/ . Child Psychot. Psychiat., Vol. 17, 1976, pp. 225 to 227 Pergamon Press. Printed in Great Britain
ANNOTATIONS SUB-CLINICAL LEAD POISONING IN CHILDREN
Donald Barltrop* Overt lead poisoning in childhood has been recognised increasingly during the last 30 years. Although the sources oflead are numerous, the predominant association is with old lead-based paint, ln the U.S.A. there are now numerous well-established lead programmes aimed at the identification ofchildren at risk so that in the year ending June 1975, 28,597 children were found to have evidence of undue lead absorption (Morbidity and Mortality Weekly Report, 1976). In the U.K. the problem has attracted less attention and it is thought that less than 100 cases are diagnosed each year with 2 - 3 deaths (Department of the Environment, 1974). Much confusion has arisen from the problem of the definition of the term "poisoning " and failure to appreciate the fate of absorbed lead. The response to the ingestion of leadcontaining materials is relatively slow so that a child with pica ingesting flakes of lead-based paint containing l,OOO;ug oflead per day is unlikely to present with clinical symptoms for 4 - 5 months (Chisolm and Harrison, 1956; Barltrop and Killala, 1967). Similarly, the return of the tissue lead values to normal after the cessation of exposure is also likely to be prolonged. Several grades of exposure may be defined which correspond with the lead content of the soft tissues. For practical purposes, soft tissue lead may be equated with the blood lead concentration (Barltrop, 1968). Children in the "normal" population (Grade 1) are likely to have a blood lead of less than 40|zg/100ml and children in Grade 2 (asymptomatic) have values in the range 40-80/ig/100ml. Clinical symptoms may, but do not necessarily, occur at blood lead values in excess of 80/Lig/100ml (Grade 3). Cerebral involvement and death may occur in association with blood lead values in excess of 100/:/g/100ml (Grade 4). The neurological sequelae oflead encephalopathy were well summarised by Byers (1959) who reported that 38% ofpost-encephalopathic children who survived were sufficiently braindamaged to warrant the description "non-competitive". Other workers have described cerebral palsy, visual impairment with optical atrophy, cranial nerve lesions, increased liability to convulsive disorders, and visuo-motor defects even in the absence of intellectual impairment (Thurston ef a/., 1955; Perlstein and Attala, 1966). Since these early reports there has been controversy as to whether sub-encephalopathic exposure to lead is of clinical significance. There are essentially two schools of thought. The first adheres to the "all or none" hypothesis which attributes neurological damage to the consequences of severe cerebral oedema accompanying encephalopathy. From this point of view there is nothing specific in the induced cerebral changes or sequelae which can be attributed to lead and the observed changes do not differ materially from the encephalopathies associated with other heavy metals or even the viral encephalitides. Thus, it is argued that while sub-clinical exposure to lead resulting in blood lead concentrations of the order of 80/ig/100ml might produce clinical symptoms, they are entirely reversible and unless encephalopathy occurs there is no likelihood of permanent neurological or behavioural impairment. This concept has been challenged by some authors with the alternative view that encephalopathy is merely a final point in a continuous spectrum of exposure and that * Paediatric Unit, St. Mary's Hospital Medical School, London W.2. 225
226
DONALD BARLTROP
increasing blood lead values merely increase the probability of cerebral damage and neurological sequelae. These hypotheses are not easy to test and few studies in this field are above criticism in their experimental design (Wiener, 1970). Thus, Moncrieff et al. (1964) described increased blood lead values in a group of mentally retarded children but failed to appreciate that this was unlikely to have been a causative association. The practice of pica may be unduly prevalent in some retarded children (Bricknell, 1976) and, in any case, blood lead values tend to return to normal after the cessation of a damaging exposure. Recently David etal. (1972) have suggested that hyperactivity might sometimes be produced by the effect of absorbed lead. This view was based on observation of children attending a psychiatric clinic who, when given a chelating agent (a substance which removes lead from the body) excreted larger quantities than controls. Their blood lead levels were in the normal range, although they differed statistically from those of the control children. Similarly, animal studies have been reported in which behavioural disturbances have been observed after relatively modest exposure to lead (Silbergeld and Goldberg, 1973). Unfortunately in both these studies, the method of selection of controls has been open to criticism. A number of recently published studies report the effect of lead in communities living close to lead smelters. Landsdown etal. (1974) studied such a group ofchildren, and found no evidence of intellectual impairement or hyperactivity, even though some of the children they identified showed blood lead levels in the 40-80/ig/100ml range. A comparable study in the U.S.A. (McNeil and Patasnik, 1974) reported similar conclusions, although, when their children were compared with a different control group, some inconsistent differences in the expected direction were found with respect to a small number of tests of motor performance and visuo-spatial ability. (Landrigan et al., 1975). It is difficult to avoid the conclusion that some of the conflicting data might reflect variations in the selection of the control groups used and that the changes reported in some children exposed to lead are probably not due to the effect of its absorption. The LQ. is known to be subject to a variety of social influences, and numerous causes of hyperactivity have, of course, been recognised (British MedicalJoumal 1975). The view expressed by some that children with blood lead levels over 20AJg/100ml are a cause for concern (Carnow, 1975) is difficult to reconcile with the available evidence. Further, there does not appear to be any a priori reason therefore to attribute behavior disorders or mental retardation to moderate increase in blood lead concentration (40-80Mg/100ml). Nevertheless where a child showing either of these problems is suspected of having been in a contaminated environment or is known to suck non-food objects, the blood lead should certainly be investigated. The discovery of a blood lead concentration greater than 40A(g/100ml is an indication of undue absorption and merits an investigation of potential sources, measures to prevent further exposure and a search for other similarly exposed children in the family group and in the locality. The urgency with which these steps are taken should be related to the severity of the exposure. Although only a minority of such children will require chelation therapy, it may even sometimes be necessary to consider removal of the child from the contaminated environment (preferably to a different but familiar setting) until the source oflead has been identified and made safe. REFERENCES Bailtrop, D. and Killala, N.J .P. (1967) Faecal excretion oflead by children. The Lancet 2, 1017-1019. Bailtrop, D. (1968) Lead poisoning in childhood. Postgrad. Med. J. 44, 537-542. Bicknell, J. (1975) Pica, A Childhood Symptom,-p.i^. Butterworth, London. British Medical Journal (1975) Editorial: Hyperactivity in Children. 4, 123-124. Byers, R.K. (1959) Lead poisoning: a review of the literature and report on 45 cases. Pediatrics 21,5^5. Carnow, B.W. (1975) Testimony at Hearing of California Air Resources Board, Sacramento, November. Chisolm. J.J. and Harrison. H.E. (1956) The exposure ofchildren to lead. Pediatrics 18. 943.
ANNOTATIONS
227
David, O., Clark, J. and Voellier, K. (1972) Lead and Hyperactivity. Ihe Lancet 2,900-903. Department of the Environment (1974) Pollution Paper No. 2, Lead in the Environment and its Significance to Man. Landrigan, P.J., Whitworth, R.H., Baloh, R.W., Staehling, N.W., Barthel, W.F. and Rosenblum, B.F. (1975) Neuropsychological dysfunction in children with chronic low-level lead absorption. The Lancet 1,708-712. Landsdowne, R.G., Shepherd, J., Clayton, B.E., Delves, H.T., Graham, P.J. and Turner, W.C. (1974) Blood-lead levels. Behaviour and Intelligence, A Population Study. Ihe Lancet 1, 538-541. McNeil, J.L. and Ptasnik, J.A. (1974) Evaluations for deleterious effects of prolonged asymptomatic elevationsof blood lead. Proc. XlVth Int. Cong. Pediatrics, Buenos Aires, 3-9 October. Moncrieff, A.A., Koumides, O.P., Clayton, B.E., Patrick, A.D., Renwick, A.G.C. and Roberts, G.E. (1964) Lead poisoning in children. Arch. Dis. Child 39, 1-13. Morbidity andMortatity Weekty Report, 29 Nov. 1975, U.S. Dept. of Health, Education and Welfare. Perlstein, M.A. and Attala, R. (1966) Neurologic sequelae of plumbism in children. Clin. Pcdiatr. 5, 292. Seppalainen, A.M. and Hernberg, S. (1972) Sensitive technique for detecting subclinical lead neuropathy. Br. J. Industr. Med. 29, 443-449. Silbergeld, E.K. and Goldberg, A.M. (1973) A lead-induced behavioural disorder. Life Sci. 1 3 , 1 2 7 5 - 1 2 8 3 . Thurston, D., Middlecamp, J.M. and Mason, E. (1955) The late effects of lead poisoning. J. Pcdiatr. 4 7 , 4 1 3 . Wiener, G. (1970) Varying psychological sequelae oflead ingestion in children. U.S. Public Health Reports 8 5 , 19.
ANNOTATIONS SUB-CLINICAL LEAD POISONING IN CHILDREN
Donald Barltrop* Overt lead poisoning in childhood has been recognised increasingly during the last 30 years. Although the sources oflead are numerous, the predominant association is with old lead-based paint, ln the U.S.A. there are now numerous well-established lead programmes aimed at the identification ofchildren at risk so that in the year ending June 1975, 28,597 children were found to have evidence of undue lead absorption (Morbidity and Mortality Weekly Report, 1976). In the U.K. the problem has attracted less attention and it is thought that less than 100 cases are diagnosed each year with 2 - 3 deaths (Department of the Environment, 1974). Much confusion has arisen from the problem of the definition of the term "poisoning " and failure to appreciate the fate of absorbed lead. The response to the ingestion of leadcontaining materials is relatively slow so that a child with pica ingesting flakes of lead-based paint containing l,OOO;ug oflead per day is unlikely to present with clinical symptoms for 4 - 5 months (Chisolm and Harrison, 1956; Barltrop and Killala, 1967). Similarly, the return of the tissue lead values to normal after the cessation of exposure is also likely to be prolonged. Several grades of exposure may be defined which correspond with the lead content of the soft tissues. For practical purposes, soft tissue lead may be equated with the blood lead concentration (Barltrop, 1968). Children in the "normal" population (Grade 1) are likely to have a blood lead of less than 40|zg/100ml and children in Grade 2 (asymptomatic) have values in the range 40-80/ig/100ml. Clinical symptoms may, but do not necessarily, occur at blood lead values in excess of 80/Lig/100ml (Grade 3). Cerebral involvement and death may occur in association with blood lead values in excess of 100/:/g/100ml (Grade 4). The neurological sequelae oflead encephalopathy were well summarised by Byers (1959) who reported that 38% ofpost-encephalopathic children who survived were sufficiently braindamaged to warrant the description "non-competitive". Other workers have described cerebral palsy, visual impairment with optical atrophy, cranial nerve lesions, increased liability to convulsive disorders, and visuo-motor defects even in the absence of intellectual impairment (Thurston ef a/., 1955; Perlstein and Attala, 1966). Since these early reports there has been controversy as to whether sub-encephalopathic exposure to lead is of clinical significance. There are essentially two schools of thought. The first adheres to the "all or none" hypothesis which attributes neurological damage to the consequences of severe cerebral oedema accompanying encephalopathy. From this point of view there is nothing specific in the induced cerebral changes or sequelae which can be attributed to lead and the observed changes do not differ materially from the encephalopathies associated with other heavy metals or even the viral encephalitides. Thus, it is argued that while sub-clinical exposure to lead resulting in blood lead concentrations of the order of 80/ig/100ml might produce clinical symptoms, they are entirely reversible and unless encephalopathy occurs there is no likelihood of permanent neurological or behavioural impairment. This concept has been challenged by some authors with the alternative view that encephalopathy is merely a final point in a continuous spectrum of exposure and that * Paediatric Unit, St. Mary's Hospital Medical School, London W.2. 225
226
DONALD BARLTROP
increasing blood lead values merely increase the probability of cerebral damage and neurological sequelae. These hypotheses are not easy to test and few studies in this field are above criticism in their experimental design (Wiener, 1970). Thus, Moncrieff et al. (1964) described increased blood lead values in a group of mentally retarded children but failed to appreciate that this was unlikely to have been a causative association. The practice of pica may be unduly prevalent in some retarded children (Bricknell, 1976) and, in any case, blood lead values tend to return to normal after the cessation of a damaging exposure. Recently David etal. (1972) have suggested that hyperactivity might sometimes be produced by the effect of absorbed lead. This view was based on observation of children attending a psychiatric clinic who, when given a chelating agent (a substance which removes lead from the body) excreted larger quantities than controls. Their blood lead levels were in the normal range, although they differed statistically from those of the control children. Similarly, animal studies have been reported in which behavioural disturbances have been observed after relatively modest exposure to lead (Silbergeld and Goldberg, 1973). Unfortunately in both these studies, the method of selection of controls has been open to criticism. A number of recently published studies report the effect of lead in communities living close to lead smelters. Landsdown etal. (1974) studied such a group ofchildren, and found no evidence of intellectual impairement or hyperactivity, even though some of the children they identified showed blood lead levels in the 40-80/ig/100ml range. A comparable study in the U.S.A. (McNeil and Patasnik, 1974) reported similar conclusions, although, when their children were compared with a different control group, some inconsistent differences in the expected direction were found with respect to a small number of tests of motor performance and visuo-spatial ability. (Landrigan et al., 1975). It is difficult to avoid the conclusion that some of the conflicting data might reflect variations in the selection of the control groups used and that the changes reported in some children exposed to lead are probably not due to the effect of its absorption. The LQ. is known to be subject to a variety of social influences, and numerous causes of hyperactivity have, of course, been recognised (British MedicalJoumal 1975). The view expressed by some that children with blood lead levels over 20AJg/100ml are a cause for concern (Carnow, 1975) is difficult to reconcile with the available evidence. Further, there does not appear to be any a priori reason therefore to attribute behavior disorders or mental retardation to moderate increase in blood lead concentration (40-80Mg/100ml). Nevertheless where a child showing either of these problems is suspected of having been in a contaminated environment or is known to suck non-food objects, the blood lead should certainly be investigated. The discovery of a blood lead concentration greater than 40A(g/100ml is an indication of undue absorption and merits an investigation of potential sources, measures to prevent further exposure and a search for other similarly exposed children in the family group and in the locality. The urgency with which these steps are taken should be related to the severity of the exposure. Although only a minority of such children will require chelation therapy, it may even sometimes be necessary to consider removal of the child from the contaminated environment (preferably to a different but familiar setting) until the source oflead has been identified and made safe. REFERENCES Bailtrop, D. and Killala, N.J .P. (1967) Faecal excretion oflead by children. The Lancet 2, 1017-1019. Bailtrop, D. (1968) Lead poisoning in childhood. Postgrad. Med. J. 44, 537-542. Bicknell, J. (1975) Pica, A Childhood Symptom,-p.i^. Butterworth, London. British Medical Journal (1975) Editorial: Hyperactivity in Children. 4, 123-124. Byers, R.K. (1959) Lead poisoning: a review of the literature and report on 45 cases. Pediatrics 21,5^5. Carnow, B.W. (1975) Testimony at Hearing of California Air Resources Board, Sacramento, November. Chisolm. J.J. and Harrison. H.E. (1956) The exposure ofchildren to lead. Pediatrics 18. 943.
ANNOTATIONS
227
David, O., Clark, J. and Voellier, K. (1972) Lead and Hyperactivity. Ihe Lancet 2,900-903. Department of the Environment (1974) Pollution Paper No. 2, Lead in the Environment and its Significance to Man. Landrigan, P.J., Whitworth, R.H., Baloh, R.W., Staehling, N.W., Barthel, W.F. and Rosenblum, B.F. (1975) Neuropsychological dysfunction in children with chronic low-level lead absorption. The Lancet 1,708-712. Landsdowne, R.G., Shepherd, J., Clayton, B.E., Delves, H.T., Graham, P.J. and Turner, W.C. (1974) Blood-lead levels. Behaviour and Intelligence, A Population Study. Ihe Lancet 1, 538-541. McNeil, J.L. and Ptasnik, J.A. (1974) Evaluations for deleterious effects of prolonged asymptomatic elevationsof blood lead. Proc. XlVth Int. Cong. Pediatrics, Buenos Aires, 3-9 October. Moncrieff, A.A., Koumides, O.P., Clayton, B.E., Patrick, A.D., Renwick, A.G.C. and Roberts, G.E. (1964) Lead poisoning in children. Arch. Dis. Child 39, 1-13. Morbidity andMortatity Weekty Report, 29 Nov. 1975, U.S. Dept. of Health, Education and Welfare. Perlstein, M.A. and Attala, R. (1966) Neurologic sequelae of plumbism in children. Clin. Pcdiatr. 5, 292. Seppalainen, A.M. and Hernberg, S. (1972) Sensitive technique for detecting subclinical lead neuropathy. Br. J. Industr. Med. 29, 443-449. Silbergeld, E.K. and Goldberg, A.M. (1973) A lead-induced behavioural disorder. Life Sci. 1 3 , 1 2 7 5 - 1 2 8 3 . Thurston, D., Middlecamp, J.M. and Mason, E. (1955) The late effects of lead poisoning. J. Pcdiatr. 4 7 , 4 1 3 . Wiener, G. (1970) Varying psychological sequelae oflead ingestion in children. U.S. Public Health Reports 8 5 , 19.
