Document Yj9QdMZyXjQok4Z7zB1bnE83k

DISCUSSION GUOUP on the SEDUCTION OP ENVIRONMENTAL EXPOSURE TO LEAD POISONING Matting of 26 May 1969 The Rockefeller Mnnity The following individuals have indicated their intention to attend: LAKHtt^ Jonathan T. , M.D# (Group Giainaa) Chairman, Department of Pediatrics State Univarsity Hospital Kings Connty Medical Canter Brooklyn, New York ALBERT, Boy B., M.D. Institute of Environmentar Medicine New York University Kadical Center 550 First Avn.Now York, New York 10016 BUXBAJOM, Joel Ni, M.D. School of Hadisina New York University Medical Center New York, New York CHASLESyOKTH, Dr* Building Beseareh Advisory Board National Research Connell Washington, D.C. CLASS, Kenneth, Professor Department of Electrical Engineering Polytechnic Institute of Brooklyn Brooklya, New York CONVEEY, Saa - Legal (ex paint chemist) National Lead Colony New York, New York BEMMIKG, Charles, Director Lawrence 0thing#r Beseareh Center U.S. Plywood-Champion Papers, Inc, Brewster, New York HOLTON, Arthur B., Vice President Sherwin-Williams Company Cleveland, Ohio 44101 KENT, Fred Asa't. Coon, of Health Eav. Health Services New York City Health Dept* 125 Worth St. Nov York, New York 10013 NEWTON, Robert C. Manager, Analytical Department Beseareh & Development Center Armstrong Cork Company Lancaster, Pennsylvania PLATOW, Raymond C., Vice President Beseareh & Development U.S. Plywood-Champion Papers, Ine. New York, New York SOUTH, L. OimfCrT""* New York, New York DILLON, Bohert M., Executive Director Sailding Beseareh Advisory Board National Beseareh Connell Washington, D.C. DODSON, Vance B. Director of Beseareh, Construction Materials Division Dewey & Alary Chemical Company Cambridge, Massachusetts N11870 0007-SWP-000005827 Cw.fKe.TC.'- '..I Nackctsi!-..* ' ivtisi:-. 4 * Synopsis of Mscl. .:! /-.rose;: til iOi'OCm k J. J.'iicn G.Ircir* Jr., //.. D Baltimore, rj. a 1 "ChiidhooJ Iced poisoning a preventable disec'.e. An e:::s::-.c program of prevention reeuircs two essential irgridients: A clear recognition as tne :cic,;ic factor: pno a cleor commitment of responsibility by physician, public health v.-o-bur, city official and arc used public to take concerted and effective action. The etiolocic pattern which can ultimately lead to irreversible load encephalo pathy consists cf a triad: The child, the parent end the piece. The ci.il.i is c toddler with exaggerated oral activities.' Use parent is a mother with inaccouc"; r.-source: tbs they emotional, intellectual, informational end/or economic) to cops with her family's needs. The place is a neglected slum housing unit with Ticking lead p:a--or*r paint within reach of a small child's grasp. Tire dynamic interaction of these factors will be disccssed, with the main emphasis on the environmental factors. In the young child, symptomatic acute lead intoxication is primarily a summertime disease: In the United States, approxi mately 30 to 85% of all cases occur between May and October. The disease is almost exclusively limited to pre-schooi children who live in houses built prior to 1940, many of which ore still h use end still contain layers of lead pigment point which have never been removed. Use principle sources of lead within such houses are the painted windowsills one door frames. Recent surveys in Baltimore indicate that 50 to 70% of oid houses in selected slum areas still contain dangerous quantities of flaking lead point. A few small chips of such point may contain lOOmgm or more of lead. (The safe daily intake of lead is less than 0.5 mgm.) The repetitive ingestion of a few small chips of such paint, if permitted to continue for more than three months, can lead to the absorption of a potentially lethal body burden of lead. Clinical manifestations tend to vary with both the age of the child and the magnitude of abnormal lead ingestion. Acute encephalopathy is mare common in children 15 to 30 months of age, while intoxication without encephalopathy in this age range usually presents as some form of hyperirritobie or aggressive behavior disturbance. Associated iron deficiency anemia is virtually clways present. The onset of acute encephalopathy fends to 0007-SWP-000005828 N11870.01 ;r. -i-s r. ... :'i r! ` ";-:tciy i!v v. .i. - 5". ? z'.zc:'z%-- - cvalusr-in. Astro - . *-i ! rui g- ~v:: _ .r, c -. era 'j L; !;:r avcic. Thus, *Se :v.-o to fisc-;1- e -cia v.'ifii -o-rgnicci sb-hiv:.. ,-.ay present v.-irh n convulsive ciscrdsr simi:!-.. ;-g id.ionsrhic epilepsy, rv.rjr.ic i.-.-puisive, eggressive i-ypsrkir--:'; behavior disorder i r.-o.-.ial rercrrlst!c:i. .Uncr-:r.:wi syndicates ir.ciu precressive'lo'is of mental furc;io.~. simulating degenerative cerebral c:s-.-sses end peripheral neuropathy. Since ti '.-re are r.z abnormal hies specific for lead intoxication on physical; exam ination and since routine examination of bloc: end urine is lik'ely to be unreveaiing, prempr diagnosis depends open a high index of suspicion on the port of the physicJor, end the per formance of certain specific laboratory tests. The most valuable of these is blood lead determination. For tepid presumptive diary r:is in the symptomatic child, the qualitative urinary cooroporphyrin test is most valuable and should be avail able in rho erne: geney ree"s of all hospitals serving high rid: populations. Prior to the advent of chelating agents, the me.-tclify from severe as'ure encephal opathy was approximately 66%-. With the cdvc.ntof first SAL end lefsr EDTA, this'mortality was reduced to approximately 33% it has recently been reported that the use of BAL end EDTA in combination, together with careful supportive therapy, can nopcrcntly reduce the mortality from acute lead encephalopathy to less than 5%. Nevertheless, the incidence of severe permanent broin damage among survivors of encephalopathy continues to be 25% or more. If survivors of on initial attack of acute lead encephalopathy ere retxpossd to abnor mal lead exposure, the incidence of severe permanent brain carnage is increased to virtually 1.00%. For this reason, the cornerstone of our current therapeutic program is prompt termina tion of environmental exposure to lead: No child with an increased body burden of lead is ever returned to a leaded home. In practical terms, this usually means brief hospitalization for treatment with BAL and EDTA followed by the administration of d-penici I lamina to the child in a convalescent home: during this time, suitable new housing is found fpr the family / or the abnormal lead sources are removed from the current home. In addition, upon return home, every effort is made to enroll the child in a nursery school or day cere center to provide the stimulation Which he needs: such stimulation usually terminates the child's pica. If the incidence of permanent injury to brain and possibly to kidney is to be substantially reduced, increased efforts must be directed toward uoily diagnosis prior to the onset of symptoms and ultimately to primary prevention of the disease. 2 .r v. v 0007 'SVIP-000005829 Currently, there i$ widc-spreca inrerccl application of techniques to the prevention of childhood plotnbiv:.-.. 7' ree t-icknicv.es v.hi ti: uio compsr- cble in cost ore currently available ond under irvt: ;;:ian. These include the defennii-.a- tion of S-aminolevulinic acid in mine. The rr.ajor :>-nblcm in the cppliccfic". of this :csr is the difficulty ir. obtaining landom urine samples -mptly from young chi Mian 12 to 24 months of age, who ore the patients ot greatest risk. Currently, the suiter.!!!:/ rf the determination of lead in heir is under intensive investigation. The technique recommends itself because of the ease of obtaining adequate samples of hair. Determination of load in blood is the most reliable. A venous blood sample is required. More sensitive methods for the determination of lead in'blood, preferably upon capillary samples of blood, would greatly facilitate this problem. Not only children, but also houses must be screened. Simple techniques ore available for this purpose. The cost of such procedures is small when compared With the cost of o single ccse of lead encephalopathy, which at the least will er.taii hospital ization for four to six weeks, not to mention the cost of long-range follow-up care, special educational facilities and, in the unfortunate few, permanent institutionalization. How much more intelligent it would be to spend our effort and substance on the systematic elimination of environmental lead exposure associated with old dwellings. Were this to be dene, childhood lead poisoning could be largely eradicated in the United States, as it apparently has been in Australia. For example, immediately following the birth of on infant of a family residing in a pre-World War II dwelling, the prospective dwelling could be inspected and sampled for lead, so that hazardous conditions could be corrected before the infant reaches the age of pica. 3 0007-SWP-000005830