Document qJKOgQ4exNgYZeLnBD9zNgpj

sooovodno u* & D O N 'T S A Y IT -WRITE IT N 27623 Reader Reaction 8. Albert RE, Shore KB, Sayers AJ, etal: Follow-up of children overexposed to lead. Environ Health Perspect 7:85L9, May 1974. g. Koenig H: FEP studies in normal newborns. To be published. 10. Perkins KC, Osld FA: Elevated blood lead in a 6-month-old breast-fed infant: The role of newsprint logs. Pediatries 67:426-7, 1976. 11. Sachs HK, Blanksma LA, Murray EF, et al: Ambulatory treatment of lead poisoning: Report of 1166 cases. Pediatrics 46:389-96, 1970. Consultant's replyi j . j u u an CHI SOLM, JR, MO, senior staff pedia trician, Baltimore (Md.) City Hos pitals; associate professor of pedi atrics, Johns Hopkins University School of Medicine, Baltimore. Dr, Magnus has addressed himself to a difficult and, as yet, unsettled ques tion: At what level of increase in lead absorption are the benefits of chelation therapy likely to outweigh its inherent risks in asymptomatic children? Also, are there other mo dalities of therapy that carry less risk? Recent studies in experi mental animals reveal that nutri tional factors are exceedingly im portant. A high fat intake, as well as dietary deficiencies of calcium, iron, copper, and zinc, increase the absorption and retention of lead in the body.1,2'3 It may not be gener ally recognized that the chelating agents used in the treatment of plumbism are not specific for lead. On the contrary, they mobilize and remove substantial amounts of other trace minerals, along with lead, including zinc, copper, and iron. For these reasons, I feel that control of exposure, proper house cleaning, and great emphasis on improved diet provide the most ju dicious therapeutic approach in the management of children with blood lead concentrations falling between 30-49 /4g/dl. It goes without saying that the single most important mo dality of therapy is the identifica tion of a particular child's source of excessive intake, followed by the prompt separation of the child from that source. It is also true that one needs to determine trends; there fore, serial measurement should be ,, made in such children in order to determine whether their blood lead concentrations either are stable, are falling, or are rising. The only evidence suggesting that blood lead concentrations in the 30-49 ftg/dl range may be followed by subtle impairment in learning and behavior comes from young an imals.4 There is no definitive evi dence on this point in children. Most of the reported human studies are retrospective and contain other im portant defects in design. One of the major deficiencies is the absence of serial blood lead measurements during early childhood. On the other hand, there is a general consensus that blood lead concentrations above 50-60 pg Pb/dl whole blood signify an unacceptable risk, particularly if associated with clear evidence of derangements in heme synthesis.4-5,6 One retrospec tive study in children provides evi dence that chelation therapy is ben eficial in those children with blood lead concentrations greater than approximately 60 pg/dl.7 It is clear that institution of che lation therapy after the onset of acute clinical symptoms in children does not uniformly prevent the oc currence of central nervous system sequelae. In my opinion, chelation therapy should be instituted prior to the onset of symptoms if con firmed blood lead levels exceed 50-60 pg/dl. This point may not have been clear in the original ar ticle in Patient Care. Occasionally, one does see asymptomatic patients Who have a very sharp rise in lead absorption associated with very brief exposure. If such brief overexposure can be promptly ter minated, then soft tissue lead levels will fall of their own accord without resort to chelation therapy. In most instances, however, overexposure is chronic, and chelation therapy would appear to be indicated. Dr. Magnus has suggested the more widespread use of the CaNaEDTA mobilization test. To obtain meaningful data, one should have timed quantitative collections and access to properly cleaned col lection bottles. Such bottles are usually cleaned with nitric acid, fol lowed by copious rinsing with dis tilled deionized water. In addition, diagnostic doses of CaN%EDTA should never be used in children -with clinical symptoms compatible with plumbism; if the symptoms are due to lead poisoning, a single diag nostic dose (sin exacerbate the illness. Alternate diagnostic tests and full therapeutic courses of che lation therapy should be used, in the hospital, in such patients. One should be cautious about the outpatient use of chelation therapy. There are now data in animals that indicate that even parenteral ad ministration of chelating agents can increase the absorption and reten tion of any excess lead that may be present in the intestinal tract.8 It is my strict policy to give chelation therapy on an outpatient basis only after the child has been separated from the abnormal sources of lead and a successful inpatient course has been completed. When using d-penicffiamine, I take the addi tional precaution to give the entire daily dose at 5-6 AM to ensure that the medication is given on an empty stomach. Past clinical experience indicates that outpatient therapy in a child with persistent pica can only make matters worse. Space does not permit a more detailed re sponse, However, the interested reader may find the references listed below of interest. 1. Klauder DS, Petering HG: Protective value of dietary copper and iron against some toxic effects of lead in rats. Environ Health Perspect 12:77-80, Dec 1976. 2. Cerklewski FL, Forbes RM: influence of dietary zinc on lead toxicity In the rat. J. Nv.tr 106:689-96, 1976. 8. Barltrop D, Khoo HE; The influence of nutritional factors on lead absorption. Postgrad Med 61:795-800, 1976. 4. Recommendations for the prevention of lead poi soning in children. Committee on Toxicology, Assem bly of Life Sciences Rational Research Council, Na tional Academy of Sciences, Jul 76. 5. Zielhuis RL: Dose-response relationships for inor ganic lead. I. Biochemical and haematological re sponses. Int Arch Occup Environ Health 36:1-18, 1976. 6. Zeilhuis RL: Dose-response relationships for inor ganic lead. II. Subjective and functional responses-- chronic sequelae---no-response levels. Int Arch Occup Environ Health 35:19-415, 1976. 7. Albert RE, Shore RE, Sayers AJ, et al: FpUow-up of children overexpo&ed to lead. Environ Health Penpect 7:83-9, May 1974. 8. Jugo S, Maljkovic T, Kostial K: Influence of che lating agents on the gastrointestinal absorption of lead. Toxicol Appl Pharmacol 34:299-63, 1976. DUP040008128 N 27623.01 PATIENT CARE / APRIL 1,1977