Document mBRQwV22V47zLyNExg9y5EdyB

. DISCUSSION GUOUP on the . REDUCTION OP ENVIRONMENTAL EXPOSURE TO LEAD POISONING Heating of 23 Map 1939 The Rockefeller University Tho following individuals have indicated their intention to attend: LANMAK, Jonathan T., M.D. (Group Chairman) Chairman, Department of Pediatrics .. State University Hospital Sings County Medical Center Brooklyn* New York ALBERT, Roy B., H.D. Institute of SaviraBmentaT Medicine New York University Medical Center 550 First Ave.- . New York, New York 10018 saxsm!, Joel Ni, M.D. School of Medicine . New York University Medical Center New York, New York . CHARLSSUDRTH, Dr* Building Research Advisory Board National Research Council Washington, D.C CLARK, Kenneth, Professor Departaeat of Electrical Engineering Polytechnic Institute of Brooklyn Brooklyn, New York ' BEMMIKG, Charles, Director Lavereaee Ottinger Research Center U.S* Plywood-Champion Papers, Inc* Brewster, New York HORTON, Arthur B., Vice President Sherwin-Williams Company Cleveland, Ohio 44101 KENT, Fred Ass't* Comm, of Health Env. Health Services New York City Health Dept. 125 Worth St. Now York, New York 10013 NEWTON, Robert C. Manager, Analytical Department Research & Development Center Armstrong Cork Company Lancaster, Pennsylvania PLATOV/, Raymond C., Vice President Research & Development U.S. Plywood-Champion Papers, Inc. New York, New York CONVERT, Saa - Legal (ex paint chemist) National Lead Company New York, Now York SJffiHl, L. OllvCfTSr. New York, New York . DILLON, Robert M., Exeemtive Director Building Research Advisory Board National Research Council Washington, D.C. DODSON, Vance H. Director of Research, 'Construction Materials Division . Dewey & Almy Chemical Company Cambridge, Massachusetts N11870 0007-SWP-000005827 - Cor.ferenc.'- Laua Rackets!!.-- ' ivtisi:-- d* A Synopsis of Msc.!. Aspect: : ' J. J.'lic" Oiirc:." Jr., IA. D. Solti.-noie, ;.y. ' J ' "Childhood lead poisoning a preventable disease. An e::':sti-.c program of prevention requires two esssnriel ingredients: A clear recognition a: :bc ;clogic factor: and a clear commitment of responsibility by physician, public health wo-iter; city official and aroused public to take concerted and effective action. The etiologic pattern which can ultimately lead to irreveisiUe lead encephalo pathy consists of a triad: Tiie child, the parent and the piece. The child Is c tcddler with exaggerated oral activities.' Tire parent is a mother with inadcauu.-n r.scurcs: tbs they emotional, intellectual, informational and/or econcmic) to cope -.vi:h nor family's needs. The place is a neglected slum housing unit with flowing lead c:g--paint within reach of a small child's grasp. Tire dynamic interaction of these factors will be discussed, with the main emphasis on the environmental factors. In the young child, symptomatic acute lead intoxication is primarily a summertime disease: In the United Sfotes, approxi mately 80 to 85% of all coses occur between May and October. The disease is almost exclusively limited to pre-school children who live in houses built prior to 1940, many of which are still in use and still contoin layers of lead pigment paint which have never been removed. Hie principle sources of lead within such houses are the painted windowsills end door frames. Recent surveys in Baltimore indicate that 50 to 70% of aid houses in selected slum areas still contain dangerous quantities of flaking lead paint. A few small chips of such paint may contain 100mgm 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 more common in children 15 to 30 months of age, while intoxication without encephalopathy in this oge range usually presents as some form of hyperirritable or aggressive behavior disturbance. A'socicted iron deficiency anemia is virtually always present. The onset of acute encephalopathy tends to 0007-SOT-000005828 N11870.01 . jicia: ; . . . "" . ... :r. ...a i"t. >* * -.spaa: r." . ' * f'ifciy s\. i. -c'.acr.c:."'; . cvaluor-/m. As. tro - . * :i :U: g- aw: -1 _ r i c; :; ;r:d 'j b; !;;; ssvetc. Thus, `-Sc two to fisc-*'*- t -:!i :!d!d with -- .'e'rrgnizei r.!-...- 'S-v... \~y present with n convulsive circrder simi:!-.. :-g idiopaihia ep:icp-.y, rbrjr.ic i.\.puis:ve. c'^rs-ssivc hvperfc ir--i: ; fcehevior disorder 01 r.-e.-.ral rercrdatic.'i. Ur.cr:r..-.-.o:i synaie.-xes ir.civ. regressive lots of trcntol function simulating degenerative cerebral e::-,,-a:es end peripheral neuropathy. Since ti re are ns clnomiaiiiiri specific for lead intoxication on physical exam ination and since rosiine examination of bleed end urine is likely to be unrevealing, prempr diagnosis depends upen a high index of suspicion on the part of the physician and the per form. ance o' f .certain sp ecific laboratory tests. The most valuable of th ese is blood le'ad determination. For repid presumptive dlcg* r:is in the symptomatic child, the qualitative urinary cooroporphyrin tesr is most valuable and should be available iii H*o time:gency roe--; of all hospitals serving high risk papulations. Prior to the advent of chcWinc agents, the martelify from severe acute snesphei- epothy wes approximately 66%-. With the cdvc.ntof first BAL end Ictcr EETA, this mortality was reduced to approximately 30%. It has recently been reported that the use or BAL and EDTA in combination, together with-careful supportive therapy, can noparently reduce rhe mortality from acute lead encephalopathy to less than 5?% Nevertheless, the incidence of severe permanent brain damage among survivors of encephalopathy continues to be 25% or more. If survivors of on initial attack of ccute lead encephalopathy arc reexposed to obner- mai 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 on 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-penicillamine 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 efibrt is made to enroll the child in 0 nursery school or day cere center to provide the stimulation which he needs: such stimulation usually terminates fhc 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 caily diagnosis prior to the onset of symptoms and ultimately to primary prevention of the disease. 2 .. i y. 0007-SWP-000005829 Currently, there is widc-spreca inrerc:! applied ion of ;c:c-.:.ir..i techniques, to the prevention or childhood plurrbis:... 7 res t-ichnicv.es whit!: uie compar- cble in cost ore currently available ana under invi;- ;ir:on. These include deferinii-.a- fion of 6-aminolevulinic acid in mine. The major : obicm in the cppliccfic". or this iesr is the difficulty ir. obtaining landom urine samples -mptly from young chi Mien 12 to 24 months of age, who ore the patients at greatest risk. Currently, the suitability of 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 lead 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 are available for this purpose. The cost of such procedures is small when compared With the cost of a single cese of lead encephalopathy, which at the least will entail hospital ization for four to six weeks, not to mention the cost of long-range follow-up care, special educational facilities arid, 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 as 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