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Development of children with elevated blood lead levels
Volume 81 Number 3
Letters to the Editor
627
Editorial correspondence
"Editorial Correspondence" or letters to the Editor relative to articles published in the JOURNAL or to topics of current interest are subject to critical review and to current editorial policy in respect to publication in part or in full.
Development o/children ~itb elefated blood lead lefels Letter 1 To the Editor: I read with interest the recent report of Kotok 1 describing the lack of significant difference in developmental scores between a group of children with elevated blood lead levels and a control group. Several comments appear to be in order. The report first alludes to an unpublished study2 describing a lack of neurologic sequelae following lead poisoning, including encephaIopathy, in 16 children. It would be most interesting to know how the deficiencies noted in adaptive and language function were related to "the mother-child relationship" to the point of excluding plumbism. Second, the difference in body lead burden between the control and lead-poisoned group in the published report may be more apparent than real. It is generally acknowledged that the blood lead "determination is less than an ideal screening test for subacute or chronic lead poisoning. It has been pointed out that the blood level represents "recent" exposure. 3 Moncrieff and Koumides~ suggested abandonment of preconceived ideas about the relationship of blood lead levels and toxicity. Studies just completed 5 underline this problem. Body lead burdens, as estimated from urinary lead excretion after chelating agents, were found by us to correlate poorly with blood lead levels in a group of clinically asymptomatic children. Third, nearly three fourths (72 per cent) of the control group were exposed to Chisolm's6 triad of factors causative in childhood lead poi-
soning: pica, dilapidated housing, and parents with inadequate resources. It therefore seems possible that, regarding their lead burden, the two groups were more equal than the mean lead levels would imply. The author's contention is that lead caused no developmental deficits in the lead-poisoned children. Perhaps the real lesson to be drawn from the study is that children with so-called "normal" blood lead levels may be at a risk equal to that of their brothers and sisters with higher blood lead levels. Phillip Nieburg, M.D. 401 Vandenberg St. Seymour ]ohnson Air Force Base, N. C. 27530 REFERENCES 1. Kotok, D.: Development of children with elevated blood lead levels: A controlled study, J. PEDIATR. 80"- 57, 1972. 2. Costeff, H., and Provence, S.: Development of children with lead poisoning. Unpublished. 3. Schroeder, H. A., and Tipton, I. H.: The human body burden of lead, Arch. Environ. Health 17: 965, 1968, 4. Moncrieff, A. A., and Koumides, O. P.: Lead poisoning in children, Arch. Dis. Child. 39: 1, 1964. 5. Nieburg, P. I., Oski, B. F., Cornfeld, D., and Oski, F. A.: The use of red cell-aminolevulinlc acid dehydrase activity as an index of body lead burden. In preparation. 6. Chisolm, J. J., Jr.: Lead poisoning, Sci. Am. 224: 15, 1971.
Replies To the Editor: Dr. Nieburg's comments underscore the complexities of evaluating the subsequent develop-
Letters to the Editor
627
Editorial correspondence
"Editorial Correspondence" or letters to the Editor relative to articles published in the JOURNAL or to topics of current interest are subject to critical review and to current editorial policy in respect to publication in part or in full.
Development o/children ~itb elefated blood lead lefels Letter 1 To the Editor: I read with interest the recent report of Kotok 1 describing the lack of significant difference in developmental scores between a group of children with elevated blood lead levels and a control group. Several comments appear to be in order. The report first alludes to an unpublished study2 describing a lack of neurologic sequelae following lead poisoning, including encephaIopathy, in 16 children. It would be most interesting to know how the deficiencies noted in adaptive and language function were related to "the mother-child relationship" to the point of excluding plumbism. Second, the difference in body lead burden between the control and lead-poisoned group in the published report may be more apparent than real. It is generally acknowledged that the blood lead "determination is less than an ideal screening test for subacute or chronic lead poisoning. It has been pointed out that the blood level represents "recent" exposure. 3 Moncrieff and Koumides~ suggested abandonment of preconceived ideas about the relationship of blood lead levels and toxicity. Studies just completed 5 underline this problem. Body lead burdens, as estimated from urinary lead excretion after chelating agents, were found by us to correlate poorly with blood lead levels in a group of clinically asymptomatic children. Third, nearly three fourths (72 per cent) of the control group were exposed to Chisolm's6 triad of factors causative in childhood lead poi-
soning: pica, dilapidated housing, and parents with inadequate resources. It therefore seems possible that, regarding their lead burden, the two groups were more equal than the mean lead levels would imply. The author's contention is that lead caused no developmental deficits in the lead-poisoned children. Perhaps the real lesson to be drawn from the study is that children with so-called "normal" blood lead levels may be at a risk equal to that of their brothers and sisters with higher blood lead levels. Phillip Nieburg, M.D. 401 Vandenberg St. Seymour ]ohnson Air Force Base, N. C. 27530 REFERENCES 1. Kotok, D.: Development of children with elevated blood lead levels: A controlled study, J. PEDIATR. 80"- 57, 1972. 2. Costeff, H., and Provence, S.: Development of children with lead poisoning. Unpublished. 3. Schroeder, H. A., and Tipton, I. H.: The human body burden of lead, Arch. Environ. Health 17: 965, 1968, 4. Moncrieff, A. A., and Koumides, O. P.: Lead poisoning in children, Arch. Dis. Child. 39: 1, 1964. 5. Nieburg, P. I., Oski, B. F., Cornfeld, D., and Oski, F. A.: The use of red cell-aminolevulinlc acid dehydrase activity as an index of body lead burden. In preparation. 6. Chisolm, J. J., Jr.: Lead poisoning, Sci. Am. 224: 15, 1971.
Replies To the Editor: Dr. Nieburg's comments underscore the complexities of evaluating the subsequent develop-