Document 6bQk1440E1xaQbMxKymeaQZ8R

tp o recognition clinic > icar le vias con r<<m edios ha tvn. dos endoscopic t/THE EXPOSURE OF CHILDREN TO LEAD By J. Julian Chisolm, Jr., M.D., a n d Harold E. Harrison, M.D. ent of Pediatrics, Johns H opkins University School of M edicine, Harriet Lane H om e of Johns H opkins Hospital, and Pediatric Division of Baltimore City Hospitals fistula permittc . a v a ila b ility of a new and effective liea e produce 3 erapeutic agent has resulted in re icho e del vias interest in lead intoxication in child- resulta d el reflui: f w Reports1" 1 em anating from various in le vias respir, 'macho demomc. 1 apis of the United States, indicate an in- iste viscere i ( sw in g recognition of this disease, par- Iinque le inf.tr >11 abdom inal . lfcolarly in urban areas. W hile edathamil Jdum disodium has proven to be of value treatment of acute episodes of i es le princip s con fisti: ration, tussc 1 d e aspirat. sophagee sc; leo-esophatic' e non es p - ibism, it cannot be used to prevent the effects of prolonged excessive absorp- lead. In children, as in adults, preof excessive exposure to lead rethe principal means of control, sound preventive program must be upon adequate environmental data. ge incidence, seasonal distribution of te manifestations and concentration among children residing in urban eas are w ell know n.1' '' Although the ion of lead fumes as a cause of in children has been reported,"7 eved that at present the ingestion i-containing paint flakes is the most m source from which children obtain ive quantities of lead. The present deals entirely with this latter type Jlposure. Data have been obtained upon the in- ' of such exposure, duration of ex- ! and the seasonal factor in the pro- 11 of lead intoxication in children. (*l % i,,secondarv" case rate among house- of index cases has also been studied. r^gWise, the relationship betw een the in- W e of severe permanent damage to the and re-exposure to lead among sur- *1V0K of an initial episode of acute lead eephalopathy has been examined. Ob- ^vations were made upon the develop mental status of affected children and the personal-social situations in which they de veloped lead intoxication. The purpose of this report is to present these data and to discuss the relative role which each of the several environmental factors may play in the production of lead intoxication in chil dren. It is hoped that this may facilitate the implementation of adequate preventive measures. CLINICAL MATERIAL AND DIAGNOSTIC CRITERIA The clinical material was derived from the pediatric clinics of the Harriet Lane Home of Johns Hopkins Hospital and of Baltimore Citv H ospital. In all, 197 children exposed to lead, including 89 patients with acute lead encephalopathy, have been studied. All dw elled in the urban slum areas of Baltimore. W ithin this group, 59 children were person ally studied bv the authors. In these children, observations on developm ental status and per sonal-social home situations were made. The studv was conducted during the vears 1952 to 1954, inclusive. An important part of the present survey was the detailed analysis of exposure factors in nine households in w hich abnormal sources of lead were demonstrated. Within these nine environm ental units, there were 9 index cases and 17 other children under 6 years of age w ho served as controls, or a total of 26 sub jects with known exposure to lead. Among the 17 control subjects of this household-study group, the in cidence of unsuspected "secondarv" cases was determined. Another group of 33 children were patients who were studied during and after hospitaliza tion for acute lead intoxication or encepha lopathy during 1952-1954. In addition, a re view was m ade of all hospital records of chil- fSubmitted May 23, accepted July 3, 1956.) This work was supported by grants from the Lead Industries Association, New York, New York, and ^O the National Institutes of Health, U.S. Public Health Servjce (G-3918). ADDRESS: (J.J.C.Jr.) Baltimore City Hospital, 4940 Eastern Avenue, Baltimore 24, Maryland. 943 944 CHISOLM - EXPOSURE OF CHILDREN TO LEAD dren admitted to the above clinics during the previous 12 vears and indexed as "lead poison ing" or "lead ingestion." Among these records, 138 contained sufficient information to estab lish and classifv the clinical diagnosis according to the criteria listed below. These constitute 138 of the 197 subjects included in this report. D iagnostic Classification: All subjects are classified in six clinical categories as follows: T y p e I. E x p o s e d - N o r m a l . Subjects with a history of ingestion of materials suspected of containing lead or with evidence of radio opaque foreign materials in the gastrointes tinal tract bv roentgenography, were classified as exposed normals, if thev had concentrations of lead in blood less than 0.06 m g /1 0 0 gm w hole blood, absence of "lead lines" in roent genogram s of long bones, normal findings in exam ination of the blood (or an anemia which responded rapidly to the oral administration of iron) and no sym ptom s attributable to lead intoxication. Subjects in this category were subdivided into tw o groups: a) those for whom exposure to lead was verified bv analytic records giving the identification and lead content of the material ingested bv the child and b) those for whom such analytic records were not available, al though the clinical record indicated that a source of lead had been found in the ch ild 's environm ent. T y p e II. A sym p to m a tic, Increased L ea d A b s o r p t i o n . T hese subjects differed from the ex posed-norm al group in that thev had elevated concentrations of lead in blood and roentgenographic ev id en ce of storage of lead in the bones, without symptoms attributable to lead intoxication. Qualitative tests for coproporphvrin in urine were positive in some of these children. T y p e III. L ea d Intoxication (w ithout E n c e p h a l o p a t h y ) . The diagnosis of lead intoxica tion w as m ade in children w ho had, in ad d i tion to evidence of increased lead absorption, several of the following manifestations: anemia resistant to iron therapy, increased urinary excretion of coproporphvrin, severe constipa tion, anorexia, hvperirritabilitv, bizarre b e havior patterns and interm ittent vom iting. In the children of this group, there were no ab normal findings in the cerebrospinal fluid. T y p e I V . L e a d E n c e p h a l o p a t h y , M i l d . In addition to fulfilling the criteria for lead in toxication, the children of this group had ab normal findings in the cerebrospinal fluid and one or more of the following signs and symp toms: persistent vomiting, hvperirritability, ataxia, intermittent convulsions and somno len ce or semistupor. Findings in the cerebro spinal fluid were considered abnormal if two or more of the following were present: in creased concentration of protein, increased pressure and pleocytosis in the cerobrospinal fluid. T y p e V . L e a d E n c e p h a lo p a th y . S e v e r e . The encephalopathy was classified as severe if the patients either convulsed continually for a minimum period of 24 hours or remained com atose for a period of 24 hours or longer, or both. The numbers of subjects in each diagnostic category were as follows: nique of Snvder. leaded" with war by a thorough r "L ead-free" water sage of distilled w. i resin column. < T he above metl for the analysis of containing greater t As concentration o 'l value the insolubl specimens caused the final extraction appreciable in man than 0.100 mg Pb I betw een pairs as <_ - countered. The pre i tions sufficient to i I. Exposed-normal (with presumed lead occurred only in tin ingestion) 41 (a) record of lead source available 14 (b) record of lead source not available 27 II. Asymptomatic, increased lead absorption 39 III. Lead intoxication without encephalopathy 18 IV. Lead encephalopathy, mild 48 V. Lead encephalopathy,severe 41 ing iron medicinally by discontinuing t! coverv of lead in fee to 1 10% . The maxin the m ean of duplic. 1.00 m g P b /2 4 hr) ; hr or greater). Tissues were quick 185 in the frozen state The remaining 12 subjects of the tot group of 197 children exposed to lead we normal control subjects in the household-st group w ho apparently had not ingested lead containing materials. They w ere then drk 105C, frozen and r< in triplicate, of aliqi genate w ere then ca method. Difficulties, centration of lead, w METHODS OF STUDY the analysis of brain T h e intensity of exposure to lead was from the mean of tr term ined bv m easurem ent of daily fecal excre other tissues variation | tion of lead in all m embers of the household^ exceed =fc82. stud y group under 6 vears of age. Pooled 2- In all suspected ca to 4-dav collections of stools w ere made m | in children in Baltin the hom e in covered l'A quart Pvrex casserole , blood and of suspecte dishes supplied bv the laboratory. Mothen ' of lead were-' routinel w ere directed to have the child defecate di I the Baltimore Citv Ht rectly into the casserole dish. In hospitals J was analysed bv a patients quantitative collection of stools j technique utilizing a made w hile the children were on meta frames. Aliquots of the pooled 2- to 4-day sam ples w ere prepared for analysis by genization of entire sam ples in a Wl blendor in which the standard brass 4 Snal color estim ation.1 painted plaster, etc., j homes by a visiting i :f`ad content was estir tire technique11 and tollows: w as replaced bv a cast iron bearing, cate aliquots were drv-ashed''9 and and for lead bv the mixed-color dithizone Lead absent--less than! Trace of lead--0.12 to J Positive for lead--12 tl Strong positive for lea<J ispinal fluid ami signs and svmiv hvperirritahilitv ns and somno- in the cerebrn 'onormal if t\\" re p resen t: in ein, increased cerobrospimt! //. S e v e r e . Tin . severe it tin inuallv for .1 or remained irs or longer h diagnostic rd lead l>le Id lilable 27 tioputliy m the total lead wen lokl-stud' ted lead- iisehold tssem lotliee tali/1'' xilisn ,on>` .ii'in- .1 1 1 " ARTICLES ie of Snvder.10 All equipm ent was "d e led" w ith warm 20% nitric acid, follow ed 'jl thorough rinsing in "lead-free" water, d-free" water was prepared bv the pasof distilled water through an ion-exchange column. Jhe above m ethod w as entirely satisfactory She analvsis of lead in feces in specim ens training greater than 1.00 m g P b '24 hr. Concentration of lead decreased below this Be the insoluble m atter present in some ecimens caused increasing interference in | final extraction step. This interference was j|redable in m anv specim ens containing less to 0.100 m g Pb 24 hr in w hich variations tween pairs as great as twofold were engntered. T h e presence of iron in concentra t e sufficient to interfere with the analvsis gorred only in the stools of patients receiv:jron m edicinallv. This w as readilv avoided ^discontinuing the iron temporarily. Rejjjj&ry of lead in feces bv this m ethod was 95 10%. The maximum allow ab le error from ean of duplicates w as -- 10% (0.100 to m g P b /2 4 hr) and =t.5% (1.00 m g Pb 24 greater). ues were quick-frozen and homogenized ie frozen state w ith mortar and pestle, were then dried to constant w eight at C, frozen and re-hom ogenized. Analyses, pplicate, of aliquots of this final homo- e were then carried out by the above Jod. D ifficulties, resulting from low con- tion of lead, w ere en countered onlv in analvsis of brain tissue in which variation I the mean of triplicates was =tl5%. In tissues variation from the mean did not d 8%, all suspected cases of lead intoxication fiildren in Baltim ore, sam ples of w hole and of suspected environmental sources ad were routinelv analvzed for lead bv Baltimore City Health Departm ent. Blood analysed bv a w et-digestion dithizone ique utilizing a spectrophotom eter for color estim ation.11 Sam ples of paint chips, Sifted plaster, etc., were collected in the es by a visiting public health nurse. The y j content was estim ated bv a semiquantitaj technique" and reported qualitativelv as s: d absent--less than 0.1% of lead of le a d -0 .1%to 1.0% of lead dve for lead--1% to 5% of lead lng positive for lead--greater than 5% of lead RESULTS In nine households selected for detailed study of exposure factors there were 9 index cases and 17 other ambulatory chil dren less than 6 years of age, who served as controls. Of the nine index cases, four had acute lead encephalopathy, two had lead intoxication and three were classified as asymptomatic, increased lead absorp tion. Data on the intensity of lead exposure were obtained in this household-studv group through the measurement of fecal excretion of lead before and after the re moval of all identified sources of lead in the houses. By balance studies it has been shown by Kehoe and his associates12 that fecal excretion of lead provides a good index of lead ingestion inasmuch as ap proximately 90% of ingested lead is ex creted in the stool. Prior to the removal of identified sources of lead, stool samples were collected concurrently from control and affected subjects. Similar collections of stools from those subjects with lead intoxi cation were made in the hospital at least 1 week after the completion of therapv with edathamil calcium disodium and again upon return to their homes after the removal of all identified sources of lead. In all, 63 satisfactory pooled, 2- to 4-dav collections of stools w ere obtained from 22 of the 24 ambulatory children under 6 years of age in eight of these nine house holds. Comparable stool samples were ob tained from six children of physicians on the pediatric staff. These were classified as "nonexposed" controls. Stool samples were collected on admission to the hospital from seven additional patients with acute lead encephalopathy. The subjects of the household study were classified according to the diagnostic cri teria outlined. The results of the analyses of the stools for lead are presented in Table I. The results of similar determinations in "nonexposed" controls and additional pa tients with encephalopathy are included in Table I as a background for the evaluation of the household-study group. All outputs of lead in feces were calculated from the I -'f - ' ;5 946 CHISOLM-EXPOSURE OF CHILDREN TO LEAD TABLE T D aily F ecal E xcretion of Lead in C hildren B efore and A fter R emoval of E nvironmental Sources of Lead* F ec . C lassification of P atien ts t .Vo. o f P a tie n ts X o. of \ Specim ens L ead O u tp u t ( m g /2!, hr) .\fean M edian Range T'J1* of Sut, H ousehold-Study G roup Normal Children Primitive societ\ Types III, IV and V At home during exposure In hospital after therapy American (hosp' Present study G 10 44.0 47.0 5.04 -104.0 5 13 0.364 0.440 0.064- 0.850 Industrial workers Types II, III, IV and V At home after exposure 8 15 0.565 0.511 0.039- 1.50 AU types of expo. Severe exposure f Type II At home during exposure Lead Poisoned Child Present study 5 14 4.16 1.11 0.116- 9.60 M ' In this table the . Household Controls 1,11,1 a,ld the poisoner; At home during exposure ii 43 0.834 0.651 0 .0 8 7 - 1.93 * are compared with . Kehoe et al.UM Thee Other C hildren single fecal evacuatio Mexican eommunitv Nonexposed controls** American children. Tl At home 6 6 0.134 0.157 0 .0 1 4 - 0 . 1 7 5 ^ these children was tha II They obtained similar Types IV' and V ilustri.nl workers. Dest During exposure* 7 7 53.4 53.4 0.373-445.0 and analytic technique * The household-study group h;is been divided according to both diagnostic classification and presence or I the poisoned children severely exposed indust sence of lead exposure, in order that the observed differences in fecal excretion of lead under these varying condition household controls is of can be seen. Each specimen represents a 4- to 4-day pooled collection of feces from the lead content of which) normal unexposed child calculated the milligrams lead excreted per 44 hours. An average of two such specimens were collected from < patient during each period of observation relative to exposure. TTaken from data or laAOJ, 1933 t Diagnostic Classification; see text for criteria. ** Nonexposed Controls: 14- to 35-month-old children of members of pediatric staff for whom there wertjfi| known environmental sources of lead. + These seven patients admitted with acute lead encephalopathy were not members of household-study | Values shown are based upon total lead content of admission stool, divided by the number of days since thel f 'lie p resen ce o f e .\ t poximately 0.8 n r 1 '* seen that thos,' previous fecal evacuation, in order to obtain mean daily excretion. pooled collections as 24-hour outputs. In m ost subjects tw o pools of 2- to 4-day col lections of stools w ere obtained during ex posure. T he data, therefore, represent ap p r o x im a te ly o n e "e x p o s u r e -w e e k " o f o b servation in the various subjects. T h e term "e x p o su r e -w e e k " is u s e d , in a sm u c h as th e sam ples w ere not alw ays consecutive. On the first lin e o f T ab le I are sh ow n the ou t puts of lead during exp osu re of six patients w ith lead encephalopathy and intoxication. T h e m ean output o f lead in this group during exposure w as 44 m g /d a y and the range w as 5 to 105 m g /d a y . Three of these had acute lead encephalopathy. T h eiy hour outputs are calcu lated from theT content of the first stool passed m ission to the hospital. A ll othe collections during exposure were the hom es. W hen these lead-poisond dren w ere rem oved from exposure bv h osp italization or, a fter dischai rem oval of all identified sources from their hom es, the daily fecal of lead fell to norm al valu es, appro^ 0.3 and 0.5 m g, resp ectiv ely (line 3). O n th e fifth lin e o f T a b le I, daily output of the 11 control Histribctiox ; Age Groups I- to 35 months aB+ months Totals \- = .4S. ''11.01. N te: ARTICLES TABLE [I F ecal E xcretion oe L ead* Type of Subject mg P b/D ay Mean Range Normal Children Primitive societyf American (hosp.)f Present study 0.088 0.13 0.83 0- 0.48 0.01- 2.2 0.09- 1.9 Industrial workers All types of exposuref Severe exposure f 3.8 7 ..(> 0- 14.0 4.0 - 14.0 Ix?ad Poisoned Children Present study 44.0 5.0 -104.0 * In this tabic the daily fecal lead output of the nor mal and the poisoned children in the household group are compared with similar data from the studies of Kehoe et a/.13,14 They determined the lead content of single fecal evacuations from children in a primitive Mexican community and in convalescent hospitalized American children. The only known source of lead for these children was that contained in their normal diet. They obtained similar determinations in exposed in dustrial workers. Despite the differences in sampling and analytic techniques, the fecal excretion of lead by the poisoned children apparently exceeds that of severely exposed industrial workers, while that of their household controls is of the same magnitude as that of normal unexposed children. t Taken from data of Kehoe et al.: J. Indust. Ilyg., 15:302, 1033. the presence of exposure to lead was ap proximately 0.8 m g of lead daily. It can be seen that those children classified as asymptomatic, increased lead absorption (line 4) occupy an intermediate position between the poisoned and the control sub jects. Thus, during exposure the poisoned children were found to be excreting ap proximately 50 times as much in the feces as the similarly exposed household controls. The results shown in Table I may be compared with the studies of Kehoe ct al.13,1* on fecal excretion of lead under various conditions of exposure to lead (Table II). It can be seen that daily fecal excretion of lead in the control subjects of the present study is of the same order of magnitude as that of the normal children studied bv Kehoe et al.'3 Even when allow ance for differences in analytic and sam pling technique is made, it is evident that the lead-poisoned children of the present study w ere excreting in the feces far greater quantities of lead than do heavily exposed industrial workers. An unexpected finding of this household study was the discovery of five additional cases of unrecognized increased lead ab sorption and lead intoxication among the 17 control subjects. All of these unsuspected cases fell within the same age range as the index cases: namely, 12 to 35 months of age. No evidence of increased lead absorp tion or ingestion was demonstrated among the older housemates (Table III). Indeed, if the index cases are included, 14 of the 15 children aged 12 to 35 months in the nine TABLE III H ousehold Study D is t r ib u t io n by a g e o f u n su spe c t e d c a ses o f a sy m pto m a tic, in c r e a s e d lea d a b so r ptio n and LEAD INTOXICATION IN HOUSEMATES OF N IN E IN D E X CASES Number of Subjects Age Groups 12 to 35 months 36-}- months Totals Subjects at Risk 6 11 17 Asymptomatic, Increased Lead Absorption and Lead Intoxication 5 0 5 Normals i 11 14 .71 .*< *^ m- 9-48 CHISOLM - EXPOSURE OF CHILDREN TO LEAD TABLE IV of le L e a d C o n t e n t o k T i s s u e s o k C i i i i . d h e n D y i n o k h o .m A c k t e L e a d K n < e i >h a u )1>a t m y items chew Patient Age , Time of (mo) Death* Lead Content Total Lead (m g P h / 1 0 0 <jm d r y fix.me) F ound in So// T i s s u e s Rib B rain ; Liver Kidney | (mg) Output of Lead in Urine] one s lead, i on tl * Bakin B. McF. 25 22 hours 39.0 i a | 10.5 8.9 15.0 anuric | ers, o N.B. I I . 11. L.I). 31 20 23 12 hours 31 days G hours 33.0 13.1 10.0 1.0 20.1 9.5 40.5 5.2 1 .4 1.1 5.5 10 . 1** 4.8 1.7 -- l i- ; i -- 2.4 I tainei ? of Ie; I total s * Time of death after institution of therapy with edathainil calcium disodium, , An f Total output of lead in urine during therapy prior to death. ' Jurat; ** Exclusive of brain, estimated lead content of which is approximately 3 mg. J sympt households were found to be ingesting po an additional 48 sources. For each of the I tion o tentially toxic quantities of lead. 105 exposed children, from one to five dif f* tainin In four patients who died during an ferent sources containing greater than IX cl obtaii acute episode of lead encephalopathy, tis ^ posun sue content of lead was determined (Table IV). Tliree of the four patients died within 24 hours after the institution of therapy TABLE V E nvironmental So u rces of L ead* sk | j mate ? if the 9 a) the with edathamil calcium disodium. Total urinary output of lead prior to death varied from 2 to 5 mg. While it is not possible to estimate accurately the total lead content of the body from these data, the content of Location Lead Content Less than 1% 1% or I f on Interior Sources lead in soft tissues can be approximated. Windowsills & frames 5 118 Aub e t a l . i s and Kehoe e t a l . 10 have found in animals and in human necropsy material obtained from individuals dying within a few days or weeks after cessation of chronic exposure to lead that from one-third to two- Interior walls painted paper painted plaster Door frames Furniture Cribs 38 16 24 32 1 15 33 31 thirds of the total lead in nonskeletal tis sues is contained in liver, kidney and brain. Skeletal stores vary greatly and reflect to a certain extent the duration of exposure. Door frames Porches & housewalls Fences & other walls Exterior Sources 3 10 0 20 27 From the data in Table IV and those of the authors quoted, we may estimate total con tent of lead in soft tissues in these children as 20 to 100 mg. In the entire series, records of identified Interior sources Exterior sources Totals 74 183 11 37 85 220 sources of lead were available for 105 chil dren. The locations of these sources about the dwellings are shown in Table V. Of the 220 samples tested which contained greater than 1 % of lead, only 4 were ob * The distribution, by lead content and location < the 305 identified possible environmental sourcesaf I to which 105 subjects in this series were exp sources were identified by analysis of paint I taken from the various surfaces in and about t which gave evidence of having been chewed. ] "conn tained from cribs and furniture. More strik ing is the fact that 116 of the 220 sources were window-sills and frames. Peeling wall paper and crumbling plaster accounted for subject one to seven such sources were identi all 105 subjects at least one source containing^ than 1% of lead was found. For 102 of the 1051 at least one source containing greater than J was found. ARTICLES 949 ich ol tin to five (lit r th an 1' n il Mnr ini III .'II ill. ' f l.-3-i 1-111- jiiiii....... d were identified among the various each child was thought to have ed. For 102 of them there was at least source containing greater than 5 % of The lead was contained in the paint ,e surfaces. The paint was old and g and frequently contained many lavX>ne or more of which may have conlead pigments in which the content d may have been 30 to 70% of the solids in the paint. attempt was made to ascertain the tion of exposure likelv to produce toxic toms. Maternal estimates of the duraof their child's ingestion of lead-conig materials frequently were either un able or unreliable. The type of exre, however, permitted an indirect estiof the probable duration of exposure, following assumptions were made: locations of the sources of lead rethat the children be ambulatory in to reach them, and b) exposure began time of ambulation, or at 12 months [e on the average. With these assump,the probable duration of exposure be estimated as the interval in months `een the child's first birthday and the at which the child was classified as iptomatic, increased lead absorption, 1 lead poisoning was discovered. the data were analysed on this basis, istically significant correlation could found between presumed duration of exjfjfre and severity of disease (exposedJonnal children excluded). Indeed, the data ted that the presumed exposure was ilar duration in all diagnostic classitons manifesting increased absorption j*ad, with or without symptoms. J^explanation for this became apparent *5? the seasonal factor was taken into Thirty-two patients in the series 'ped acute lead encephalopathy prior years of age. The relationship be/f the seasonal factor and the presumed of exposure is shown for each of ^Spatients in Figure 1, in which the of the child's first birthday is joined bar with the month of onset of acute encephalopathy. The length of each bar, therefore, represents the assumed dura tion of exposure in months for each child. In the upper portion of Figure 1 the chil dren passing their first birthdav between May and September are shown. Thev were presumed to have been ingesting lead during some part of this 5-month summer period (when the peak incidence of acute lead encephalopathy occurs), yet they did not become ill until the summer of the following year as they approached 24 months of age. In the lower portion of Figure 1 are shown those patients reach ing their first birthdav during the winter months prior to April. They became ill dur ing the first summer after the presumed on sets of ingestion. Reading from the top to the bottom of Figure 1 the probable dura tion of ingestion, therefore, becomes pro gressively shorter and approaches a mini mum of 3 months. Within this group of 32 patients there was no statistically significant correlation between month of first birthday and severity of, or survival during, acute lead encephalopathy. Excluding December, the distribution of births by month in the group does not differ significantly from the monthly distribution of births in Baltimore for the years 1951 to 1953 inclusive, during which most of the patients were born. In this small group the peak in births during December, and the passage of the older infants through their first summer of ambu lation without symptoms, suggests that 5 to 6 months of lead ingestion may elapse prior to the onset of acute lead encephal opathy. The possibility that a minimum exposure period of 3 months is required, after which the advent of summer becomes the control ling factor in the production of symptoms, is also suggested by the following finding. In the entire group there were 14 children with unequivocal evidence of excessive lead ingestion including identification of at least one environmental source containing greater than 1 % of lead, but with no evi dence of increased lead absorption. Eight of these fourteen normal-exposed children N`-'-o: W rreS al m&T 930 C H ISO L M - E X PO SU R E O F C H IL D R E N T O L E A D RELATIONSHIP BETWEEN MONTH OF FIRST BIRTHDAY AND MONTH OF INCIDENCE OF ACUTE ENCEPHALOPATHY follow ed f( 16 patients tinued ingc months or SUMMER SUMMER posure and lead after lopathy. Th survivors of analysed, wi during the whether the the occurrei in the cent) posure to le the followi sidered evid age to the b recurrent co disorder. 01 0 MONTH OF F IR ST B IR T H D A Y 0 IN C ID ENC E - SURVIVAL <" D IE D having these strated one < 12 fulfilled statistically, - J 1 F 1M 1 A M 1J 1J 1A ' S o' n ' d' j ' f ' m' a MONTH i If i MJ JA3 0 'N' D / {. tion betwee: vere sequel] following rc opathy (X2 = Fic. 1. In this graph the acute lead encephalopathy month of onset of acute symptoms for each of the 32 prior to 2 years of age is shown on the right. On the patients who developed left is the month of the i tion betweei child's first birthday. These points are joined bv a bar. The length of each bar, therefore, represents t h e | lead is more assumed duration of lead exposure (in months) for each child. Twelve months of age was selected as the I surviving an average age of am bulation. The nature of the exposure in this series required that the child be ambula lopathy. Am' tory in order to reach the sources of lead in his environment. In this m anner a relation between pre posure was > sumed duration of exposure to lead and the seasonal factor in the production of symptoms can be | demonstrated. were less than 15 months of age. Con versely, among the 89 patients with en cephalopathy, the youngest was 15 months of age. Although these data on duration of ex posure were indirectly deduced, they are supported by histories obtained from many parents, who stated that they had seen their children ingesting paint flakes or had found plaster particles in the child's stools since the time the child had begun to walk. It was also observed that among patients who survived an initial episode of acute lead encephalopathy and were re-exposed to lead, recurrent acute episodes of encepha lopathy usually did not occur until the fol lowing summer. An analysis of the occurrence of severe 1 Re l a t i o n b e t w permanent damage to the brain among sur- i Levi vivors of an initial attack of acute lead encephalopathy indicates the importaix* of continued environmental exposure to lead in increasing the incidence of < nervous system sequellae. In the series 61 survivors of acute lead opathy were treated more than 12 prior to evaluation of sequellae (I with citrate, 16 patients; therapy wi Known re-exposi Koknown re-ex; 28 patients; and therapy with calcium disodium, 17 patients). F'itl the group were lost from follow-up. six of the sixty-one patients (citrate^ tients; BAL, 19 patients; and calcium disodium, 14 patients) have I *Four survivi Us uncertain, a t Sequellae = > `'ere behavior . ARTICLES 951 followed for 1 year or longer. Of these 46 patients, 14 were known to have con tinued ingestion of lead for periods of 2 months or longer, 4 had doubtful re-ex posure and 28 had no known re-exposure to lead after the initial episode of encepha lopathy. The incidence of sequellae in the survivors of acute lead encephalopathy was analysed, without regard to type of therapv during the acute phase, to determine whether there was any association between the occurrence of severe permanent residua in the central nervous system and re-ex posure to lead. Presence of one or more of the following manifestations was con sidered evidence of serious permanent dam age to the brain: severe mental retardation, recurrent convulsions and severe behavior disorder. Of the 23 survivors classified as having these "severe sequellae," 6 demon strated one of these criteria, 5 had two and 12 fulfilled all three (Table VI). There is, statistically, a highly significant associa tion between the occurrence of such "se vere sequellae" and re-exposure to lead following recovery from mild encephal opathy (X2 = 14.30, P < 0.01). The correla tion between sequellae and re-exposure to lead is more difficult to assess in the group surviving an episode of severe encepha lopathy. Among the 20 severe cases, re-exposure was uncertain in 4. These four, all of whom had permanent residua in the brain, are omitted from Table VI. If these doubtfully re-exposed cases are considered as not re-exposed, X , = 2.68 and P > 0.1 (re-exposure is not statistically significant). For the entire group of- survivors of mild and severe encephalopathy there is no sig nificant correlation between sequellae and the duration of acute encephalopathy, type of therapy during the acute phase or con centration of lead in blood after the acute illness. The loss of patients from follow-up does not vitiate the analysis. In survivors not re-exposed to lead there is no correla tion between sequellae and age of incidence at the 18, 24, or 30-month levels. DISCUSSION The ages and seasonal distribution of symptomatic cases in this series are the same as those reported for children by various investigators.3'5 Eighty-eight of the one hundred five cases of acute lead intoxication occurred during May, June, July, August, and September. Ninety of the one hundred five cases occurred in chil dren between the ages of 12 and 36 months. It need only be re-emphasized here that homes in which the children of this series lived had several features in common: they were old and in varying states of deteriora tion and disrepair. In the homes visited, TABLE VI R elation* b e t w e e n I ncid en c e o p S ev er e S e q u ella e in t h e C e n t r a l N e r v o u s S ystem and R e -ex po su r e to L ead follow ing R ecovery prom an I nitial E pisode of A cute L ead E ncephalopathy Acute Lead Encephalopathy Severe Cases* M ild Cases W ith Sequellae] No Sequellae W ith Sequellae No Sequellae Known re-exposure to lead 7 0 70 No known re-exposure to lead 8 6 2 17 X* = t .89; P < 0 .0 5 Xs = 11 .35; PCO.Ol * Four survivors of severe acute lead encephalopathy, who sustained sequellae but in whom re-exposure to lead was uncertain, are omitted from the table. (See text for discussion.) f Sequellae = severe, permanent, residual damage to the brain (severe mental retardation, convulsive disorder severe behavior disturbance). '(W. 952 C H ISO L M - E X P O SU R E O F C H IL D R E N T O L E A D crumbling, painted plaster or loose paint chips from walls, ceilings, door frames, win dow-sills, outside porches and fences were readily accessible to the hands and mouths of inquisitive small children. The data of the present study show the intensity of this type of exposure; but they cannot be ap plied directly to such questions as the minimal quantity of lead toxic for children or the maximal safe content of lead in liquid paint. Among the environmental data pre sented, two factors stand out; the intensity of lead exposure provided by a small quan tity of paint flakes and the role of the season in precipitation of acute lead en cephalopathy. The data in Table I on fecal excretion of lead may be utilized as a measure of the quantity of lead ingested by the various groups of subjects in the household study. The difference between the poisoned and the nonaffected children in these house holds does not require statistical analysis; for the mean daily fecal excretion of lead in the poisoned children exceeded, by 50fold, that of the controls in which it fell within the normal expected range. In Table II it can be seen that the mean daily fecal output of lead bv the lead-poisoned chil dren (44 mg Pb/dav) exceeded, by ap proximately sixfold, that of a group of se verely exposed industrial workers (7.6 mg Pb/dav) and, by elevenfold, that of work ers in various trades in which exposure to lead is less severe. The groups of industrial workers chosen for comparison14 were ex posed to lead-containing dust, much of which is swallowed with the saliva. As in the children of the present study, the principal mode of absorption in these work ers would be through the gastrointestinal tract. It has been pointed out that the oc currence of lead encephalopathy in adults has usually been associated with intense exposure.17 The more frequent occurrence of encephalopathy in children as compared with adults may depend in part upon their more intense exposure rather than upon any inherent biologic differences between child and adult. Lehman18 recently reviewed the litera ture and concluded that the average daily ingestion of not more than 1.5 mg of lead is without harm. Kehoe e t a l . 12 have found that significant retention of lead in the tis sues occurs when, in addition to normal dietary intake, adult volunteers are fed 2 mg of soluble lead (as lead acetate) daily. The data in Table I are in accord with these conclusions. Under the sponsorship of the American Academy of Pediatrics, the Committee on Hazards to Children of the American Standards Association studied the problem and recommends that paints may be considered safe for use on chil dren's toys and furniture and housing in- ij teriors if the lead content does not ex-i ceed \ % of the total solids.19 Paints and jj other surface coatings meeting this speci- | fication and those relating to other po-f" tentially toxic metals may be labelled: "conC forms to American Standard Z 66.1-1955.^ It is essential to recognize that this recom mendation applies only to the two or threes layers of paint usually applied to a surface; .; not to multiple layers of paint as may bg| found in old deteriorated housing. As thdj number of layers increases or when af layer of paint containing lead pigments is added, the quantity of lead per unit are increases to the point where even a small! flake may contain an excessive amount ofj lead. The magnitude of exposure to lead ; associated with the ingestion of a few smalL paint flakes is emphasized if we calculate^ the quantities of paint flakes necessary toj yield the amounts of lead found in stools of the lead-poisoned children: example, 44 mg of lead would be equivale to the ingestion of 0.88 gm or less of flakes containing 5 % or more of lead, or? 4.4 gm of flakes containing \ % of lead, example of the size and quantity of chips necessary to yield potentially amounts of lead is shown in Figure In Table V the location and lead tent of environmental sources of lead shown; 102 of these 105 children were jj posed to at least one source conta greater than 5% of lead. No case of lead toxication has been found where the Fic. 2. Exai Four small pa fragments wa removed from His feces, wh evacuation, cc almost daily i 10 months pri< source of lea in the driei data applv lead is pres well as a pi< solids appro with a satis ceivable tha housing wi; many layers as 1% of le children m; hazard to sn Evidence cates that, mately 3 mt the advent < continued e> ling environ tion of acuti Although th the ARTICLES 953 I OUi`l*P Fig. 2. Example of size and quantity of paint fragments containing a potentially toxic quantity of lead. Four small paint chips are shown with a cigarette for comparison of size. The aggregate weight of these fragments was 2.68 gm; they contained 254 mg (or 9.52) of lead. W ith the fingernail they were easily removed from a door frame upon which a patient with acute lead encephalopathy was known to chew. His feces, w hich were obtained on admission to the hospital and 48 hours after the last previous fecal evacuation, contained 180 mg of lead. The mother stated that this child had been ingesting paint flakes almost daily from this and other sources (containing similar concentrations of lead) for approximately 10 months prior to hospitalization. source of lead contained less than \ % of lead n the dried paint surface. The present data apply to old housing. Inasmuch as lead is presently used as a paint drier as well as a pigment, 1% of lead in total paint solids approaches the minimum consistent "nth a satisfactory house paint. It is con ceivable that poor maintenance of modern housing with resultant accumulation of ^any layers of paints (containing as little 35 1% of lead) on surfaces accessible to children may in the future constitute a hazard to small children. Evidence has been presented which indi cates that, after a minimum of approxi mately 3 months of this type of exposure, ^he advent of summer (in the presence of continued exposure to lead) is the control ling environmental factor in the precipita tion of acute lead encephalopathy (Fig. 1). ^though the mechanism of this phenomenn is not fully understood, experimental C'ddence has been obtained in animals "'hich indicates that vitamin D and the actinic ravs of the summer sun increase ^ absorption of lead from the intestine.5 It has also been suggested that the in creased heat of the summer leads to de hydration and acidosis in small children and in this manner may play a role in the production of encephalopathy.20 In the present study no reliable data could be ob tained concerning vitamin D intake in view of the sporadic use of vitamin D-fortified evaporated and fresh milk products by the subjects. Among the patients interviewed, a history of no vitamin D supplement during winter or summer was given by about half of the cases. When the probable duration of exposure exceeded 3 months, no correlation could be demonstrated between increasing severity of disease and further monthly increments in exposure. This finding may be explained by the interplay of two other factors: the magnitude of lead ingestion observed in the household-study group, and the sea sonal factor in the precipitation of acute symptoms. It emphasizes the urgency during the summer months of the prompt removal of children manifesting asymptomatic in creased lead absorption from such intense 954 CHISOLM - EXPOSURE OF CHILDREN TO LEAD exposure to lead. The data indicate that, in such a patient, acute encephalopathy may develop if exposure is permitted to continue but a few weeks longer. Frequency of ingestion, is, of course, an important consideration. Long-term data obviously could not be obtained on this point. The data in Table I represent, at most, only 1 "exposure-week" in time. The repetitive ingestion of a few particles from one of the identified sources of lead several times during that week would be compati ble with this data. Tissue contents of lead (Table IV) give an approximation of the amounts of lead which may be absorbed under these conditions. The finding in the household study of five "secondary" cases among the six con trol subjects aged 12 to 35 months is sig nificant. If confirmed, it indicates that a larger public health aspect of this disease exists in old housing areas than has here tofore been recognized. Furthermore, wher ever an index case is found, his environ mental contacts under 3 years of age should be submitted to careful clinical and labo ratory examination. Although the need for identification and removal of environmental sources of lead is well known,3-21 a highly significant cor relation between re-exposure to lead and the incidence of severe permanent sequellae in the central nervous system in sur vivors of an initial episode of acute en cephalopathy has not previously been re ported. This indicates that immediate and absolute prevention of re-exposure may, perhaps, be the single most important long term factor in the eventual outcome in such patients. In our experience this has been satisfactorily accomplished only by burning the old lead-containing paint com pletely away or by transfer of the child to a new dwelling in good repair. The term "pica" is frequently used in as sociation with both lead poisoning and with mental defect in children. Thus, in the minds of many, plumbism and mental de ficiency are frequently associated. This is not so with respect to the ingestion of other toxic substances, a single ingestion of which, suffices to produce symptoms. The wont of toddlers in the 1-year-age group to taste and eat a large variety of foreign ma terial is well known and is considered to be a part of their normal behavioral pattern, at least for a short span of time. In the present study all members of the household group were submitted to psycho metric examination. Within this group no striking developmental deviations could be found between the affected and the non- affected members. In addition, 28 patients who were not re-exposed were psycho- metrically evaluated 1 year after recovery from acute lead intoxication and encepha lopathy. The distribution of intelligence quotients on the basis of the revised Stan- ford-Binet Intelligence Scale, Form L, was ows: 9 Intelligence Quotient 60- 69 70- 79 80- 89 90- 99 100-109 110-119 Numbers of Patients oo 2m 5 yjk 9 5 4 Jm These findings would agree with the con cept that the ingestion of foreign material] exhibited by these children was not manifestation of mental deficiency, but that ^ the ready availability of a highly toxic ma-' terial in the environment was the important factor. This is certainly supported by the high "secondary" attack rate found among the control subjects of the household study. If the assumptions are made that flaking, lead-containing paints are widely distrib uted in old housing, that there are large numbers of infants and toddlers living such a physical environment and that nor| mal as well as defective children may re ily ingest amounts of lead sufficient! produce intoxication, the question Why is lead intoxication not more lent than the numbers of cases prese recognized would indicate? Many of lesser degrees of intoxication may| unrecognized unless sought out (as cated by the cases") or ma' gestion. In sti tion of ingestie duce overt sig However, p< in those subjc may, in part, greater ingesti of this report ; population of similar physic; spect to mater plumbism, mo were aware o' paint or had h poisoning. Sign 33 mothers, wl, volved, were n considered the child was eatin him." Such ma understandable calculation tha flakes may con of lead. It is the minute quantitic leads to lead in* that no mother to prevent this face of crumblii be recognized t both interior an is probably the mental factor ii prevention of cl The corrective ents wh6 attem] consisted large; which may be been ineffectual, toremove the soi wise, was the lac vision of the afft the thirty-three i who worked at week away from home they left neighbors or in t Sixof the mother - w.: ARTICLES cated by the incidence of "secondary cases") or may be the result of lesser in gestion. In still other children the dura tion of ingestion may be insufficient to pro duce overt signs of lead intoxication. However, personal-social factors elicited in those subjects studied bv the authors may, in part, account for the relatively greater ingestion of lead in the subjects of this report as compared with the larger population of children who may live in similar physical environments. W ith re spect to maternal information concerning plumbism, mothers were asked if they were aw are of their child's ingestion of paint or had heard of the danger of lead poisoning. Significant is the fact that 14 of 33 m others, while aware of the danger in volved, were not concerned because they 9onsidered the amount of paint flakes their child was eating to be insufficient "to hurt him." Such maternal statements are quite Understandable in view of the preceding Calculation that less than 1 gm of paint 2S m ay contain highly toxic quantities flead. It is the repetitive ingestion of these lute quantities of such paint chips which to lead intoxication. If it is conceded it no mother can reasonably be expected ifprev en t this type of ingestion in the of crumbling paint and plaster, it will be recognized that proper maintenance of interior and exterior painted surfaces probably the most important environltal factor in the long-term aspect of mention of childhood lead intoxication. ie corrective efforts taken by the parwho attem pted to curb the ingestion sisted largely of punitive measures iich may be said, prima facie, to have been ineffectual. Only one had attem pted remove the source of lead. Common, likewas the lack of close parental superion of the affected children. Thirteen of thirty-three mothers were wage earners worked at least several days of each ek aw ay from home. While away from ie they left their small children with ibors or in the care of older children, fof the mothers had more than three chil- dren less than 5 years of age. They stated that in order to get various types of house work done, they shut the children-in other rooms for short intervals; in these rooms sources of lead were found. Several of the children in the hospital dem onstrated an excessive desire for af fection. From the point of view of the child, the ingestion of foreign material was an obvious attention-getting device in some, particularly in those who had been punished for it. Many others appeared to nibble inadvertently upon the window sills and door frames as thev gazed out into the street. In these, boredom was apparently conducive to the lead ingestion, and may be attributable to the lack of an emotionally and intellectually stimulating environment. Many parents reacted by an overprotective attitude following their child's recovery from acute lead encephalopathy. They fre quently sought advice about play activities for their child; the diminution in pica was often striking. SUMMARY AND CONCLUSIONS A study of some environmental, behav ioral and social factors in the production of lead poisoning in children in an urban com munity has been reported. Most significant among the environ mental data presented were the magnitude of the exposure to lead from repetitive in gestion of small quantities of leaded-paint flakes, and the role of the seasonal factor (summer) in the precipitation of acute lead encephalopathy. The predominance of these two factors may explain the absence of any significant correlation between severity of disease and increments (beyond a minimum of 3 months) in the probable duration of exposure. It was concluded that a child without symptoms but having increased absorption of lead, recognized during the summer months, may progress to severe en cephalopathy within a few weeks if the sources of lead are not promptly identified and eliminated. The present studies demonstrate that ex posure to lead may be intense in children 956 CHISOLM-EXPOSURE OF CHILDREN TO LEAD over 1 year of age living in dilapidated dwellings in which flaking leaded paint is readily accessible. The amounts of lead found in the feces of the poisoned children in the present study exceeded that found by others in the feces of exposed industrial workers. This suggests that the higher in cidence of lead encephalopathy among children as compared with adults may, in part, result from their relatively greater ex posure. The importance of continued environ m ental exposure to lead in increasing the incidence of severe permanent damage to the brain among survivors of an initial at tack of acute lead encephalopathy was demonstrated. The correlation between the occurrence of such sequellae and re-ex posure to lead in patients recovering from mild acute encephalopathy was statistically highly significant. It was concluded that removal of lead from the child's environ m ent is the only adequate protective m eas ure in such cases. T he high proportion of children aged 12 to 35 months with average intellectual capacity found among cases of lead in toxication, and the high incidence of un suspected cases found among 12- to 35month-old housemates of the index cases dem onstrate the importance of the environ m ental aspect of the problem in urban slum areas. This high incidence of "secondary cases'' emphasizes the physician's obliga tion to examine carefully and promptly all environmental contacts under 3 years of age w herever an index case is found. The developmental factors in the child and the social situations in the home which may intensify the ingestion of lead-con taining materials were discussed. While the responsibility of parents to protect their children from environmental hazards is not denied, no mother can reasonably be ex pected to prevent the repetitive ingestion of a few paint chips when these are readily accessible. As lead is widely used as a paint drier, continued good maintenance of painted surfaces would appear to be more pertinent to the long-range prevention of childhood plumbism than specific limita tions on the content of nonpigment lead in fresh paint. The various environmental data all point to the conclusion that, where housing has been perm itted to deteriorate, exposure to lead may be of such intensity as to outweigh such individual variables as mental retardation and emotional malad justments in the child. Such intense ex posure is a preventable hazard to normal small children, and, as such, constitutes a public health problem which may be more extensive than has heretofore been thought to exist. Pending the wider availability of better housing, preventive measures will have to be adapted to individual home situations and to the available facilities within a given community. Basic to any preventive pro gram are facilities for the prompt identifi cation and removal of environmental sources of lead, as has been emphasized by others.3' 21 Equally im portant is a compre hensive social investigation of the home in order to evaluate the circumstances under which the child obtained toxic quantities of lead and to determine whether the iden tified sources of lead can be adequately re moved, or whether a change of dwelling is $ required to prevent further dangerous ex- s posure to lead. ACKNOWLEDGMENTS The authors wish to acknowledge the co operation of the Baltimore City Health De partm ent, and of Huntington Williams, M.D., D.P.H., Commissioner, who made its services freely available to us. Miss Jean Askin, B.S., performed all of the psychom etric examinations included in this report. Mr. Peter Wei performed lead analyses of the feces and tissues. REFERENCES 1. Bvers, R. K., Maloof, C. C., and man, M.: Urinary excretion of children. Am. J. Dis. Child., 87 1954. 2. Bessman, S. P., Rubin, M., and The treatment of lead A method for the removal ing the 1954. 3. Williams, and Sa\ I young ( 230, 194. .Vlellins, R demiolo I of lead 158:15. 5. Rapoport, | poisonin study of sonal in. Child., ( 6. Williams H. B., ] Jr.: Lea of batte 1933. Wvllie, J. poisonin terv cas. 1954. 8. Methods f. in Biol America 9. Official an. sis, 5th cultural 10. Snyder, L. for detei microme 19:684, 11. Kaplan, E the auth. 12. Kehoe, R. Bamback periment and excr diagnosis ing. J. I 1943. 13. Kehoe, R. On the i of lead; in infant 15:301, 14. Kehoe, R. J.: Lead certain It 306, 193 15. Aub, J. C.. and Rezn more, W 16. Kehoe, R. A Lead ab: tion to tl J. Indust. 17. Hamilton, limitalead in omental t, where eriorate. nsity as ibles as maladnse ex normal `itutes a he more thought f better have to tuations i a given ive proidentifinmental sized by comprehome in s under uantities lie idenatelv reelling is rous ex- e the coalth DeV'illianis. io made d all <>f luded in ed some ,ues. ad CllSil,f lead in 87:54S. .eikin, So ilopathy" lead dur- ARTICLES 957 ing the acute stage. Pediatrics, 14:201, 1954. Williams, H., Kaplan, E., Couchman, C. E.. and Sayers, R. R.: Lead poisoning in young children. Pub. Health Rep., 67: 230, 1952. Mellins, R. B., and Jenkins, C. D.: Epi BA demiological and psychological study of lead poisoning in children. J.A.M.A., 158:15, 1955. Rapoport, Nl., and Rubin, M. I.: Lead poisoning. A clinical and experimental study of the factors influencing the sea sonal incidence in children. Am. J. Dis. Child., 61:245, 1941. 0. Williams, H., Schulze, W. H., Rothchild, H. B., Brown, A. S., and Smith, F. R., Jr.: Lead poisoning from the burning of battery casings, J.A.M.A., 100:1485, m.: 1933. Wvllie, J.: A family outbreak of lead poisoning from burning of storage bat tery casings. Canad. M. A. J., 70:287, 1954. Methods for Determining Lead in Air and in Biological Materials. New York, American Public Health Ass'n., 1944. Official and Tentative Methods of Analy sis, 5th Ed. Association of Official Agri cultural Chemists, 1940, p. 397. Snyder, L. J.: Improved dithizone method for determination of lead: Mixed-color micromethod at high pH. Analvt. Chem., 19:684, 1947. Kaplan, E.: Personal communication to the author. iehoe, R. A., Cholak, J., Hubbard, D. M., Bamback, K., and McNarv, R. R.: Ex perimental studies on lead absorption and excretion and their relation to the diagnosis and treatment of lead poison ing. J. Indust. Hyg. & Toxicol., 25:71, 1943. [ehoe, R. A., Thamann, F., and Cholak, J.: On the normal absorption and excretion of lead; lead absorption and excretion in infants and children. J. Indust. Hvg., 15:301, 1933. hoe, R. A., Thamann, F., and Cholak, J.: Lead absorption and excretion in certain lead trades. J. Indust. Hvg., 15: 306, 1933. Aub, J. C., Fairhall, L. T., Minot, A. S., and Reznikoff, P.: Lead Poisoning. Balti- >more, Williams & Wilkins, 1926, p. 53. ehoe, R. A., Thamann, F., and Cholak, J.: Lead absorption and excretion in rela tion to the diagnosis of lead poisoning. J. Indust. Hvg. & Toxicol., 15:320, 1933. Hamilton, A., and Hardy, H. L.: Industrial Toxicology, 2nd Ed. New York, Hoeber, 1949, p. 80. 18. Lehman, A. J.: Quarterly Report to the Editor on Topics of Current Interest: Lead in decorative paint for children's tovs and furniture. Quart. Bull., A. Food and Drug Officials U.S., 20:36, 1956. 19. American Standard Specifications to Mini mize Hazards to Children from Residual Surface Coating Materials (Z 66.1 -- 1955). New York, American Standards Association, 1955. 20. Blackman, S. S., Jr.: The lesions of lead encephalitis in children. Bull. Johns Hopkins Hosp., 61:1, 1937. 21. Bvers, R. K., and Maloof, C. C.: Edathamil calcium-disodium (Versenate) in treat ment of lead poisoning in children. Am. J. Dis. Child., 87:559, 1954. SUMMARIO IN INTERLINGUA Le Exposition de Juveniles a Plumbo Es reportate un studio de certe factores de milieu e mores in le production de invenenamento a plumbo in juveniles in un communitate urban. Le plus significative del datos de milieu hie presentate es le magnitude del exposition a plumbo associate con le repetite ingestion de parve quantitates de squamulas de color a plumbo e le factor saisonal (i.e. le importantia del estate) in le precipitation de acute encephalopathia a plumbo. Le predominantia de iste duo factores explica possibilemente le ab sentia de un correlation significative inter le severitate del morbo e augmentos del probabile duration del exposition (ultra un minimo de 3 menses). Esseva concludite que un caso de asymptomatic augmento del absorption de plumbo que es recognoscite durante le estate pote progreder a sever encephalopathia intra alicun septimanas si le fonte del plumbo non es promptemente identificate e eliminate. Le diurne ingestion medie de plus que 1,5 mg de plumbo es potentialmente toxic. Un medietate del matres interviewate esseva inconscie del facto que minuscule quantitates de colorante pote continer concentrationes toxic de plumbo. Le presente studios demonstra que exposi tion a plumbo pote esser intense in juveniles de plus que 1 anno de etate qui habita domicilios decrepite in que squamulas de colorantes a plumbo es facilemente accessibile. Le con centrationes de plumbo trovate in le feces del invenenate juveniles in le presente studio excedeva le concentrationes de plumbo trovate 1' m tf