THE
EXPOSURE
OF
CHILDREN
TO
LEAD
By J. Julian Chisolm, Jr., M.D., and Harold E. Harrison, M.D.
Department of Pediatrics, Johns Hopkin.r University School of Medicine, Harriet Lane Home of Johns Hopkinr hospital, and Pediatric Divi.sion of Baltinvre City Hospitals
(Smmbmitteci \lav 2:3, accepted July :3, 1956.)
This work was supported by grants from the Lead Indumstries Association, New York, New York, amid
from the National Instittmtes of Health, U.S. Public Health Service (G-3918).
ADDRESS: (J.J.C.,Jr.) Baltimore City Hospital, 4940 Eastern Avenue, Baltimore 24, Maryland.
943
T
HE AVAILABILITY of a new and effective tilerapeumtic agemit has resumbted inre-newed interest in lead intoxication in
child-hood. Reports’1 emanating from various
parts of the United States, indicate an in-creasing recognition of this disease, par-ticumharhy in urban areas. While edathamih
cahciumm disodiumm has proven to be of value
in the treatment of acumte episodes of
phumbism, it cannot be used to prevent the
toxic effects of prolonged excessive
absorp-tion of lead. In children, as in adults,
pre-vention of excessive exposure to bead
re-mains the principal means of control.
A sound preventive program must be based upon adequate environmental data. The age incidence, seasonal distribution of the aeumte manifestations and concentration
of cases among children residing in urban
sham areas are well known.’, Although the
inhalation of lead fummes as a cause of
pluimbism in children has been reported,’ it is believed that at present the ingestion
of head-containing paint flakes is the most
common soumrce from which children obtain
excessive qumantities of bead. The present
report deals entirely with this hatter type
of exposure.
Data have been obtained umpon the
in-tensity of such exposure, duration of
cx-iostmne and the seasonal factor in the
pro-duction of head intoxication in children.
The “secondary” case rate among
houmse-mates of index cases has also been stumdied.
Likewise, the relationship between the
in-cidence of severe permanent damage to the
brain and ne-exposure to lead among
sur-vivors of an initial episode of acumte lead
eneephahopathy has been examined.
Oh-servations were macic uion the
develop-mental status of affected children and the
personal-social situations in which they
de-veboped lead intoxication. The pumrpose of
this report is to present these data and to diseumss the relative role which each of the several environmental factors may play imi the production of lead intoxication in ehil-dren. It is hoped that this may facilitate the implementation of adequate preventive measumres.
CLINICAL
MATERIAL
AND
DIAGNOSTIC
CRITERIA
The climiicab material was derived from the
pediatric chimiics of the Harriet Lane Home
of Johns Hopkins Hospital and of Baltimore
City Hospital. In all, 197 children exposed to head, incbumdimig 89 patients with acute head
emieephahopathv, have beemi stumdied. All
dwelled in the urban slum areas of Baltimore.
Within this group, 59 children were
perso)n-ally studied by the aumthors. In these children,
observations omi developmental status and
per-sonal-social home situations were made. The
study was conducted dtmring the years 1952
to 1954, imichumsive.
An importamit part of the presemit survey
was the detailed amialysis of exposure factors
in nine households in which abnormal sources
of head were demomistrated. Within these mime
environmental units, there were 9 index cases
and 17 other children under 6 years of age
who served as comitrols, or a total of 26
sub-jects with known exposure to head. Among the
17 comitrol subjects of this household-study
group, the incidemice of ummistmspected
“see-ondanv” cases was determined.
Another group of 33 childremi were patients who were studied dumring and after
hospitaliza-tion for acumte lead imitoxication or
emicepha-hopathv dumring 1952-1954. Imi addition, a
cliii-dren admitted to the above chimiics during the
previous 12 ears amid indexed as “lead
poison-ing” or “lead ingestion.” Among these records,
138 contained sumfficient information to
estab-lish amid classify the clinical diagnosis according
to the criteria listed below. These constitute
138 of the 197 subjects included in this report.
DIAGNOSTIC CLASSIFICATION :All subjects are
classified in six clinical categories as follows:
Type I. Exposed-Normal. Subjects with a
history of imigestion of materials suspected of comitaimiing head or with evidence of
radio-opaqume foreign materials in the
gastrointes-timial tract b roentgemiography, were classified
as exposed normals, if they had concentrations
of lead in blood hess than 0.06 mg/100 gm
whole blood, absence of “bead lines” in
roent-genograms of bong bones, normal findings in
examination of the blood (or an anemia which
responded rapidly to the oral administration
of iron) amid no symptoms attributable to lead
imitoxication.
Sumbjects in this category were subdivided
into two groups: a) those for whom exposure to
bead was verified by analytic records giving the
idemitification amid lead content of the material
im#{236}gestedby the child and b) those for whom
such analytic records were not available,
ah-thoumgh the clinical record indicated that a
source of bead had been found in the child’s
environment.
Type II. Asyniptomatic, Increased Lead
Ab-sorption. These sumbjects differed from the
cx-posed-normal group km that they had elevated
concentrations of lead in blood and
roentgeno-graphic evidence of storage of bead in the
bones, without symptoms attributable to lead
intoxication. Qualitative tests for
copropon-phvrin in urine were positive in some of these
chihdremi.
Type III. Lead Intoxication (without
En-cephalopathy). The diagnosis of bead
intoxica-tiomi was made imi children who had, in
addi-tion to evidence of increased bead absorption,
several of the following manifestations : anemia
resistant to iron therapy, increased urinary
excretion of coproporphyrmn, severe
constipa-tion, anorexia, hvprirnitabibity, bizarre
be-havior patterns amid intermittent vomiting. In
the chihdremi of this group, there were no
ab-normal fimidimigs imi the cerebrospinal fluid.
Type IV. Lead Encephalopathy, Mild. Imi
addition to fulfilling the criteria for lead
in-toxicatiomi, the children of this group had
ab-normal findings in the cerebrospimial flumid amid
omie or more of the folbowimig signs amid
svmp-toms : persistemit vomiting, hvperirritabihity,
ataxia, intermittemit comivimlsiomis and
sommio-lence or semistupor. Findings in the
cerebro-spinal fluid were considered al)miormah if two
or more of the following were present:
‘in-creased concemitration of proteimi, increased
pressure amid pheoctosis in the cerol)rospinal
fluid.
Type V. Lead Eucephalopathy, Severe. The
emicephabopathv was classified as severe if the
p:itients either convumhsed comitimiuabhy for a
minimum period of 24 hours or remained
comatose for a period of 24 hours or longer,
or both.
The miumbers of subjects iii each diagmiostic
category were as follows:
I. Exposed-normal ( with presumiied head
ingestion) 41
(a) record of lead source available 14
(b) record of lead source not available 27
II. Asyniptoniatic, increased lead
absorption 39
III. Lead intoxication without encephalopathy 16
IV. Lead encephalopathy, miiild 48
V. Lead encephalopathy, severe 41
185
The remaining 12 subjects of tile total
group of 197 childremi exposed to lead were
normal control subjects in the household-studs’
group who apparemitly had miot iiigested
bead-containing materials.
METHODS
OF STUDY
The intensity of exposumre to head was de-termined by measurement of daily fecab
excre-tion of bead in all members of the
household-study group under 6 ears of age. Pooled
2-to 4-day collections of stools were made in
the home in covered 13 quart Pyrex casserole
dishes sumpplied l)\ the laboratory. Mothers
were directed to have the child defecate
di-rectly into the casserole dish. In hospitalized
patients quantitative collection of stools were
made while the chibdremi were on metabolism
frames.
Aliquots of the pooled 2- to) 4-day stool
samples were prepared for analysis b
homo-genizatiomi of emitire samples km a ‘Waring
blendor in which the stamidard brass bearing
was replaced by a cast iromi bearimig.M
Dumphi-cate aliquots were dr’-ashed’ amid amiahvzed
tech-ARTICLES
nique of Smi’der.’ All equipment was
“de-headed” with warm 20% nitric acid, followed
i)\’ a thoro)ugh rimising in “lead-free” water.
“Lead-free” water was prepared by the
pas-sage of distilled water through ami ion-exchange
resimi cobummi.
The above method was entirely satisfactory
for the amialysis of head imi feces in specimens
contaimiimig greater than 1.00 mg Pb/24 hr. As concemitratiomi of lead decreased below this
value the insoluble matter presemit in some
specimens caumsed increasing interference in
the fimial extraction step. This interferemice was
1I)l)reci11)he imi mans’ specimens containing less
thami 0.100 mg Pb/24 hr imi which variatiomis
l)etweeml h)1ir5 as great as twofold were
en-cO)untered. The presence of iron imi
comicentra-tions sumfficient to imiterfere with the amialysis
occimrred omily iii the stools of patients
receiv-imig iromi medicinally. This ‘aS readily avoided
h)\’ cliscontinumimig the iromi temporarily.
Re-cover of lead in feces by this method was 95
to 110f. The maximumm allowable error from
the meami of dumplicates was ±10% (0.100 to)
1.00 mg Pb24 hr) amid 5% (1.00 mg Pb 24
hr or greater).
Tissues were (1tmick-frozemi amid homogenized
in the frozemi state with mortar amid pestle.
The’ were themi dried to comistamit weight at
105 #{176}C, frozemi amid re-homogemiized. Amialvses, in triplicate, of ahiqumots of this final
homo-genate were then carried out by the above
method. Difficulties, resuhtimig from low
comi-cemitration of head, were emicoumitered only imi
the analysis of braiii tissue in which variatiomi
from the mean of triphicates was ±15%. Imi
other tissumes variatiomi from the mean did not
exceed 8%.
Imi all sumspectedl cases of head intoxicatiomi
in childremi km Baltimore, samples of whole
blood amid of suspected emivironmentah soumrces
O)f head were roumtimiehy analyzed for lead by
the Baltimore Cit Health Department. Blood
was amialysed IW a wet-digestion dithizone
technio1ue utilizimig a spectrophotometer for
final color estimation. ‘ Samples of paimit chips,
1)ainted plaster, etc. , were collected imi the
homes iy a visitimig pumbhic health nurse. The
lead comitemit was estimated b a
semiquantita-tive techmii(jue’ ‘ and reported qualitatively as
follows:
Lead absent-less thaml 0. 1% of lead
Trace of lead-O.1% to 1.0 O)f head
Positive for Iea(l-1’. to 5 of lead
Strong positive for lead-greater than 5% of head
RESU LTS
In nine houmseholds selected for detailed
study of exposure factors there were 9
index cases and 17 other ambulatory
cliii-dren less than 6 years of age, who served
as controls. Of the nine index cases, foumn
had acute lead encephabopathy, two had
head intoxication and three were classified
as asymptomatie, increased bead
absonp-tion. Data on the intensity of head exposure
were obtained in this household-study
group through the measumnement of fecal excretion of bead before and after the
re-moval of all identified soumnces of lead in
the houses. By balance studies it has been
shown by Kehoe audi his associates’2 that
fecal excretion of head provides a good
index of bead ingestion inasmuch as
ap-proximately 90 of ingested head is
cx-creted in the stool. Prior to the removal of
identified sources of lead, stool samples
were collected concurrently from control
and affected sumbjects. Similar collections of
stools from those sumbjects with head
intoxi-cation were made in the hospital at beast
1 week after the completion of therapy
with edathamil calcium disodium and
again upon nettmrn to their homes after the
removal of all identified soumnees of lead. In all, 63 satisfactory pooled, 2- to 4-day
collections of stools were obtained from
22 of the 24 ambulatory children umnder 6
years of age in eight of these nine
houmse-holds. Comparable stool samples were
oh-tamed 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 eneephahopathy.
The sumbjeets of the houmseholci stumdy were
classified according to the diagnostic
en-teria oumthined. The resumbts of the analyses
of the stools for bead are presented in Table
I. The resumlts of similar determinations in
“nonexposed” controls and additional
pa-tients with eneephalopathiy are included in
Table I as a I)ackground for the evakmatiomi
of the houmsehohd-study group. All oumtpumts
(‘lasxific(,lion of Paiienist
Xo. of Palienis
\#{252}. of Specimens
Mean Median Raige
6
7
().13
53.4
0:157
‘13.4
0.012-- 0.175
‘FABLE I
i)AILY FEOAL ExeloETmoN or LEAm) mN ChILDREN BEFORE ,Nm) .‘FTEmo REiuovtm.
OF ENVIHONMENTAL So110(Es OF LF.,D*
Lead Output (mg/2 hr)
!!ousehold-Stms(Iy (irolip
‘I’ypes ILL, IV amal V At hommme (luring CXj)OSUC I nhospital after therat’
6 10 44 .0
0.362
7 .0 0.24()
3 .01 -1
0 .
062-04.0
0.85()
Iypes IL, Ill, IV ammil V
At hoimme alter CXI)OSUF S 1 0.565 0.511 0.039- 1.50
Type II
At home (luring exposure .5 1 .16 1.1 1 0 .I 16- 9.60
household (omitroIs
At homne (luring exposure 11 3 0.83’2 0.651 0.057- 1 .93
Other Children
* The household-study group has been divided according to both oliagnostic ciassifleatio)ml amid presemmee or
ab-semmce of lead exposure, in order that the observed differences in fecal excretion of lead under these varying (Omiditiomis can he seen. Each specimen represents a - to 4-day pooled collection of feces frommi the lea(l (omitemit of which is
calculated the milligrams lead excreted per 4 hours. An average of two such specimmiens were collected from each patient during each period of observation relative to exposure.
tDiagnostic Classification; see text for criteria.
** Nonexposed Controls: 12- to 35-month-old children of mnenihers o)f pediatric staff for whomu there were mmo known environmemital sources of lead.
These seven patients admitted with acute lead encephalopathy were miot mnenil)ers of household-study group.
Values shown are based upon total lead content of admission stool, (Iivi(Ied by the nunul)er of olays simmoe the last
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-bections 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 umsed, inasmuch as the samples were not always consecutive. On the first line of Table I are shown the
out-puts of lead dumning exposumre of six patients
with lead encephalopathy and intoxication.
The mean oumtput of lead in this group
dumning exposumre was 44 mg/day and the
range was 5 to 105 mg/day. Three of these
had acute head encephahopathy. Their
24-hour outputs are calculated from the bead
content of the first stool passed after
ad-mission to the hospital. All other stool
collections during exposumre were made in
the homes. When these lead-poisoned ehil-dren were removed from exposure to bead
by hospitalization or, after discharge, by
removal of all identified sources of head
from their homes, the daily fecal excretion
of lead fell to normal vahumes, approximately 0.3 and 0.5 mg, respectively
(
hues 2 and 3). On the fifth line of Table I, the mean daily oumtput of the 11 control sumbjects inNomiexposeol comitrols**
At home 6
Types IV and V
‘l’ABLE II
FE(’AI. I:XCI(ETION 01.
Type of Subject
rug Ph/1)ay
Mean Range
0.08S
0.43
0.83
0- 0.28
0.01-0.09- 1 .9
asymptomatic, increased! lead absorption
(line 4) occupy tn imitermnediate positiomi
1)et\Veen the poisone(l and the control
sub-jects. Thums, during exIM)sure the poisoned
children were foumnd to be excreting
ap-proximately 50 times as much in the feces
as the similarly exposed hotmsehohd controls.
The resumbts shown in Table I may be
compared with the studies of Kehoe
et all 14 on fecal excretion of head umnden
varioums conditions of exposure to head!
3.8 0- 14.0 (Table II). It can be seen that daily fecal
7.6 2.0 - 14.0 excretion of head in the control suibjects of the present stumdly is of the same ondler of
manitumde as that of the normal children
44(1 5.0 -1(14(1 ‘- .
Studlled by Kehoe et all Evemi when
allow-ance for differences imi analytic amid
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 bead than do heavily exposed
industrial workers.
An umnexpected finding of this household
stumdy was the discovery of five additional
cases of uinrecognized increased lead
ab-sorption and head intoxication among the
17 control subjects. All of these umnsumspected
eases fell within the same age range as the
index eases: namely, 12 to 35 months of
age. No evidence of increased head
absonp-tion on ingestion was demonstrated among
the older houmsemates (Table III). Indeed, if the index cases are ineluided, 14 of the 15 children aged 12 to 35 months in the nine
the presence of exposumne to lead was
ap-proximately 0.8 mug of head daily. It can
be seen that those children classified as
‘I’ABLE 111
947
X2=9.28. P(0.01 Normal (hildremm
l’rimnitive So)oietf
ArIIeri(nmm (Imosp.) f Present StIl(ly
ln(iustrial workers
All ty)es of exl)osuret S(’vere exposuret
iC1l(l Poisomied (hildremm
Present StU(lV
* 1mmthis tal)le the (hiily fecal lead output of the
mior-nuil ami(l the poisomie(l childremi imi the household group
are comnj)are(l with simiiilar data from the studies o)f
Kehoe ci /14 determnined the lead comitemit of
simigle fecal evacuations froni childremi in a primmiitive
\Iexioami oommimnumutv and in comivalescent hospitalized
.\nleri(ami chiloiremi. ‘I’he omily known source of lead for
these (hil(lrdn smms that containe(1 in their nornial (liet. ‘Fliey obtaimie(l similar (ietermninatiomis iii exposed
in-(lustrial vorkers. l)espite the differemices imi samn)limig 110(1 ammalytie teehmuques, the fecal exeretiomi of lead by
the 1)oisomie(l childremm ai)paremitly excee(ls that of severely exposeol imi(lustrial workers, while that of their
household comitrois is of the sanie ltiagmmitu(le as that of
miormmmal umiexposed childremi.
t ‘l’akemi fromim (lata of Kehoc el al :J. 10(1(1st. Ilyg., 1.5:30?, 1933.
IIousEImoLm) STI’I)Y
l)IsTImImiuTIoN BY AGE OF UNSUSPECTED CASES OF ASYMPTOMATI(, INCIIEASEI) LEAD ABSORFION AND
mEAL) mNToxIc’ATIoN IN HOt’SEMATES OF NINE INL)EX CASES
Age Groups
Number of Subjects
Subjects a! Risk
Asymplomalie, 1nereased
Lead Absorption an(l ‘iorrna1s
Lea(1 Intoxicotion
1’2 to 35 mmiontlis
36+ muomiths
6 11
5
0 11
.5 1
Patient
Age
(mo)
Time (If Death*
Rib Brain Liver Kidney
Total Lead
JOlZIi(1 ifl
Soft Tissues
(nig)
Output of
Lead i’i
Urinet
B. M(F. 25 hours 39.9 1.1 10.5 8.9 15.0 ammurie
NB. 34 Uhours 33.0 1.0 6.1 9.5 4(1.5 .5.2
11.11. 2() Sldays 13.1 1.4 4.1 5.5 10.1 4.8
LI). 3 6hours 10.0 1.7 - - - ‘L4
* Time of death after imistitution of therapy with edathanmil calciumn disodium.
t Total output of lead in urimie during therapy prior to death.
** Exclusive of brain, estimated lead content of which is approximately 3 mug.
TABLE IV
1Eu) CONTENT 01’ ‘[‘ISSUES 01’ CHILDREN l)YING FUOM AOL’TE LEAI) ENeEI’II.moe.TlIY
households were found to be ingesting po-tentially toxic quantities of lead.
In four patients who died during an
acute episode of lead encephalopathy,
tis-sue content of lead was determined (Table
IV). Three of the foumr patients died within
24 houmrs after the institution of therapy
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 bead in soft tissues can be approximated.
Aumb et al) and Kehoe et a!.” 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-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. 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 soumnees 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-tamed 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
Lead Content (mg Pb/lou gemdry tissue)
an additional 48 sources. For each of the
105 exposed children, from one to five dif-ferent sources containing greater than 1%
TABLE V
ENvIRONMENTAL Sotit (‘ES OF LEA D
location
Lea(l (‘ontent
---
-
-Less than 1% 1% or More
Interior Sources
Wimidowsills & framnes S 116 Interior walls
painted paper 38 16
paimited plaster 24
Door frames 1 15
Furniture 3 3
Cribs 3 1
Door frames
lxterior Sources
3 10
Porches & housewalls 6
Fences &other walls ‘2 7
Interior sources
Totals
74 183
Exterior sources 11 37
85
* ‘rhe distributiomi, I)’ lead comitemit amid location, of
the 305 idemitified possible enviromimental sources of lea(l
to which 105 subjects iii this series were exposed. These sources were identified by amialysis of paint sera)imigs
taken fromn the various surfaces imi amid about the homnes which gave evidence of having beemi ehewe(1. For each subject one to seven such sources were idemitified. For
all 105 subjects at least one source contaimiing greater than 1% of lead was found. For 102 of the 105 subjects at least one source containing greater than 5% of lead
of lead! were identified among the varioums
itemiis each child! was thought to have
chewed. For 102 of themn there was at beast
one soumrce comitaimiing greaten than 5% of
head. The lead! was comitained in the paint
on the stmrfaces. The paint was old andi
flaking and frequenthy contained many
lay-ens, one on more of which may have
con-tamed head pigments in which the content
of bead may have been 30 to 70% of the
total solids in the paint.
Au attempt was made to ascertain the
duration of exposumne likely to produmee toxic
symptoms. Maternal estimates of the
duna-tion of their child’s ingestion of
head-con-taming materials frequently were either
un-obtainable or umnnehiable. The type of
cx-posuire, however, permitted an indirect
esti-mate of the probable dumnation of exposure,
if the following assumptions were madle:
a) the hocations of the soumnccs of lead
ne-quiredi that the Cliihdlncn be ambulatory in
order to reach them, and b) cxposumne began
at the time of ambulation, on at 12 months
of age on the average. With these
assump-tions the probable dumnation of exposure
coumbd be estimated as the interval in months
i)etwcen the child’s first birthday and the
age at which the child was classified! as
asymptomatic, increased bead absorption,
on clinical lead poisoning was discovered.
When the diata were analysed on this basis,
110 statistically significant correlation could
l)e found between presumed dumration of
cx-posune and severity of disease (exposed-normal children cxchumded). Indeed, the data
imi(licated that the presummedi exposumne was
of similar diunation in all diagnostic
classi-fications manifesting increased absorption
of beadi, with on vitbioumt symptoms.
An explanation for this became apparent
when the seasonal factor was takemi into
accoummit. Thirty-two patients in the series
(leveboped acumte lead encephalopathy prior
to 2 years of age. The relationship
be-twcen the seasonal factor and the presummed
diuration of exposumne is shown for each of the Patients in Figumne 1, ill which tile
month of the child’s first birthday is joined
by a bar with the month of onset of acute
enccphahopathiy. The length of each ban,
therefore, repnesemits the assumed
diuna-tiomi of exposumne in mouths for each child. In the uli)pcr portion of Figure 1
tue
chil-dnen passing their first birthday between
May and September are shovmi. They were
presumed to have been ingesting bead
during some pant of this 5-montll summer
period (when the peak incidence of aeumte
lead cncephalopathy oecumns), yet they did
not become ill until the summmen 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 dumning the wimiter
months prior to April. They became ill
dun-ing the first summer after the presumed
on-sets of ingestion. Reading from the top to
the bottom of Figure 1 the probable
duna-tion of ingestion, therefore, becomes
pro-grcssiveby shorter and approaches a
mini-mum of 3 months. Within this groump of 32 patients there was no statistically significant
correlation between month of first birthday
and severity of, or sumrvival dumning, acumte head encephabopathy. Excluding December, the distribumtion of births by month in the
group does not differ significantly from the
monthly distnibumtion of births in Baltimore
for the years 1951 to 1953 inehumsive, dumning
which most of the patients were born. In
this small group the peak in births dumning December, and the passage of the olden infants thnoumgh their first summer of ambu-lation without symptoms, suggests that 5
to 6 months of head ingestion may elapse
prior to the onset of acumte bead
encephal-opathy.
The possibility that a mimiimum exposure period of 3 months is nequmired, after which the advent of summmcr becomes tile
control-hing factor in the produmetion of symptoms,
is also stmggested by the following finding.
In the entire groump there were 14 children with umnequmivocal evidence of excessive bead ingestion including identification of at least
one environmental soumrce containing
greater than 1% of bead, bumt with no
cvi-denec of increased bead absorption. Eight
MONTH
OF
INCIDENCE
OF
ACUTE
E NC E PH A LO PAT H V
A-SUMMER
p
0-p
0 MONTH OF FIR5? BIRTHDAY
0 .. INCIDNt-$URVSVA$.
U .. . a’DED
_J I F ‘ M #{149}A P.1 ..I ‘ J ‘ S 0 ‘ N
#{149}
D ‘ J#{149}
F MONTHN’A M’J’J’AS O’N’D
FIG. 1. In this graph the month of onset of acute symptoms for each of the 32 pmtieiits who (leveloped acute lead encephalopathy prior to 2 years of age is shown on the right. On the left is the month of the (hiil(lS first birthday. These points are joined by a bar. The length of each bar, therefore, represemits the
asSunledi (luration of leadl exposumre (in miionths) for each childi. Twelve months of age was selected as the
average age of ambimlation. The nature of the exposure in this series required that the child be
ambula-tory in order to) reach the sources of lead in his environment. In this manner a relation between pre-suuie(l dltmration of exposimre to) lead and the seasonal factor in the production of svmptonis can ie diemliOlistratedi.
RELATIONSHIP
BETWEEN
MONTH
OF
FIRST
BIRTHDAY
AND
0-were less than 15 months of age.
Comi-versehy, among the 89 patients with
en-cephalopathy, the youngest was 15 months
of age.
Although these data on duration of
cx-posure were indirectly dedumced, they are
sumpported 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 acumte lead
eneephabopathy and were re-exposed to
lead, necumrnent acumte episodes of
encepha-lopathy usually did! not oecumn umntil the
fol-bowing stmmmer.
An analysis of the occumrnence of severe permanent damage to the braimi among
sumr-vivors of all initial attack of acute lead!
encephalopathy indicates the importance
of continued environmental exposure to
lead in increasing the incidence of central
nervous system sequmelbae. Imi tile entire
series 61 survivors of acumte bead
emicephiab-opathy were treated more than 12 months
prior to evalumation of sequmehlae (therapy
with citrate, 16 patients; therapy with BAL,
28 patients; and therapy with edathamil
calciumm d!isodhum, 17 patiemits). Fifteen of
the gnoump were lost from follow-up.
Forty-Six of the sixty-one patients (citrate, 13
pa-tients; BAL, 19 patients; amid! ed!athamil
Severe Cases*
With No
Seqnellaet Sequellae
‘3
Mild Cases
With
Seqnellae
0 6
No Sequellae
x24.89; P<0.05
7 0
17
x214’35; P<0.01
* Four survivors of severe acute lead encephalopathy, who sustained sequehlae hut in whom re-exposure to lead
was umicertaimi, are omnitted from the table. (See text for discussion.)
tSequellae=severe, permanent, residual damnage to the brain (severe mnental retardation, convulsive disorder
severe behavior disturbance).
followed for 1 year or longer. Of these
46 patients, 14 were known to have
con-timlued! imigestion of lead for periods of 2
I1R)fltl1S or longer, 4 Ilad! (louh)tful
re-ex-posure amid! 28 had! 110) kmiown re-exl)osure to)
lead! after tile initial episode of
encepha-lopathy. The incidence of sequehlae in the
survivors of acute head encephalopathy was
analysed, without regard to type of therapy
during the acute phase, to determine
whether there was any association between
the occurrence of severe permanent ncsidua
in the central nervous system and
re-ex-1)OStmne to bead. Presence of one on 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 sequchlae,” 6
demon-stnated one of these criteria, 5 had two and
12 fulfilled all three (Table VI). There is,
statistically, a highly significant
associa-tion between tile occurrence of such
“se-vere scquebhae” and re-exposure to head
following recovery from mild
encephal-opathiy (X2 = 14.30, P < 0.01). The
conreba-tion between sequcllae and re-expostmre to lead is more difficult to assess in the group
sumrvivimig an episode of severe
encepha-lopathy. Among the 20 severe cases,
re-ex-posure was umneertain in 4. These four, all
of whlom had permanent residuma in the
brain, are omitted from Table VI. If these
doumbtfuhly re-exposed cases arc considered
as miot ne-exposed, X = 2.68 amid! P > 0.1 (ne-exposumre is not statistically significant). For tile entire group of sumrvivons of mild! and severe encephalopathy there is no sig-nificant correlation between scqucbhae and
the duration of acute encephahopathy, type
of therapy during the aetmte phase or con-centration of bead in blood after the acute
illness. The loss of patients from follow-up
does not vitiate the analysis. In survivors
not re-exposed to bead there is no correba-tion between sequelbae 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 Eighty-eight of the one hundred five eases of acute lead intoxication occurred during May, June, July, August, and September. Ninety of the one hundred five cases occurred in ehil-drcn 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
deteniora-tion and disrepair. In the homes visited,
‘FtI31E VI
HEmTION BETWEEN IN(’Im)ENCE OF SEVERE SEQI’ELLAE IN THE CENTRAL NEnvous SYSTEM AND RE-EXP0SI’UE TO) LE.smi FOLLOWING ltEoOVEIOY FROM AN INITIAL EPISODE OF ACUTE LEAm) ENcEpmmALomATmIY
Kmiown re-exposure to lead
No kmiowmi re-exposure to Iea(l
crummbhing, painted plaster on loose paint
chips from walls, ceilings, door frames,
win-dow-sills, oumtside 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 exposumne; 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 qumantity 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
50-fold, 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
outpumt of lead by the lead-poisoned chil-dren (44 mg Pb/day) exceeded, by ap-proximately sixfold, that of a group of
se-vereby exposed industrial workers (7.6 mg
Ph/day) and, by ehevenfold, that of
work-ens in various trades in which exposure to bead 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 woumhd be through the gastrointestinal tract. It has been pointed out that the
oc-cumrrence of lead encephabopathy in adults has usimably been associated with intense exposumne.’7 The more frequent occurrence of encephalopathy in children as compared with adults may depend in part upon their more intense exposumre rather than upon any inherent biologic differences between child and adult.
Lehmanh8 recently reviewed the
hitena-tune and concbumdcd that the average daily ingestion of not more than 1.5 mg of head
is without harm. Kehoc et al.12 have found
that significant retention of bead 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-tenors if the lead content does not
cx-ceed 1% of the total sohids.19 Paints and
other surface coatings meeting this
speei-fication and those relating to other
po-tentially toxic metals may be labelled :
“eon-forms to American Standard Z 66.1-1955.” It is essential to recognize that this
recom-mendation applies only to the two or three
layers of paint usually applied to a sumrface;
not to multiple layers of paint as may be
found in old deteriorated housing. As the
number of layers increases on 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 magnitumde 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 to
yield the amounts of lead found in the
stools of the lead-poisoned children: 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 1% 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 bead
con-tent of environmental sources of lead are
shown; 102 of these 105 children were
ex-posed to at least one source containing
greater than 5% of lead. No case of lead
Fic. 2. Example of size and quantity of paint fragments containing a potentially toxic (nantity of lead. Four sniall paint chips arc shown with a cigarette for comI)arisomi o)f size. The aggregate weight of these
fragments was 2.68 gIn; they contaimied 254 mug (or 9.5) of lead. With the fingernail they were easily
removed! fromn a door frame upon which a patient with acumtc lead encephalopathy was known to chew. His feces, which were obtained on admission to the hospital and 48 hours after the last previous fecal evacuation, comitained 180 mg of head. The miiother stated that this child had been ingesting paint flakes
ahmiiost daily from this and other sources (contaimiing similar concentrations of head) for approximately 10 months prior to hospitabization.
soumrce of head eontaimicd less than 1% of head in the dried paint surface. The present
(lattt t))hy to Old! houmsing. Inasmuch as
head! is presently used as a paint dIner as
vehi as a pigment, 1% of lead in total paint
SOhidIS approaches the minimum consistent
vithi a satisfactory houmse paint. It is
con-ceivabbe that poor maintenance of modern
houmsing with resultant accumulation of
many layers of paints (containing as little
as 1% of bead) on surfaces accessible to
children may in the future constitute a
hazard to small children.
Evidence has been presented vhichi
mdi-cates that, after a minimum of
approxi-mately 3 months of this type of exposure,
the advent of summer (in the presence of continued exposumne to lead) is the
control-bing envirominiental factor in the
precipita-tion of acumte lead! encephabopathy (Fig. 1).
Although the mechanism of this phenome-non is not fully understood, experimental evidence has been obtained in animals
which indicates that vitamin D and the
actinie rays of the summer sun increase the absorption of lead from the intestine.5
It has also i)een sumggested that the
in-creased! heat of the stmmmer leads to
dc-hydration and acidosis in small children
and in this manner may play a role in the production of eneephabopathy.#{176} In the
present study no reliable data coumk! be
01)-tamed concerning vitamin D intake in view of the sporadic umse of vitamin D-fortified! evaporated and fresh milk pnodumcts by the
subjects. Among the patients interviewed, a
history of no vitamin D sumpplemcnt during
winter or summer was given by aboumt half of the eases.
When the probable duration of exposure exceeded 3 months, no correlation could be
demonstrated between increasing severity
of disease and further monthly increments in exposumne. This finding may be exphained
by the interplay of two other factors : the
magnitude of bead ingestion observed in the household-study group, and the sea-sonal factor in the precipitation of acute symptoms. It emphasizes the urgency during
Intelligence Quotient
60- 69 70- 79
80- 89
90- 99
100-109 110-119
Numbers of Patients
3
9
5 9
5
4
exposure to lead. The data indicate that, in such a patient, acute encephabopathy
may d!evelOp if exposumre is I)enmittedl to)
contiiiue btmt a few weeks lomiger.
Frequency of ingestion, is, of course, an important consideration. Long-term data obvioumsly 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 head 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-tofone been recognized. Furthermore, wher-even 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 321 a highly significant cor-relation between re-exposure to lead and the incidence of severe permanent sequel-lae in the central nervous system in sur-vivors of an initial episode of acute en-ccphalopathy 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 corn-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, phumbism and mental de-ficiency are frequently associated. This is miot so with respect to the ingestion of other
toxic substances, a single ingestion of
which, sumffices to produce symptoms. The
wont of toddlers in the 1 -year-age group to taste and eat a large variety of foreign
ma-tenial is well kmiown and is collsid!ered to be a part of their normal behavioral pattern, at least for a short span of time.
In the present study all membens 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 ne-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
as follows:
These findings woumid agree with the con-cept that the ingestion of foreign material exhibited by these ehibdrcn was not a manifestation of mental deficiency, butt 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 houmsehold study. If the assumptions are made that flaking, lead-containing paints are widely distnib-uted in old housing, that there are large numbers of infants and toddlers hiving in such a physical environment and that non-mal as well as defective children may
read-ily ingest amounts of lead sufficient to
produce intoxication, the question arises: Why is lead intoxication not more pneva-lent than the numbers of cases presently recognized would indicate2 Many eases of lesser degrees of intoxication may go
mdi-955
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-dumee overt signs of bead intoxication.
However, personal-social factors elicited
lll those subjects studied by 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. With re-spect to maternal information concerning
phumbism, mothers were asked if they
were aware of their child’s ingestion of paint or had heard of the danger of lead
poisonimig. Significant is the fact that 14 of
33 mothers, while aware of the danger
in-volved, were not concerned because they
considered the amount of paint flakes their
child was eating to be insumfficient “to humrt
him.” Such maternal statements are quite
umidlerstamidlabbe in view of the pneeed!ing
calcumbation that less than 1 gm of paint
flakes may contain highly toxic qumantitics
of lead. It is the repetitive imigestion of these minumte quantities of sumch paint chips which
beads to bead intoxication. If it is conceded
that no mother can reasonably be expected
to prevent this type of ingestion in the
face of cntmITIl)hing paint amid plaster, it will
be recognized that proper maintemiance of
both interior and exterior painted sumnfaces
is probably the most important
environ-mental factor in the long-term aspect of
prevemition of childhood head intoxication.
The corrective efforts taken by the
par-cuts who attempted to curb the ingestion
consisted largely of punitive measures
which may be said, prima facie, to have
been ineffectumab. Only one had attempted to remove the soumrce of head. Common,
like-\vise, was the back of close parental
super-vision of the affected children. Thirteen of
the thirty-tiiree mothers were wage earners
who \vorkedl at least several d!ays of each
week away from home. Wiiiie away fnom
home they heft their small children with
neighbors or in the care of old!cr children.
Six of the mothers had more than three
chil-dren hess than 5 years of age. They stated that in order to get various types of house-work done, they shumt the chibdren in other rooms for short intervals; in these rooms
soumnees of bead were found.
Several of the children in the hospital
demonstrated an excessive desire for
af-feetion. From the point of view of the child, the ingestion of foreign material was
an obvious attention-getting device in
some, particumlarly in those who had been pumnished for it. Many others appeared to nibble inadvertently upon the window sills and door frames as they gazed oumt into the street. In these, boredom was apparently
conducive to the lead ingestion, and may be
attributable to the back of an emotionally
and intellectually stimulating environment.
Many parents reacted by an overprotective
attitude following their child’s recovery
from acute lead encephahopathy. They
fne-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-ional and social factors in the production of bead poisoning in children in an umnban
corn-mumnity has been reported.
Most significant among the environ-mental data presented were the magnitumde of the exposure to bead from repetitive in-gestion of small quantities of headed-paint flakes, and the role of the seasonal factor
(summmer) in the precipitation of acute lead eneephalopathy. The predominance of these two factors may explain the absence of any significant correlation between severity of disease and increments (beyond a minimumm of 3 months) in the probable duration of exposure. It was eonclumded that a child
withoumt symptoms bumt having increased
absorption of lead, recognized dumring the
summer months, may progress to severe en-cephalopathy within a few weeks if the sources of lead are not promptly identified and eliminated.
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 encephabopathy among children as compared with adults may, in part, result from their relatively greater cx-posure.
The importance of continued environ-mental 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 sequelhae and re-ex-posure to lead in patients recovering from mild acute encephahopathy was statistically
highly significant. It was concluded that
removal of lead from the child’s environ-ment is the only adequate protective meas-ure in such cases.
The 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 eases found among 12- to 35-month-old housemates of the index cases demonstrate the importance of the environ-mental aspect of the problem in urban slum areas. This high incidence of “secondary eases” emphasizes the physician’s obiiga-tion to examine carefully and promptly all environmental contacts under 3 years of
age whenever 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-taming materials were discussed. While the responsibility of parents to protect their children from environmental hazards is not denied, no mother can reasonably be cx-peeted to prevent the repetitive ingestion of a few paint chips when these are readily accessible. As lead is widely umsed! as a paint drier, continumed 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 vanioums environmental data all point to the conclusion that, where housing has been permitted to deteriorate, exposure to bead may be of such intensity as to outweigh such individual variables as mental retardation and emotional malad!-justments in the child. Such intense cx-posune is a preventable hazard to normal small children, and, as sumch, constitumtes a public health problem which may be more extensive than has heretofore been thought to exist.
Pending the widen 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
21 Equally important is a compre-hensive social investigation of the home in order to evaluate the circumstances umnder which the child obtained toxic quantities of lead and to determine whether the
iden-tified sources of lead can be adequmately
re-moved, on whether a change of dwelling is required to prevent further dangerous
cx-posure to lead.
ACKNOWLEDGM
ENTS
The authors wish to acknowledge the co-operation of the Babtimonc City Health Dc-partment, 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 imi this report. Mr. Peter Wci performed some lead analyses of the feces and tissues.
REFERENCES
1. Byers, R. K., Mahoof, C. C., amid
Gush-man, M. : Urimiary excretion of lead in
children. Am.
J.
Dis. Child., 87:548,1954.
2. Bessman, S. P., Rubin, NI., and Leikin, S.:
. The treatment of head
dur-ing the acute stage. PEDIATRICS, 14:201, 1954.
3. Williams, H., Kaplan, E., Couchman, C. E., and Sayers, R. R. : Lead poisoning in
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230, 1952.
4. Meblimis, R. B., and Jenkins, C. D. :
Epi-demiological and psychological study
o)f lead poisoning in children. J.A.M.A.,
h58:15, 1955.
5. Rapoport, M., and Rubin, M. I. : Lead
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stumdy of the factors influencing the
sea-sonab incidemice in children. Am.
J.
Dis.Child., 61:245, 1941.
6. Williams, H., Schuhze, W. H., Rothchild,
H. B., Brown, A. S., and Smith, F. R.,
Jr. :
Lead poisoning from the burningof battery casings, J.A.M.A., 100:1485,
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7. Wvbhie,
J.
: A family outbreak of leadpoisoning from burning of storage
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J.,
70:287,1954.
8. Methods for Determining Lead in Air and
ill Biological Materials. New York,
American Public Health Ass’n., 1944.
9. Official amid Tentative Methods of
Analy-sis, 5th Ed. Association of Official
Agni-cultural Chemists, 1940, p. 397.
10. Snyder, L.
J.
: Improved dithizone methodfor determination of lead : Mixed-color
micromethod at high pH. Analyt. Chem.,
h9:684, 1947.
1 1. Kaplan, E. : Personal communication to
the author.
12. Kehoc, R. A., Chohak,
J.,
Hubbard, D. M.,Bamback, K., and McNary, R. R. :
Ex-pcrimcntah studies on lead absorption
and excretiomi and their relation to the
(liagmiosis and treatment of lead
poison-ing.
J.
Imidumst. Hyg. & Toxieol., 25:71,1943.
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J.:
On the normal absorption and excretion of lead; head absorption and excretion in infants and children.J.
Indust. Hyg., 15:301, 1933.14. Kchoe, R. A., Thamann, F., and Cholak,
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: Lead absorption and excretion in certain lead trades.J.
Indust. Hyg., 15: 306, 1933.15. Aub,
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C., Fairhall, L. T., Minot, A. S.,and Reznikoff, P. : Lead Poisoning.
Balti-more, Williams & Wilkins, 1926, p. 53.
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Lead absorption and excretion inncla-tion to) the diagnosis of lead poisoning.
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J.
Dis. Child., 87:559, 1954.SUMMARIO
IN INTERLINGUA
Le
Exposition
de
Juveniles
a Plumbo
Es reportate un studio de certe faetores de
milieu e mores in he production de invenena-mento a plumbo in juveniles in un communitate urban.
Le plus signifleative del datos de milieu hic presentate es he magnitude dcl exposition a plumbo associate con be repetite ingestion de parve quantitates de squamubas de color a
plumbo e be factor saisonal (i.e. Ic importantia
dcl estate) in be precipitation de acute
ence-phabopathia a plumbo. Le predominantia de
iste duo factores exphica possibihemente he
ab-sentia de un correlation significative inter be
sevenitate del morbo e augmentos dcl probabile
duration dcl exposition (umltra un minimo de 3
menses). Esseva concludite que un caso de
asymptomatic augmento dcl absorption de
phumbo que es recognoscite durante be estate pote progreder a sever encephalopathia intra
alicun septimanas si be fonte del phumbo non
es promptemente identifleate e eliminate. Le diurne ingestiomi medic de plus que 1,5 mg de
pbumbo es potentialmente toxic. Un medietate
dcl matres interviewate esseva inconscic 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 ({ui habita
domi-cihios decrepite in que sqimamulas de coborantes
a plumbo es facilememite accessibile. Le
eon-cemitrationes de plimmbo trovatc in he feces del
per ahtere autores in le feces de exponite obre-ros industrial. Iso pare indicar que le plus alte incidentia de encephahopathia a plumbo inter juveniles in comparation con aduiltos es possibihemente in parte be resultato del rela-tivemente plus alte grado de exposition.
Es demonstrate be impontantia del factor de continue exposition a plumbo in augmentar le imicidentia de sever lesiones permanente del cerebro inter superviventes de un initial attacco de acute encephahopathia a plumbo. Le con-relation inter le occurrentia de tal sequelas e he re-exposition a plumbo in patientes convales-eente ab leve episodios de acute encephalo-pathia esseva statisticamente multo signffica-tive. Esseva concludite que le elimination de plumbo ab be milieu del patiente es non sol-mente le sol adequate mesura de protection sed etiam un importantissime mesura thera-peutic in Ic tractamento de tal casos.
Le abte proportion de juveniles de etates de inter 12 e 35 menses con capacitate in-tellectual medic qumi es trovate inter he casos de
intoxication a plumbo e be abte incidentia de non-suspeete casos trovate inter br codomici-lianios del mesme etates demonstra le impor-tantia del aspecto ambiental del problema imi areas urban de habitationes substandard. Iste alte incidentia de “casos secundani” accentua be obligation del medico de examinar eaute- e
promptemente omne codomicibiarios de minus
que 3 anrios de etate quandocunquc umn easo de invenenamento a plumbo es trovate.
Omne he vane datos relative al milieu urban
supporta he conclusion que in situationes in quc
on ha permittite mm deterioration del
condi-tiones domicihiani, he exposition a plumbo pote
esser si intense que illo deveni un factor plus importante que vaniabibes individual, COO
pen exempbo be retardation mental o be mabad-justamento emotional del juveniles mesme. Tal grados de exposition a plumbo representa pro
