Document aJJN5p6aXreKqmyVzygOVdZvb

U>l |1? " SEP^ms p h o t o c o p y pnc-vr;' -. g e is in g e r me d ic a l l ib r a r y NOTICE: THIS MAT."'*-1 : *.v 3= PROTECTED EY CCr ..\ - . ;i LAW (TITLE 17. U.S, CODE; clinic del I'Oi. . ucilt- lia esMl:e opic non THE EXPOSURE OF CHILDREN TO LEAD By J. Julian Chisolm, Jr., M.D., and Harold E. Harrison, M.D. Department of Pediatrics, Johns Hopkins University School of Medicine, Harriet Lane Home of Johns Hopkins Hospital, and Pediatric Division of Baltimore City Hospitals rmitte fe { rj^HE a v a il a b il it y of a new and effective mental status of affected children and the iduce un j X therapeutic agent has resulted in re- 1 vias in- I ^..'smniT!eTHnlcTciTntcc-;:catiori in ciiikl- :1 refluxo ? liood. Reports1-4 emanating from various 5 respira- l parts of the United States, indicate an in emonstra cere con creasing recognition of this disease, par infante ' ticularly in urban areas. While edathamil calcium disodium has proven to be of value personal-social situations in which thev 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 ninal as- in the treatment of acute episodes of the implementation of adequate preventive rrincipa] J nlumbism, it cannot be used to prevent the measures. fistulas toxic effects of prolonged excessive absorp tusse, e tion of lead. In children, as in adults, prepirution 1 cation of excessive exposure to lead re CLINICAL MATERIAL AND DIAGNOSTIC CRITERIA ?ee sugphagee. es pos mains the principal means of control. . A-pffi4gp^e_program must be The clinical material was derived from the elinics of the Harriet Lane Home wsed upon adequate gmnunmeiiUl.dala. anf Johns Hopkins ff0SDital and of Baltimore ts clinic e e re,e arii- TlIe^igeTnciH5niceeer,sese5ass;oonnaall ddiissttrriibbuuttiioonn ooff (lit- acute manifestations and concentration f cases among children residing in urban fC'iittvy fHfoosspoititaal.l 'I'n a"ll, 197 crhTirld5ren expos-edr to lead, including 89 patients with rente lead encephalopathy, have been studied. All pro le per ub- ila. Ri sser ?e. U le tir ompte !um areas are well known.1- * Although the dwelled in the urban slum areas of Baltimore. '.nluilation of lead fumes as a cause, of Within this group, 59 children were person- ilumbism in children has been reported,'T allv studied by the authors. In these children, is bej^&sd-thakaL^^ observations on developmental status and per- if lead-containing. paint flakes is: the most iimnion^3rceTr5irwEicE*3u!3lSroBfaffi" TDnal-sopial home situations were _studv was conducted during the ..to 1954, inclusive. made. The years 1952 ncessive quanrities^TS3TTEeTprS?5F' An important part of the present survey vport deals entirely with this litter type was the detailed analysis of exposure factors f exposure. in nine households in which abnormal sources Data hare been obtained upon the in- of lead were demonstrated. Within these nine ''nsity of such exposure, duration of ex- environmental units, there were 9 index cases >sure and the seasonal factor in the pro-' and 17 other children under 6 years of age fiiction of lead intoxication in children. I The "secondary" case rate among house mates of index cases has also been studied. Likewise, the relationship between the inklence of severe permanent damage to the ;,rain and're-exposure to lead among surivors of ah .initial episode of acute lead "'icephalopatfev has been examined. Ob- who 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 incidence of unsuspected "sec ondary" cases was determined. Another grpup of 33 children were patients who were studied during and after hospitaliza tion for acufel lead intoxication or encepha lopathy during 1952-1954. In addition, a re "rt-uttons were made upon the, develop- view was made of all hospital records of chil- 1 Submitted May 23, accepted July 3, 1956.) Hiis work Was supported by grants frCip the Lead Industries Association, New York, New York. and "Tn the National Institutes orn^ltRTTTST'ubl'Ic Health Service (G-3918L ADDRESS: (f.J.C Jr.) Baltimore City .Hospital, 4940 Eastern Avenue, Baltimore 24, Maryland. 943 N39096 f r-1, 944 CHISOLM - EXPOSURE OF CHILDREN TO LEAD dren admitted to the above clinics during the previous 12 years and indexed as "lead poison ing" or "lead ingestion." Among these records, 138 contained sufficient information to estab lish and classify the clinical diagnosis according to the criteria listed below. These constitute 138 of the 197 subjects included in this report.. Dia g n o s t ic Cl a s s if ic a t io n : All subjects are classified in six clinical categories as follows: Type I. Exposed-Xormal. 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 by roentgenograpny, were classified as exposed normals, if they had concentrations of lead in Hood less than 0.06 mg /100 gm whole blood, absence of "lead lines" ia roent genograms of long bones, normal findings in examination of the blood (or an .anemia which responded rapidly to the oral administration of iron) and no symptoms attributable to lead intoxication. Subjects in this category were subdivided into two groups: a) those for whom exposure to lead was verified by analytic records giving the identification and lead content of the material ingested by 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 child's environment. Type II. Asymptomatic, Increased Lead Ab sorption. These subjects differed from the ex posed-normal group in that they had elevated concentrations of lead in blood and roentgenographic evidence of storage of lead in the bones, without symptoms attributable to lead intoxication. Qualitative tests for coproporphyrin in urine were positive in some of these children. Type III. Lead Intoxication (without En cephalopathy). The diagnosis of lead intoxica tion was made in children who had, in addi tion to evidence of increased lead absorption, several of the following manifestations: anemia resistant to iron therapv, increased urinary excretion of coproporphvrin, severe constipa tion, anorexia, hyperirritabilitv, bizarre be havior patterns and intermittent vomiting. In the children of this group, there were no ab normal findings in the. cerebrospinal fluid. Type IV. Lead Encephalopathy, Mild. In addition to fulfilling the criteria for lead iut<i\ic.iti-.m, the children of this group had ab normal findings in the cerebrospinal fluid and nique o( one or more of the following signs and svmp. Jaded" toms: persistent vomiting, hvperirritabilitv. bv a th ataxia, intermittent convulsions and sonim,. `Lead-fn lence or semistupor. Findings in the cerebro jage of d spinal fluid were considered abnormal if tun resin cob or more of the following were present: in The a! creased concentration of protein, increased far the c pressure and pleocytosis in the cerobrospitu! containin fluid. As conet Type V. Lead Encephalopathy, Severe. Tin value tli encephalopathy was classified as severe if the : "specimen patients either convulsed continually for r i the final minimum period of 24 hours or remained appreeui! comatose for a period of 24 hours or longer, . than 0.T or both. ! between The numbers of subjects in each diagnostic counterei category were as follows: Hons suf I. Exposed-normal (with presumed lead occurred ingestion) 41 mg iron (a) record of lead source available 14 hy discc (b) record of lead source not available 27 ooverv oi II. Asymptomatic, increased lead absorption III. Lead intoxication without encephalopathv ]< IV. Lead encephalopathy, mild 4'- V. Lead encephalopathy, severe 41 to 110%. the meai 1.00 mg hr or gre Tissue ISr in the The remaining 12 subjects of the tola! group of 197 children exposed to lead wen normal control subjects in the household-stud', group who apparently had not ingested leadcontaining materials. Thev we 105C, f in triplic genate w method. 1 centration METHODS OF STUDY the anah> The intensity of exposure to lead was de termined by measurement of dailv fecal excre i from other the tiss tion of lead in all members of the household- ! * exceed In all study group under 6 years of age. Fooled T to 4-day collections of stools were made i: the home in covered 13s quart Pvrex casserole dishes supplied by the laboratory. Mothers were directed to have the child defecate di rectly into the casserole dish. In hospitalized patients quantitative collection of stools wete made while the children were on metabolism frames. j in childi blood an of lead the Balti was ana >teehnrqu' ^ final coin painted Aliquots of the pooled 2- to 4-dav stun! samples were prepared for analysis by homo genization of entire samples in a Wariiiblendor in which the standard brass bearin'- , homes b lead coit five tech follows: was replaced by a cast iron bearing." Dm'!" cate aliquots were dry-ashed"',J and ami! < J for load hv the mixed-color dithizono Lead al True t, i'ti.itiv Stun,'- i ARTICLES 945 :al fluid and <T: of Snyder.10 All equipment was "de- ; ar ' vmp. tl" with warm 207. nitric acid, followed ?rii Jility, ;,v a thorough rinsing in "lead-free" water. lnd sonrno- Lead-free" water was prepared hr the pashe cerebro- . .ae of distilled water through an ion-exchange raal if two ;esin column. 'resent: in. The above method was entirely satisfactory , increased :,ir the analysis of lead in feces in specimens robrospinal v,mtaining greater than 1.00 mg Pb/24 hr. \s concentration of lead decreased below this etere. The \,due the insoluble matter present in some vere if the .[iccimens caused increasing interference in ally for a ;he final extraction step. This interference was remained mpreciable in many specimens containing less or longer, than 0.100 mg Pb. '24 hr in which variations aetween pairs as great, as twofold were en diagnostic , countered. The presence of iron, in concentra- :ions sufficient to interfere with the analysis lead 41 5 14 able 27 iccurred only in the stools of patients receiv ing iron medicinally. This was readily avoided by discontinuing the iron temporarily. Ke-overy of lead in feces by this method was 95 so 110S. The maximum allowable error from as .he mean of .duplicates was =1055 (0.100 to iopathy IS 1.00 mg Pb, 24 hr) and szo% (1.00 mg Pb 24 4S il hr or greater). Tissues were quick-frozen and homogenized '85 ' ota! :b,, >verc >ld-studv ed Iead> in the frozen state: with mortar and pestle. They were then dried to constant weight at Ul5'C, frozen and re-homogenized. Analyses, "t triplicate, of aliquots of this final homoi'tnite were: then carried out by the aoove method. Difficulties, resulting, from low con centration of lead, were encountered only in 'he analysis of brain'tissue in which variation was de him the mean of triplicates was =t=15S. In al exor usebold>oled 2* -tlier tissues variation from the mean did not ; .wed =*8%. In all suspected cases of lead intoxication lade is asserofc in children in .Baltimore, samples of whole blood. an4 of suspected environmental sources doth f lead were routinely analyzed for lead by :ate S-; 'lie Baltimore-City Health Department. Blood italized was analysed by a weRcUgestion dithizone Is were ^(.`hnique utilizing a - spectrophotometer for iboliia nrial color estimation.11 Samples of paint chips, p tinted plaster, etc., were collected in the / stool! -v,mes by a visiting public health nurse. The homo-: Taring learing; " :id content -was estimated; bv technique1'- and reported I'lllows: a semiquantltaqualitatively as DupS-, aly2*d! ted- fe.id absent--less than 0.1" of lead Trace of lead--O.IS to 1,0% of lead Tositive fei lead--IS to 5% of lead Strong positive for lead-4gre4ter than 5% of lead RESULTS In nine households selected for detailed study of exposure factors there were 9 index cases and IT 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-study 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 associates13 that fecal excretion of lead provides a good index of lead , ingestion inasmuch as ap proximately 9(5? 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 km those subjects with lead intoxi cation were made in the' hospital at least 1 week after the completion ' of therapy 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 were obtained from 22 of the 24 ambulatory children under 6 years of age in eight of these nine house holds. Comparable stool1 samples were ob tained from six children of physicians on the pediatric staff. These1 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. Tlfe 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 946 CHISOLM - EXPOSURE OF CHILDREN TO LEAD f TABLE I Da il y Fe c a l Ex c r e t io n o f Le a d in Ch il d r e n Be f o r e a n d Af t e r Re mo v a l o f En v ir o n me n t a l So u r c e s o f - Le a d * Classification of Patients^ Types III, IV and V At home during exposure In hospital after therapy Types II, III, IV and V At home after exposure Type II At home during exposure Household Controls At home during exposure .Vo. of Patients Xo. of Specimens Mean Lead Output (mg/Zi hr) Median | Range Household-Study Group 0 I 61 5I 8j 1 10 j 44.0 18 0.362 11 13 j 0.365 ! o| H j 2.16 1i | ii ! 23 ! .0.882 27.0 0.240 0.511 1.11 0.051 5.04 -104.0 0.062- 0.850 0.039- 1.50 0.116- 9.60 0.087- 1.93 Xonexposed controls** At home Types IV and V During exposure* j 6| 1 7i 6 7 Other Children 0.132 0.157 53.4 53.4 0.012- 0.175 0.373-223.0 * The household-study group has been divided according to both diagnostic classification and presence or ab sence of lead exposure, in order that the observed differences in fecal excretion of lead under these varying conditions can be seen. Each specimen represents a 2- to 4-dav pooled collection of feces from the lead content of which is calculated the milligrams lead excreted per 24 hours. An average of two such specimens were collected from each patient during each period of observation relative to exposure. t Diagnostic Classification; see text for criteria. ** Nonexposed Controls: 12- to 33-month-old children of members of pediatric staff for whom there were no known environmental sources of lead. t These seven patients admitted with acute lead encephalopathy were not members of household-study group \ alues shown are based upon total lead content of admission stool, divided by the number of days since the Iasi previous fecal evacuation, in order to obtain mean daily excretion. . pooled collections as 24-hour outputs. In most subjects two pools of 2- to 4-day col lections of stools were obtained during ex posure. The data, therefore, represent ap proximately one "exposure-week" of ob servation in the various subjects. The term "exposure-week" is used, inasmuch as the samples were not always consecutive. On the first line of Table I are shown the out puts of lead during exposure of six patients with lead encephalopathy and intoxication. The mean output of lead in this group during exposure was 44 mg/dav and the range was 5 to 105 mg/day. Three of these had acute lead encephalopathy. Their 24hour outputs are calculated from the lead content of the first stool passed after ad mission to the hospital. All other stool collections during exposure were made in the homes. When these lead-poisoned chil dren were removed from exposure to lead by hospitalization or, after discharge, by removal of all identified sources of lead from their homes, the daily fecal excretion of lead fell to normal values, approximately 0.3 and 0.5 mg, respectively (lines 2 and 3). On the fifth line of Table I, the mean daily output of the 11 control subjects in Normal Oh ' Primitivt Americai Present 5 Industrial i All types Severe es Lead Poiso - Present s 1 * In this mal and th are compar -Kehoe et tu single feeal <\ Mexican cr 'i American c j these childr ' They obtai dustrial wo and analyti the poisom severely ex; household c normal une> f Taken f. ! 15:302. 1933 the preser proximate! be seen t ( i Dis t i i 12 :jr, I \- = !).-is. ARTICLES 947 Range -104.0 - 0.850 1.30 9.60 1.98 0.1*5 !3.0 ab> mentions which a rom ead were no v group the last TABLE If Fe c a l Kx c u e t h j s o k Le a p * I tjpe of Subject mg Pl/Dmj itean Range .Normal Children Primitive society! America n (hasp.)! Present study 0.088 0.48 0.88 (>- 0.28 0.01- i.i 0.09- 1.9 Industrial workers All types of exposure! Severe exposure! 3.8 T.fi 0- 14.0 2.0 - 14.0 Lend Poisoned Children Present study 44.0 3.0 -104.0 * In this table the daily fecal lead output of the nor mal and the poisoned children in the household group .ire compared with similar data from the studies of Kehoe et al.aM They determined the lead content of single fecal evacuations from children in a primitive Mexican community and in convalescent hospitalised American children. The only known source of lead lor '.h'Se children was that contained in their normal diet. They obtained similar determinatioi in exposed iuilustrial workers. Despite the differences in sampling .uni analytic techniques, the fecal excretion of lead by the poisoned children apparently exceeds that of t verely exposed industrial workers, while that of their imusehold controls is of the same magnitude as that of I'irmal unexpose'' children. + Taken from data of Kehoe et at.: J. Indust. Hvg., 11:802, 1933. the presence of exposure to lead was ap proximately 0.8 mg of lead daily. It can he seen that those children classified as asymptomatic, increased lead absorption (line 4) occupy an intermediate position between the poisoned and the control sub jects. Tims, 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 et ai.1'-1* on fecal excretion of lead tinder various conditions of exposure to lead (Table II). It oan 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 by Kehoe et ah33 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 were 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. Xo evidence of increased lead absorp tion or ingestion was demonstrated among the older housemates (Table III). Indeed, if the index .eases are Included, 14 of the 15 children aged 12 to 35 months in the nine TABLE III >ir 24; lead ir adstool de is : chil- ! lead by lead stion itelv tad teas | S SB I Ho u s e h o l d St u d y Dis t r ib u t io n b y a g e or UNSUSPECTED c a s e s o f a s y mp t o ma t ic , in c r e a s e d l e a d a b s o r p t io n a n d LEAD INTOXICATION IN HOUSEMATES OF NINE " VDEX CASES Age Groups 12 to 35 months 36+ months Totals Subjects at Risk 6 11 ' Sumber of Subjects ! Asymptomatic, Increased j Lead Absorption and j Lead Intoxication. !5 |0 ! Sormals 1 11 14 X! = !).28. 1`<0.01. TABLE IV gg lead were idet Le a h Co n t e s t o f Tis s u e s o f Ch il d r e n Dy in g f r o m Ac u t e Le a d En c e p h a l o p a t h y yms each chile (Jjewcd. For 102 Patient Age (mo) Time "J Death* Lead Content (mg Pb/l'jO gm dry tissue) Rib 1 Brain Liver | Kidney Total Lead Found in Soft Tissues (mg) Output M. Lead '-'i Vriiu t one source cont. {sad. The lead u DB the surfaces, faking and frequ R. McF. X.B. ILK. L.D. 45 hours 39.9 1 1.1 10.5 j 8.9 3-1 14 hours 33.0 i 1.0 46.1 ! 9.5 SO Si days 13.1 ! 1.4 4.1 J 5.5 43 6 hours 10.0 : 1.7 -- 15.0 40.5 io.r* anuriv 5.1 4.s 4.4 05, one or more ained lead pigrr of lead may hafetal solids in the * Time of death after institution of therapy with edathamii calciutn disodium, An attempt v f Total output of lead in urine during therapy prior to death. ** Exclusive of brain, estimated lead content of which is approximately 3 mg. duration of expo symptoms. Mate households were found to be ingesting po an additional 48 sources. For each of the Son of their ch tentially toxic quantities of lead. 105 exposed children, from one to five dif taining material- In four patients who died during an ferent sources containing greater than l' obtainable or v acute episode of lead encephalopathy, tis Insure, howevei sue content of lead was determined (Table IV). Three of the four patients died within TABLE V mate of the pro if the followin 24 hours after the institution of therapy En v ir o n me n t a l So u r c e s o f Le a d * t) the location; with edathamii 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 location Lead Content Less than 1% 1% or J/urr paired that the order to reach t at the time of flf age on the i of the body from these data, the content of Interior Sources tioas the prol lead in soft tissues can be approximated. Windowsills & frames 5 110 could be estim; Aub et fll.15 and Kehoe ct alf" have found Interior walls between the c & in animals and in human necropsy material painted paper painted plaster 38 4-1 10 34 | age at which obtained from individuals dying within a Door frames 1 15 asymptomatic, few days or weeks after cessation of chronic Furniture 3 3 or clinical leac exposure to lead that from one-third to two- Cribs 3 1 When the data 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 wails Exterior Sources 3 10 6 0 27 d o statistically be found betwposure and ss normal childn 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 85 440 I indicated thai of similar dui Stations man of lead, with An explana 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 sources of Uato which 105 suhjects in this series were exposed. Thesources were identified by aualysis of paint sernpia--taken from the various surfaces in and about the hoin< which gave evidence of having been chewed. For <ai when the sc account. Thi developed ac to 2 years tween the se; tained from cribs and furniture. More strik ing is the fact that 116 of the 220 sources were window-sills and frames. Peeling wallpaper and crumbling plaster accounted for subject one to seven such sources were identified. l': i duration of all 103 subjects at least one source containing S Ale patients than 1% of Scad was found. For 104 of the 1H5 .-ml]<<!- at least one source containing greater than 5% of lea- oionth of tin was found. by a bar wt ARTICLES 949 lead were identified among the various TH > items each child was thought to have - Jicwi'd. For 102 of them there was at least mi Output of ,mo source containing greater than 5% of Lead in lead: The lead was contained in the paint ac# v ,ni the surfaces. The paint was old and i diking and frequently contained many lay- nnuric ,rs, one or more of which may have con 5 . tained lead pigments in which the content # 4.8 ,.f lead may have been 80 to 7 of the 2.4 total solids in the paint. An attempt; was made to ascertain the Juration of exposure likely to produce toxic A'mptoms, Maternal estimates of the dura ir each of the tion of their child's ingestion of lead-con me to five dif- taining materials frequently were either un eater than IS obtainable or unreliable. The type of ex posure,. however, permitted an indirect esti mate of the probftble duration of exposure, if the following assumptions were made: o f Le a d * ,i) the locations of The sources of lead re- rad Content juired that the children be ambulatory in mler to reach them, and b) exposure began 1% 1% or Hat A the time of. atolbelslion,, or at 12 months f age on tlie average. With these assump- e Sources imis the probable duration of exposure 11C could be estimated as the interval ih months tetween the child's first birthday and the 10 32 at which die child was classified as 15 .wmptom&tic, inepeasbd lead, absorption, 3 >t clinical lead pouching was discovered. 1 When the date, wfare analysed oa this basis, terior Sources 10 20 - 'in statistically significant correlation could v found between presumed duration of ex*>sure and severity of disease (exposed"irmal children excluded). Indeed; the data Totals 183 37 220 ^Heated that 'the presumed exposure was 'f s&nilar duration in all diagnostic classi' rations manifesting increased absorption f lead, with hr without syipptoms. An explanation for this became apparent ent and locationf ten the seasonal factor was foken into lental sources of ;*, count. Thirty-two patients in the series were exposed. LdaCutSS ; tj e2'fbypeeadrsadosftealgeea.d tbhnece'prehlaalatidpariisthhyipp' rbioer- >ii chewed. Fo p ` een the: seasonal factor and the presumed were hidentified. R '^ration of ejkpasore ft shown for each of * containing g*Jj fi*. pat^nte'in J?We 1, in which the Ifthlns^ofSof the child's fijst birthday1 is joined ' a bar with this naohth bf onset1 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 birthday between May and September are shown. They 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 birthday during the winter mouths prior to April. They became ill dur ing the first summer after the presumed on sets . pf 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 diistilibution of births by month in the group does not differ significantly from the monthly distribution of births in Baltimore lor the: years 1951 to 1953 inclusive, during whicli most of the patients were born. In this sfoall group the peak In births during December, And the passage of the older infants through their first summer of ambulatlori without svmptoms, suggests that 5 to 6 months of lead digestion may elapse prior to the onset of acute lead encephal opathy. The possibility that a minimum exposure perMlrf 3 months Is required, after which die advent of summer becomes the control ling' factor in: the production of symptoms, is also suggested by the following finding. In thfe entire group there were 14 children with pjiequivocal evidence of excessive lead ingestion including identification of at least one ettiritoameiitsl source containing greater than IS of lead, but with no evi dence of increased dead absorption. Eight of these fourteen normal-exposed children 930 CHISOLM - EXPOSURE OF CHILDREN TO LEAD RELATIONSHIP BETWEEN MONTH OF FIRST BIRTHDAY AND MONTH OF INCIDENCE OF ACUTE ENCEPHALOPATHY SUMMER SUMMER Qo00" 0 MONTH OF FIRST BIRTHDAY O'* INCIOCNCC - SURVIVAL II - DIED 3 ON0 MONTH ON Fig . 1. In this graph the month of onset of acute symptoms for each of the 32 patients who develop acute lead encephalopathv prior to 2 years of age is shown on the right. On the left is the month of t:. child's first birthday. These points are joined bv a bar. The length of each bar, therefore, represents t! assumed duration of lead exposure (in months) for each child. Twelve months of age was selected as th average age of ambulation. The nature of the exposure in this series required that the child be ambuL tor,- in order to reach the sources of lead in his environment. In this manner a relation between pri sumed duration of exposure to lead and the seasonal factor in the production of symptoms can 1* demonstrated. Jjllowed fo {6 patients, tfnued inge months or posure and lead after fopathy. TI Survivors ot analysed, v. during tht whether th the occurrt T. in the cen posure to ; ~lhe follov sidered evi page to the .recurrent disorder. having th. strated on 12 fulfills statistical! tion betw vere seqt following opathv (> tion betv lead is m surviving lopathy. . posure w were less than 13 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 bv histories obtained from many parents, who stated that they had seen their children ingesting parnc Hakes or had found pilasfer panicles in die 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 seven permanent damage to the brain among sur | vivors of an initial attack of acute lem* encephalopathy indicates the importano of continued environmental exposure f lead in increasing the incidence of cento nervous system sequellae. In the entin series 61 survivors of acute lead enceplw i opathv were treated more than 12 month! prior to evaluation of sequellae (therap ! with citrate, 16 patients; therapy with BM 28 patients; and therapy with edatbam calcium disodium, 17 patients). Fifteen > the group were lost from follow-up. Fortsix of the sixty-one patients (citrate, 13 p tients; BAL. 19 patients; and edath. ' calcium disodium. 14 patients) have 1 Rr l a t h >s Known r> No know * Four W;i> uni i T S-(P l*i,vvri- 1 .D ARTICLES fr>i 'HDAY AND OP HY -a --a at' - ho develop 5 month of 4 yte, represents t as selected as#- child be ambei don between jr ;ymptoms can* iih'owcd for 1 year or longer. Of these 4f) patients, 14 were known to have con tinued ingestion of lead for periods of 2 mouths 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 tope of therapy during, the acute phase, to determine whether there was- any association between the occurrence of severe:permfenent residua in. the central, nervous system and re-ex posure to dead. 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 sequelae," 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 retefepbsure to lead following recovery -fro . mild1 encephal (X*opathy = 14.30, ? < 0.01). The correla tion between sequelae 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-ex posure was uncertain in 4. These 'four, all of whom had permanent residua in the brain, are omitted from Table Yl. IF these doubtfullv re-exposed eases are considered as not re-exposed. X, -- 2.6-S and P > (U (re-exposure is not stati.stieallv .significant'. For the entire group of survivors of mild and severe encephalopathy there is no sig nificant correlation between seqiudlae 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 fo lead there is no correla tion between sequellue and age of incidence at the IS, 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.-'-' 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. ence of sevs ain among of acute to le import l exposure 1 nee of cei* In the enb ead encepb lan 12 mofll ;llae (the ipy with B/ ith edatb* :s). Fifteeft ow-up. Fat' titrate, 13 J id edath s) have b TABLE VI Re l v t io x b e t w e e n In c id en c e o p Se v e r e Se q c e l l a e is t h e Ce n t r a l Ne r v o u s Sy s t e m a n d Re -e x p o s u r e t o Le a d f o l l o w in g Re c o v e r y f r o m a n In it ia l Ep is o d e o f Ac u t e Le a d En c e p h a l o p a t h y Acute Lead Encephalopathy Known re-exposure to lead y>n known re-exposure to lead Severe Canes* With Sequellaef Xo Sequellae 70 *6 X**4.89; P<0.05 ; i j j 1 4 | ! [ Mild Casts With, Sequellae Xo Sequellae 70 8 IT X*-14.35; PC0.01 * Four survivors of severe acute lead encephalopathy, who sustained sequeHae but in whom re-exposure to lead "'is uncertain, are omitted from the table. (Sec text for discussion.) t SequeUacsevere, permanent, residual damage to the brain (severe mental retardation, convulsive disorder v-verc behavior disturbance). I 952 CHISOLM - EXPOSURE OF CHILDREN TO LEAD I crumbling, painted plaster or loose paint Lehman15 recently reviewed the litem- cIupFFrornwansTceilings, cloorlramesTwin-' ture and concluded that the average daii\ dow-sills, outside porches and fences were" ingestion of not more than 1.5 mg of Ituui readilv accessible to the hands and mouths is without harm. Kehoe ct al.v- have found of inquisitive smalTcHlldren. The chlta of that significant retention of lead in the tis the present study show the intensity of this sues occurs when, in addition to normal type of exposure; but they cannot be ap dietary intake, adult volunteer? are f! plied directly to such questions as the 2 mg of soluble lead (as lead acetate) dailv. minimal quantity of lead toxic for children The data in Table I are in accord with or the maximal safe content of lead in these conclusions. Under the sponsorship o! liquid paint the American Academy of Pediatrics, the | Among the environmental data pre Committee on Hazards to Children of the sented, two factors stand out: the intensity ^American Standards Association studied of lead exposure provided bv a small quan the problem and recommends that paints tity of paint flakes and the role of the mav be considered safe for use on clril season la precipitation' of acute lead en dren'stoys and furniture ancTEouslnginU/ cephalopathy. tenors if the lead content does not. ex- The data in Table I on fecal excretion of ~^ee3~If'~QOli&J~'totar sofidsT^HPamts and lead may be utilized, as a measure of the other surface coatings meeting this speci - Fig . 2.E Four small fragments quantity of lead ingested by the various fication and those relating to other po removed ft 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; tentially toxic metals may be labelled; "con forms to American Standard Z 66.1-1955." _It Is essential to recognize that this-ifinmv. mendationappIies~milv to: die two, or three His feces, evacuation, almost dail ~10 months for the mean daily fecal excretion of lead in the poisoned children exceeded, bv 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 by the lead-poisoned chil dren (44'mg Pb/day) exceeded, by -ap proximately sixfold, that of a group of se verely exposed industrial workers (7.6 mg Pb/day) and, by elevenfold, that of work ers in. various trades in which exposure to lead is less severe. The groups pf 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 stud}-, 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 encephalopathv 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 anv inherent biologic differences between child and adult. "TayerilirpamFuSM surface: TouffffTirQ^^ the number of layers increases or when a layer of paint containing lead pigments is added, the quantity of lead per unit area increases to the point where even a small flake may contain an excessive amount of lead. The magnitude of exposirreL-ta-leadassociated with the insrestionLoi-a. fent-smalL paint flakes is emphasized if we calculate the^quauiitltte to yieldthe~amo^^ stops' of the: Iead-pjrisQnM-4^jMj^n.: for example, 44 mg of lead would be equivalent to the ingestion of 0.88 gm or less of paint flakes containing 5% or more of lead, or to 4.4 gm of flakes containing IS of lead. An example of the size and quantity of paint chips necessary to yield potentially toxic amounts of lead is shown in Figure 2. In Table V the location and lead con tent of environmental sources of lead are shown; 102 of these 105 children were ex posed to at least one source containin'-! greater than o\L of lead. No case of lead in toxication has been found where the on'v source of in the d data app lead is p well as a solids app with a sa ceivable t housing ' many lay as 1% of children hazard tc Evider cates th; matelv 3 the adve continue! ling envi tion of a Althougl non is r evidence which i actinic t the alva ARTICLE': 953 1 the Jitera- v '<? daily 5 of lead 12 have found `ad in the tjs. to normal eers are fed icetate) daily accord with ponsorship of ?diatrics, the ildren of the don studied. '< that paints use on ehij- housing in. oes not exfaints and l this specL J other pa. Fig . 2. Example of size and quantity of paint fragments containing a potentially toxic quantity of lead. Four small paint cliips arc shown with a cigarette for comparison of size. The aggregate weight of these fragments was 2.68 gm; they contained 234 mg (or 9.55) of lead. With the fingernail they were easily removed from a door frame upon which a patient with acute lead encephalopathy was known to chew. jelled: "con* His feces, which were obtained on admission to the hospital and 48 hours after the last previous fecal i-i9sr this recta, wo or three 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. o a surface;; source of lead contained less than 1% of lead It has also been suggested that the in as may :fe in the dried paint surface. The present creased heat of the summer leads to de- As the' data apply to old housing. Inasmuch as hydration and acidosis iinn small children i when a; lead is presently used as a paint drier as and "nTtKis"manner may plav a role in the pigments is, well as a pigment, 1% of lead liTtotaTpaint production of encephalopathy.-0 In the r unit are solids approacEestEe minimum consistent "pfesentlitu5y~no reliable data could be ob- ers a snat ^SISIlaHslactorv'irouse 'pamETtls com~~~tained concerning vitamin D intake in view amount; of eciyable that poor maintenance of modern of the sporadic use of vitamin D-fortified re. to ieal: housing with resultant accumulation of evaporated and fresh milk products by the rfew saal? jnanylavers ot parnts (containing as little subjects. Among the patients interviewed, a ?. calculate ns IS of lead}" on surfaces accessible to history of no vitamin D supplement during Pessary *; TfilfOren future constitute winter or summer was given by about half rid In ttef , lazard to small children. of the cases. Idrea:. fori '1 Evidence has been presented which indi- When the probable duration of exposure aquivalstst? ! Oates that, after a minimum of approxi exceeded 3 months, no correlation could be ss of pal# mately 3 months of this type of exposure, demonstrated between increasing severity ead, or to, die advent of summer (in the presence of of disease and further monthly increments -.lead. As tontinued exposure to lead) is the control in exposure. This finding may be explained r of patt# ling environmental factor in the preOipita- by the interplay of two other factors: the a% tea*: `ton of acute lead encephalopathy (Fig. 1). magnitude of lead ingestion observed in ;ure 2. j Although the mechanism of this phenome the household-study group, and the sea had GW*;.; non is not fully understood, experimental sonal factor in the precipitation of acute Head ijP':i ' vidence has been obtained in animals symptoms. It emphasizes die urgency during Were e& '' iich indicates diat vitamin D and the die summer months of the prompt removal antainfef '{Jtinic rays of the summer sun increase of children manifesting asymptomatic in f lead si the ofl$ ' absorption of lead from the intestine.5 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 die 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 toxic substances, a single ingestion which, suffices to produce symptoms. Tl,, wont of toddlers in the 1-ycar-age group [, taste and eat a large variety of foreign ma terial is well known and is considered to 1,. a part of their normal behavioral pattern at least for a short span of time. In the present study all members of tin household group were submitted to psychometric examination. Within this group nr. striking developmental deviations could L found between the affected and the nonaffeeted members. In addition, 28 patientwho were not re-exposed were psyeliumetrically evaluated 1 year after recoven from acute lead intoxication and encepha lopathy. The distribution of intelligence quotients on the basis of the revised Stanford-Binet Intelligence Scale, Form L, was S follows: cated by cases") or gestion. Ir fion of ing< fiace overt ' However jn those s oay, in p greater in of this rep population similar pi spect to r plumbism, -were awa paint or h poisoning. 33 mother yolved, w consideret exists- in i old housing areas than has here- Intelligence Quotient .Yumbers of Patients child was him." Sue totore been recognized. Furthermore, when- . - 60- 69 3 understan ever an index case ! is found, his environ 70- 79 o ealculatior mental contacts under 3 years of age should be submitted to careful clinical and labo ratory examination. 80- 89 90- 99 100-109 110-119 5 9 flakes ina- of lead. It * vL. minute qi Although the need for identification and leads to If removal Of environmental sources of lead These findings would agree with the con- that no m is well known,3'21 a highly significant cor cept that the ingestion of foreign material ( to preven relation between re-exposure to lead and exhibited Ey~~these children was not face of err the incidence of severe permanent sequel- rnanHestat!on~of mental deficiency, but that be recogn lae in the central nervous system in sur ,'tHe"reacIy"avaiiabiUty of a highly toxic mu- both inter: vivors of an initial episode of acute en- teriaTm the environment was the important- -is probab cephalopathy has not previously been re- factor. This is certainly supported by tin ^ ported. Tliis indicates that immediate and '"ThgFTa5gcondarv" attack rate found amonc f mental fi. absolute^reveption of re-exposure may, the control subjects of the household study.* preventio ^CTEpsT^^Se'll^plnoitimmEEISSfe,-. If the assumptions are made that- fink-in;: The co -term factor ia"!Ke^v^ lead-containing paints are widely distrib [ents who consisted such patients, labour experience this has tited in old housing, that there are large which m. been satisfactorily accomplished only by numbers of infants and toddlers living ic been inei burning the old lead-containing paint com- 'sucfLaTphysIcaTenvironment andthat nor- to remove pletely away or by transfer of the child to malaswell as defective children may reacP~ wise, war a new dwelling in good repair. ily ingest amounts of lead sutficienTT vision of The term "pica" is frequently used in as- norotluce~TnIoxication, the question arises sociation with both lead poisoning and with iJS^MTleaTTnfoxication not more~jireva the thirtx who >vor mental defect in children. Thus, in the lent than the numbers of cases presently Week u minds of many, plumbism and mental de- recognized would indicate? Manv caw- hoim* th fidelity are frequently associated. This is oTTesstTTlegfecTTT intm-irviHnoT^i.- v -PH'-'hbnr not so with respect to the ingestion ot other unrecognized unless maudit out fas r Six oi tin ARTICLES 933 ingestion o! j can d by the incidence of "secondary T 's. The] c.i'-fs") or may be the result of Jesser in-at /oup f3^ at`stioh.~Tn still other children the dura f foreign ma- tion of ingestion may be insufficient to pro sitiered to be duce overt signs of lead intoxication.- iorul pattern, However, personal-social factors elicited dren less than 5 years of age. Thev 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 aibers of die *d to psychoiis group no ms could bi nd the non- 28 patients ere psycho. :er recovery id encephaintelligence wised Stanorm L, was in those ~su&]ecfr"studiecl by the authors demonstrated an excessive desire for af may. In part, .account for the relatively fection. From"the point of view of the greater ingestion of lead in . the- subjects child, the ingestion ai foteigil material Was" of this, report as compared with the larger an obvibijs atferifiob-geffing device-In' population of 'children who stay live in similar physical environments. With re-_ "punlglleig'lfel^ _ I2I spect to maternal information concerning mBlaielaSlvertStly upon. the window ss ills plutfibism, mothers were ashed . if they '^annddd^omor'rfrlafmeeSs^aFs tthSey^ggaazSedd'oouutriinnttoo&i e" were aware of their child's Ingestion of "street."' in' tSlieier^oretipm was apparently paint or had heard of the danger of lead conducive to thelead ingestion, and may be poisoning. Significant, is the .fact that 14 of attributable' to the lack of aa emotionally jind intellectually stimulating-environment. volved, were not concerned because they Many parents reacted by an overprotective mbers of ^atients considered thiem >unt of paint: Me# their attitude following their child's recovery ,-hiid ^ hurt from acute lead' encephalopathy. They fre- liim.'^Sueh matefriai statemitnfr'are1 q^ito "queatly soasht advice about play activities S f "iiruIeStSnda'blfe in view of the preceding for their child; the diminution In pica was 2 calculation that less than 1 gtn of paint often striking. 5 9 K Hakes may contain highly toxic quantities of lead. It is ffad repetitive ingestion of these SUMMARY AND CONCLUSIONS minute quantities of such paint chips which A study of some environmental, behav a the conn materia! -as not /, but that toxic n*aimportan* ;d by tb xids to fad intosibiiHmirif" iPis conceSed that ho'mbther ca'ii reasonably be expected to prevent this type of ingestion in the face of crumbling print and jfaster, ft will be recognized that proper maintenance of I'oth interior aiict e aor surfaces 'L-Qiafebiy i... i i-Tj 1 M L iihpoF . .. r-f. it-U- 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 exposMe to lead^onTreoefitive in gestion. of, quantities of leaded-paint n5tes71g<c^^factor id among old study it flaking y disbrih are larc living fc The" "ddrifeetlvd el&^s T`j*rf^rthe jfaC mts who attempted to curb tie ingegtion consisted largely of iwn|fciyi| itaeasjqres iiich niav laraSTIS" (siimmefyih Ole precipitation of acute lead encephalopathy. The predominance of these two factors tmy explain the absence of any significant ectfreladon between severity of disease and incitements (beyond a minimum of 3 months) in the probable duration of that n- f lay read- Icient *n arise e preva' iresend) ly caf may? as m0. joiion ofj.fa a bic-lTsirtpffiw mothers wese earftm bo worked at least several days of dseli 'vek away from home. While away firom `omc they left theft small cMMiren with Neighbors or in the care of older children, hx of the mothers bad more fata three chil exposure. It whs concluded that a child without symptoms but having increased absorption: of lead, recognized during the summer month, 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 exposureftodjadlnaF^dlntense in children 956 CHISOLM - EXPOSURE OF CHILDREN TO LEAD over I year of age living, in dilapidated childhood plumbism than specific limita dwellings in w;JSch flaking leaded paint is tions on the content of nonpigment lead E 'readily accessible. The amounts of lead~ 'freSK~-paint TTievario"us--environmental "'found in tEeTeces of the poisoned children poIntloThe conclusion that, when- in the present study exceeded that found by housing has been permitted to deteriorate, others in the feces of exposed industrial exnosmeToleaHl^^ as workers. This suggests that the higher in to outweighsuch individual variables as cidence of lead encephalopathy among inenlsTIreto children as compared with adults may, in ~lustoCTfs"m*TEe~''cI5I5I Such Intense cv part, result from their relatively greater ex posure is a preventable hazard to normal posure. small children, and, as such, constitutes a The importance of continued environ public health problem which may be more mental exposure to lead in increasing the extensive than has heretofore been thought incidence of severe permanent damage to to exist. the brain among survivors of an initial at Pending the. wider availability of better tack of acute lead encephalopathy was housing, preventive measures will have to demonstrated. The correlation between the be adapted to individual home situations occurrence of such sequellae and re-ex- and to the available facilities within a given posure to lead in patients recovering from community. Basic to any preventive pro mild acute encephalopathy was statistically gram are facilities for the prompt identifi highly significant. It was concluded that cation and removal of environmental removal of lead from the child's environ ment is the only adequate protective meas others.3,21 Equally important is a compre- ure in such cases. liensive social investigation of the home in The high proportion of children aged order to evaluate the circumstances under 12 to 35 months with average intellectual which the child obtained toxic quantities capacity found among cases of lead in of lead and to determine whether the iden toxication, and the high incidence of un tified sources of lead can be adequately re suspected cases found among 12- to 35- moved, or whether a change of dwelling is month-old housemates of the index cases required to prevent further dangerous ex demonstrate the importance of the environ- posure to lead. mental aspect of the problem in urban slum areas. This high incidence of "secondary ACKNOWLEDGMENTS cases6 emphasizes the physician's obliga tion to examine carefully and promptly all environmental contacts under 3 vears of age wherever 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 The authors wish to acknowledge the co operation of the Baltimore Citv Health-Dt1partment, 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 psychometric examinations included in this report. Mr. Peter Wei performed some lead analyses of the feces and tissues. denied, no mother can reasonable be ex- REFERENCES pccted to^rfcvenFTIvc~repcHtiveingesH^ of a few paint chips wjien these are readilv _^-acccssii>le. As lead is widely used as a paint ~^ancr7~Toutimicd good maintenance of jpaintccTsfirfaces would appear to ho more ~ pertinent to the long-range prex; 1. Byers, 11. K., Maloof, C. C., and Cush man, M.: Urinary excretion of lead in children. Am. J. Dis. Child., 87:54-S. 1954. 2. Bessman. S. P., lfubiii, M., and Leikin. S The treatment of lead cncephalopatb' A method for the removal of lead d ms 4. 15. Au' 16. Ke 17. II. ARTICLES 937 limitalea mental where iorate, sitv as les as naiad>e exlonnal ites a more ought better ve to itions given promtifiental ;d by raprene in irtder. titles y reQgis ; ex- ; coDeims, J lade 1 1 of i in MB# ins; the acute stage. Pe d iat r ic s , 14:201. 1934. I Williams, H., Kaplan, E., Couchman, C. .. and Sayers, K. R.: Lead poisoning in voung children. Pub. Health Rep.. 7: 2-30, 1932. 4. M ellins. R. B., and Jenkins, C. D.: Epi demiological and psychological study of lead .poisoning in children. J.A.M.A., 158:15, 1933. 3. Rupoport M, and Rubin, M. L: Lead poisoning. A clinical and experimental study of the factors influencing the sea sonal ineidfenee in children. Am. Dss. Child., 61:24-5, I?4L 6. Williams, H,, Schulze, W. H., Rothchild, ff. B., -Browns, A.. S, and Smith, F. R., Jr.: Ledd poisoning from the burning of batten* casings, J.A.M.A., 100:1433, 1183. ' 7. Wyflie, J.: A family outbreak of lead poisoning from burning of storage bat ten* casings. Canad. M. A. if., 70:287, 1 8. Methods for Determining Lead in Air and in- iillological Materials. New York, American Public Health Ass'n., 1944. 9. Official-: and Tentative Methods of Analy sis. 5th Ed. Association of Official Agri cultural Chemists, 1940, p. 397. 10. Snyder, L. J.: Improved ditbizone method for determination of lead: Mixed-color mjtafemethod ;at high pH. Analvf Chem., 1&884, 1947. 11. Kaplan, E.:- Personal communication to thp author. 12. Kehoe, R. A., Cholak, J., Hubbard, D. M., Rambaek,. K, .and McNary, 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, ilk 13. Kehqe,?R. A., Thamann, F., and Cholak, J.: On.-we normal absorption and excretion of had; lead absorption and excretion in infants and children. J. Indust. Hvg., 15:301, 1983. 14. Kehpe, R. A., Tfeaiaarm, F., and Cholak, J.: lead, absorption and excretion in cerfeia lead trades. J. Indust. Hvg., 15: 3ti, 1,933. 13. Aub*: J: G., Fairhall, L. T., Minot, A. S., and fleznikoff, P.: Lead Poisoning. Balti more, Williams & Wilkins, 1926, p. 53. 16. Kehofc, 11 A,, Thainann, F., and Cholak, J.: Lead absorption and excretion in rela tion to tbs diagnosis of lead pi J. Indust. Hvg. & Toxicol., 15:320,1 Hamilton, A,, and Hardy, H. L.: Industrial T.i\i. Ingv. 2nd Ed. New York, I Indict'. D-JV. p. Ml. IS. Lehman. A. }.: Quarterly Report to the Editor on Topics of Current Interest: Lead in decorative paint for children's toys 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 -- 1935'. New York, American Standards Association, 1353. 20. Blackman. S.^STTTrTTTlie lesions of lead encephalitis in children. Bull. Johns Hopkins Hosp, 61:1, 1937. 21. Byers. R. K., and Maloof, C. .; Edathamil calcium-dfeodium1 (Yersenate) in treat ment of lead poisoning in children. Am. J. Dis. Child, 87:559,1954. SUM MARIO 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). Eslseva concludite que un caso de asymptomatic augment del absorption de plumbo quje es recognoscite durante le estate pole progreder a sever eneephalopathia intra alicun septimanas si le fonts del plumbo non es promptqmente ideatifleate e eliminate. Le diume ingestion ajedle de plus que 1,5 mg de plumbo es potentialmente toxic. Un medietate del matres intervfewate esseva inconscie del facto que minuscule quantitates de colorante pote continfer eonefentationes: toxic de plumbo. Le present studios ctemMstra que exposi tion a plumbo pote :esser intense in juveniles de plus que 1 anno de elate qui habita domicilios decrepite in qua squamulas de colorantes a plumbo es: facilemenfce aceessibile. Le concentrationes de plitaft&o trovajte In le feces del invenenate Juveniles in le presente studio excedeva le ecracenterttonss de plumbo trovate 958 CHISOLM - EXPOSURE OF CHILDREN TO LEAD per aitere autores in Ie feces de exponite obreros industrial. Iso pare indicar que ie plus alte incidentia de encephalopathia a plumbo inter juveniles in compaction con adultos es possibilemente in parte le resultato del relativemente plus alte grade de exposition. Es demonstrate le impprtantia del factor de continue exposition a plutabo in augmentar le incidentia de sever lesidnes permanente del cerebro inter superviventes de un initial attacco de acute encephalopathia a plumbo. Le cor relation Inter le occurrenjia de tal sequela e le re-exposition a plumbo in patientes eonvalescente ab leve episodios de acute encephalo pathia esseva statisticamOnte multo significa tive. Esseva concludite que le elimination de plumbo ab Ie milieu del paliente es non solmente le sol adequate mesura de protection sed etiam un importantissime mesura thera peutic in Ie tractamento dfe tal casos. Le alte proportion de juveniles de etates de inter 12 e 35 menses con capacitate in tellectual medxe qui es trovate inter le casos de intoxication a plumbo e le alte incidentia t],. non-suspecte casos trovate inter lor codomicj. liarlos del mesme etates demonstra le iirtportantia del aspecto ambiental del problema in areas urban de habitationes substandard. 1st,, alte incidentia de "casos secundari" accentu-i le obligation del medico de examinar caute- e promptemente omne codomidliarios de minus que 3 annos de etate quandocunque un casn de invenenamento a plumbo es trovate. Omne le varie datos relative al milieu urlw.i supporta le conclusion que in situaf mes in qn.on ha permittite un deterioration del conditiones domidliari, le exposition a plumbo pntv essfir si intense que illo deveni un factor plus importante que variabiles individual, cornu per exentplo le retardation mental o le maladjustamento emotional del juveniles mesme. Tal grados de exposition a plumbo representa pro normal infantes e juveniles un hasardo que es prevenibile. IIlos constitue un problema de sanitate public que possibilemente plus ex tense que lo que on ha previemeote supponite. hypo De? r o n depletk I fined as t stores of iron on currently a requirements c that this defini iorage deplet include consk level. This nu tion of the ter usage. The te: times used in used for des tion characte chromic anerr with the anen experimental distinction ne tion and defic I hope to mak encounter iro depletion ai anemia, so th terms becom deficiency" v Jo the clinic merely the ? 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