theory, and practice. New York: Guilford Press, 2000:206-34.

6. Preventing lead poisoning in young children: a statement by the Centers for Disease Control -- October, 1991. Atlanta: Department of Health and Human Services, 1991.

7. National Research Council. Measuring lead exposure in infants, children, and other sensitive populations. Washington, D.C.: National Academy Press, 1993.

8. Preventing lead poisoning in young children: a statement by the Centers for Disease Control -- January 1985. Atlanta: Department of Health and Human Services, 1985.

9. Markowitz ME, Clemente I, Rosen JF. Children with moderately elevated blood lead levels: a role for other diagnostic tests? Environ Health Perspect 1997;105:1084-8.

10. Mushak P, Crocetti AF. Methods for reducing lead exposure in young children and other risk groups: an integrated summary of a report to the U.S. Congress on childhood lead poisoning. Environ Health Perspect 1990;89:125-35.

11. Department of Housing and Urban Development. Moving towards a lead-safe America: a report to Congress. Washington, D.C.: Office of Lead Hazard Control, 1997.

12. Needleman HL. Childhood lead poisoning: the promise and abandonment of primary prevention. Am J Public Health 1998;88:1871-7.

13. Environmental Protection Agency. 40 CFR 745. Lead: identification of dangerous levels of lead. Final Rule. Fed Regist 2001;66:1205-40.