COMMUNITY HEALTH

Asymptomatic

Lead

Poisoning

in 85

Chicago

Children Some Diagnostic, Considerations

Therapeutic, Prognostic and Sociologic

OWEN M. RENNERT, M.D.,* PAUL WEINER, PH.D.,** JOHN MADDEN, M.D.**

LEAD poisoning

is

a

continuing major

pediatric problem of urban centers. Chicago alone reports 3,500 cases annually,’ which indicates a need for greater preventive efforts and improvement in detection and treatment before symptoms develop. Lead encephalopathy has high morbidity and mortality despite advances in treatment of lead poisoning. One study 2 notes neurologic sequelae in 39 per cent of children with lead intoxication in the absence of acute encephalopathy, and persistent neurologic abnormalities in 82 per cent of the cases where encephalopathy was present.

Our observations from November, 1966, to October, 1967, at the outpatient clinic of the

University of Chicago indicate the scope of the problem. This study defines criteria for diagnosis of asymptomatic lead poisoning; we present a protocol for outpatient treatment; and we discuss possible sequelae, emphasizing the need for community involvement for effective prevention. -

* From the Departments of Pediatrics istry, University of Florida College

and Biochemof Medicine,

Gainesville, Fla. 32601. ** The Department of Pediatrics, Pritzer School of Medicine of The University of Chicago, Chicago, Ill. 60637. Supported in part by NIH undergraduate training grant 2T1-HE51t18; the Developmental Physiology training grant Tl-HD0054; General Research support grant 623; and a grant from the U. S. Children’s Bureau’s Children and Youth Project awarded to the City of Chicago Board of Health.

Patients Under

Study

From

November, 1966, to May, 1967; 85 children with blood lead levels greater than 60 pug. per 100 ml. were seen at the University of Chicago pediatric outpatient lead clinic. These patients had been discovered through a case-detection program by the Chicago Health Department in which departmental members and members of community organizations make door-to-door surveys in high-risk neighborhoods of practically all children under seven years old. All suspect children were subjected to a screening test consisting of determining blood lead levels by atomic absorption spectroscopy at the laboratories of the Board of Health.

Outpatient

Treatment

With each child

Program

physical examination was thorough history obtained performed with special emphasis on (1) achievement of developmental milestones, (2) comparison of patient to peers, (3) mother-child relationship, (4) feeding history with special emphasis on duration of bottle feeding, and (5) ability or desire to socialize. Blood specimens were and

taken for

tests

a

a

of blood lead, blood

urea

nitro-

(BUN), hemoglobin, hematocrit, leukocyte count and differential, erythrocyte appearances (basophilic stippling) and erythro-

gen

cyte fluorescence. Urine

was

examined for

9

FIG. 1.

Age distribution

of 85 children with lead

studies and for coproporphyrins. of the abdomen and distal femora X-rays were examined. (knees) A social worker also visited each patient’s home, evaluating the physical and social conditions in the household. Four days after his initial visit, each child began the following two-dose program of intramuscular chelation therapy (given four -to six hours apart in the outpatient department): routine

vals with blood lead determinations for at least one year thereafter. The possible sequelae of lead poisoning and its effects on brain, kidneys and hematopoietic system were outlined in detail to the parents of every child prior to therapy. This

approach

’~ I:~imereaprtrl.

On the fourth day, a 1?-hour urine specimen for lead determination was obtained, and two weeks after treatment, a repeat blood lead study was done. Additional courses of chelation therapy were then begun if the blood lead level was still greater than 60 jug. per 100 ml. But whether further treatment was given or not, every child was followed at three-month inter-

10

was

probably partially responsible

for their excellent cooperation in bringing back their children for follow-up supervision. .

calcium dzsixlium versenate.

poisoning.

Family Characteristics Our 85 patients ranged in age from 11I months to seven and one-half years old, with more than 35 per cent about two years old (Fig. 1). As an average, the patient was one of four children. In 32 cases the patient was the youngest sibling; in 21, the oldest. Five patients were one of twins, but in only one instance did both in one set have lead poisoning. In seven instances, more than one child in the family had a history of pica for leadcontaining materials.

.

Clinical and Laboratory Findings We assumed that each of the 85 children had lead poisoning, since each had a blood lead value greater than 60 ftg. per 100 ml. It was encouraging, therefore, to find that 90

.

TABLE 1.

Laboratory Findings in 8.i Chicago Children witlt A symptomatic Lead Poisoning (Blood Lead Levels ’260 p.g.j 100 ml.)>

asymptomatic. We were surprised to find little positive correlation between other laboratory examinations usually useful in helping to establish a diagnosis of plumbism (Tables 1, 2). Ten per cent had significant coproporphyrinuria at the initial clinic visit, and 6 per cent demonstrated significant anemia. The examination having the per

cent

were

greatest correlation with the blood lead level

radiologic demonstration of increased density at the metaphyseal ends of the long bones (Tables 1, 3). The difficulty in recognizing the existence of lead poisoning in an asymptomatic child can be emphasized further. In only 11 per cent were three familiar laboratory criteria satisfied : anemia, coproporphyrinuria, lead lines,

was

lead shadows in the abdominal x-ray films, stippled red blood cells. Forty-six children, or 54 per cent, had elevated blood leads with no other laboratory evidence of lead poisoning (Table 2). The continued finding of a blood lead level greater than 60 ~.g,/100 ml. over several weeks was not associated with a significant increase in the number of positive results obtained by other diagnostic means

(Table 3). Inpatient

Treatments

Chelation therapy is not always free of risk. In the presence of high blood lead levels it may induce encephalopathy or deterioration TABLE 2. Numbers

*

of the patient’s condition within the first 24 hours of treatment.3 We therefore hospitalized for treatment all children with blood lead levels greater than 150 ~g.f 10(l ml. The initial blood lead values in our patients ranged from 60 to 190 ~,~./1lJO ml, We noted that one course of therapy resulted in lowering the initial values 50 to 60 per cent. We noted no overt signs of encephalopathy during therapy. Side effects included mild drowsiness in the first 48 hours in 15 per cent of the children. Problems in

Diagnosis

There were wide discrepancies between the blood lead values reported by the local Board of Health and those obtained in our own laboratory. Our values ranged as much as 50 per cent above or below the referred values with no definable pattern. Such variation may represent laboratory error, but if it does not, then two pertinent questions arise: (I) Did the children with increasing blood lead values continue to ingest lead-containing objects between the time of initial screening and their arrival in our clinic? (2) If we concur with the prevailing belief that a blood lead value greater than 60 ~,~. j104 ml., the original value for all of our patients, is toxic, should we assume that those children in whom our laboratory found blood lead values below 60 /is./ 100 ml. were no longer at risk from their

of 85 Children u41fi None to 5 Diagnostic Lraboratory Criteria* for A symptomatic Lead Poisoning

Anemia, coproporphyrinuria, &dquo;lead lines,&dquo; lead in the abdomen, stippled red blood cells.

11

TABLE 3. Laboratory Findings in 28 Children with A symptomatic Lead Poisoning uilfi Two Blood Lead Levels ’2:.60 ¡;.g.j 100 ml.

disease? Westerman et al.4 report that bone stores of lead remain toxic for 18 or more months after blood lead levels are in a nontoxic range. Exposure to sunlight or stressful stimuli (febrile illnesses, etc.) may mobilize enough bone stores to convert asymptomatic lead poisoning to a symptomatic state. We thus treated every child in whom the Board of Health had found a blood lead level of 60 p.g./l00 ml. or greater. Problems in

Therapy

In view of the prolonged duration of toxic lead stores,-, how long should treatment be continued? Blood lead values alone are not the sole criteria for adequacy of therapy. Chelation of lead in blood with EDTA or BAL represents a major advance in plumbism management; the inability of these agents to successfully bind bone stores of lead,6 however, enters into the problem of when to conclude treatment. A drop in blood lead level to below 20 ~,g.l 100 mal. and a urinary lead excretion of less than 80 ~g./100 ml. per 24 hours constitute reasonable criteria for the adequacy of therapy. In our clinic it is the practice to treat every child who has a history of pica with ingestion of paint or plastic, a blood lead level greater than 20 p.g./l00 ml., and one additional positive laboratory finding. This treatment is kept up until both the blood lead levels and the urinary lead excretion have become normal. In this group of 85 children each child required at least two and some required three courses of chelation therapy. None had developed encephalopathy 18 months later, and none exhibited any neurologic deficit. Since none had symptoms before therapy, we cannot truly evaluate the over-all effect of treatment. It is possible that none would have

12

developed symptoms even without the tion therapy, but this seems unlikely. Lead and the Central Nervous We

find

chela-

System

literature on the effects of small amounts of lead on the nerrelatively vous system or of the psychologic consequences of asymptomatic lead poisoning as seen in our totally asymptomatic children. The end results of severe lead poisoning with encephalopathy 9-12 and the effects on mixed groups of children-some asymptomatic and some with encephalopathy 13, 15 -are well documented. Even if adequate diagnostic criteria for subcan

no

clinical lead poisoning become established, we can still foresee considerable difficulties in assaying the intellectual effects of asymptomatic lead levels; data on premorbid intelligence almost inevitably would be lacking. Mothers’ reports are crude measures at best, and at worst are totally misleading. One possible though admittedly difficult approach would be to follow a group of children with asymptomatic lead levels over an extended period to determine any decrease in intellectual function. If the prolonged presence of small amounts of lead is deleterious, the dimensions of the problem of plumbism and its treatment expand far beyond that of

merely avoiding encephalopathy. ’

Sociologic Facets

.

wipe out childhood plumbism requires unlikely massive rebuilding of our slums.

To an

We believe there are problems leading to pica, however, aside from the availability of paint chips and plaster, the solution of which may protect those children forced to remain in deteriorating dwellings. Our observations, like those of Jenkins and Mellins, 12 Millican et al.,16 Lourie et al.,l1 suggest that emotional

.

factors also may be

implicated.

For

example,

child in a family is afusually only fected, even in those families with twines. The youngest child appears to be af£ecterl with greater frequency than might be expected by chance. Perhaps this child receives the least attention from an overburdened mother; his pica may be an indicator of emotional deprivation. This hypothesis, if proven correct, furnishes another argument for giving aid to economically derived mothers to help them care for their children. Other community efforts might be in the direction of group counseling technics, and other channels for local comone

munity support. Acknowledgment The authors thank Dr. F. H.

Wright for

gestions and criticisms, and Miss G. Covey

his sung. for

pro-

fessional assistance.

References 1. 2.

3.

4.

5.

6.

7.

8.

MTS lead poisoning program, Chicago Board of Health. Perlstein, M. A. and Atalla, R.: Neurologic sequelae of plumbism in children. Clin. Pediat. 5: 292, 1966. Chisolm, J. J., Jr.: Disturbances in the biosynthesis of heme in lead intoxication. J. Pediat. 64: 174, 1964. Westerman, M. P.: Concentrations of lead in bone in plumbism. New Eng. J. Med. 273: 1246, 1965. Rapoport, M. and Rubin, M. I.: Lead poisoning; a clinical and experimental study of the factors influencing the seasonal incidence in children. Amer, J. Dis. Child. 61: 245, 1941. Goodman, L. S. and Gilman, A.: The Pharmacological Basis of Therapeutics, 2nd ed. New York, Macmillan Company, 1955, p. 1013. Oliver, B. E. and O’Gorman, G.: Pica and blood lead in psychotic children. Develop. Med. Child. Neurol. 8: 704, 1966. Benson, P. F. and Chisolm, J. J., Jr.: Reliable qualitative urine caproporphyrin test for lead intoxication in young children. J. Pediat. 56:

Unpublished communication,

759, 1960. 9. Chisolm, J. J., Jr. and Harrison, H. E.: The exposure of children to lead. Pediatrics 18: 943, 1956. 10. and —: The treatment of acute lead encephalopathy in children. Ibid. 19: 2, 1957. 11. Mellins, R. B. and Jenkins, C. D.: Epidemiological and psychological study of lead poisoning in children. JAMA 158: 15, 1955. —

12.

C. D. and in children; a

Jenkins.

Neurol. 13.

Mellins, R. B.: Lead poisoning

study of forty-six 77: 70, 1957. Psychiat.

cases.

Arch.

Byers, R. K. and Lord, E. E.: Late effects of lead poisoning on mental development. Amer. J. Dis.

Child. 66: 471, 1943. R. K.: Lead poisoning; review of the literature and report on 45 cases. Pediatrics 23: 585, 1959. 15. Thurston, D. L., Middelkamp, J. N. and Mason, E.: The late effects of lead poisoning. J. Pediat. 47: 413, 1955. 16. Millican, F. K., Lourie, R. S. and Layman, E. M.: Emotional factors in the etiology and treatment of lead poisoning. Amer. J. Dis. Child. 91: 144, 1956. 17. Lourie, R. S., Layman, E. M. and Millican, F. K.: Why children eat things that are not food. Children 10: 143, 1963. 14.

Byers,

13