ANNOTATIONS

but in only a few of the controls. Geipel therefore considers them a typical mongoloid trait but it is worth noting that dissociated ridges are also found in other abnormal conditions. SARAH B. HOLT

REFERENCES 1. Cummins, H., Midlo, C. (1943) Finger Prints, Palms and Soles. Philadelphia: Blakiston (reprinted in

2. Geipel, G. (1964) ‘Die Haufigkeit und die Verteilung der Perlschnurleisten auf den Hi4nden von geistig

3. Holt, S. B., Lindsten, J. (1964) ‘Dermatoglyphic anomalies in Turner’s syndrome.’ Ann. hum. Genet.,

1961 by Dover Press).

normalen Menschen und Mongoloiden.’ Humangenetik,. 1, 157. -0 “-t M, 0 1 .

4. pfeiffer, R. A Schulte, zu Eerge, U. (1964) ‘Untersuchungen zur Frage der Handleisten und Furchen bei Extremi&tenmissbildungen.’ 2. menschl. Vererb. u. Konstitutionslehre, 37, 611.

5 . Wolf, U., Brehme, H., Reinwein, H. (1964) ‘Zum Thema: Longitudinale Leistenverlaufe auf der Handflache des Menschen.’ Humangenetik, 1,149.

LEAD POISONING IN CHILDREN THERE is ample evidence that lead intoxication in children may produce brain damage or even death. The treacherous nature of the condition is underlined by Dr. J. J. CHISOLM Jr. in his review on p. 529 of this issue, where he discusses the possibility that a long-sustained minor elevation in blood-lead level may cause continuing brain damage-an alarming thought considering in how many children an abnormally high absorption of lead passes unnoticed. Moreover, even a slight excess in blood-lead level indicates access to a source of lead and a ,potential danger that further exposure will produce overt encephalopathy. The commonest source of the lead is ingestion of old paint. This is favoured by pica and poor economic circumstances, often associated with crumbling plaster on the walls and flaking paint on the woodwork. Thus the prevention of plumbism in children is fundament- ally the concern of the public health authorities. The role of the physician starts when prevention has failed.

It has been suggested that lead intoxication in childhood may be followed by chronic renal damage in adult life.‘. lo However, TEPPER15 found no definite evidence of renal in- jury 20-35 years after acute lead intoxication in 139 subjects he investigated.

The symptomatology of acute lead encephalopathy is widely recognised, but at this advanced stage of lead poisoning the prognosis is poor even with prompt and expert medical treatment. The dramatic clinical picture, characterised by coma or drowsiness, convulsions, papilloedema and pallor, often heralded by persistent vomiting, indicates a very serious condition indeed. Estimates vary but the mortality of acute encephalopathy may be as high as 25 per cent, and in spite of treatment about half the survivors are left with neurological sequelae. 4* 6- 8 y l4

The aim of the clinician is early diagnosis but he is handicapped because lead-absorption may continue for months with no specific clinical manifestations. Indeed, many children with increased lead absorption are entirely symptomless. 2* 31 6 9 The early clinical features are ill-defined and include irritability, anorexia, occasional vomiting and mild anaemia, but these are so common that the diagnosis of lead intoxication is often not considered at this stage. The familiar signs of lead poisoning in adults-neuritis, colic and lines on the gums -are rarely seen in children, and, though a history of pica may be elicited by direct question- ing, it is often absent.

The difficulty in arriving at a clinical diagnosis is well illustrated by the high proportion of undiagnosed cases revealed by surveys. In Baltimore, Maryland: for example a raised

569

DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY. 1965, 7

blood-lead level (over 0.05 mg. per 100 ml.) was present in 44 per cent of the 333 children studied; about two-thirds of these children were selected on the basis of a positive urinary coproporphyrin test, but there was no significant difference in the blood-lead values of children with or without coproporphyrinuria. In another study in Baltimore,l blood-lead levels over 0.06 mg. per 100 ml. were found in 43 of 116 children (37 per cent) who came to a hospital outpatient department with a history of having eaten plaster or paint. In a door- to-door survey in Cleveland, Ohio, GRIGGS and othersQ found a high urinary concentration of lead and coproporphyrin I11 in 27 per cent of children from old houses but in only 3 per cent of children of similar social status who had been removed to new houses. In Britain, MONCR~EFF and his colleagues13 found blood-lead levels over 0.036 mg. per 100 ml. in 45 per cent of 122 children with mental retardation or severe behaviour disorders.

The alarming findings of these surveys tend to produce a ‘lead-consciousness7 which is often followed by a rapid rise in the number of cases diagnosed. For example, the interest aroused by Professor MONCRIEFF’S article13 led WOODS and WALTERP in Bristol to estimate the blood-levels in 30 mentally subnormal children, of whom 20 had a history of pica and the remainder mental deterioration. They found a raised blood-lead level in 12 children (40 per cent), in 3 of whom there was a strong suspicion that lead poisoning had caused their mental subnormality. This kind of experience was familiar in the United States about 10 years ago. For example, after publicity campaigns in New York the notifications of lead poisoning increased from 1 case in 1950 to 80 in 1954.11 Again in a Chicago hospital in which no cases had been diagnosed for some years, 21 cases were reported in the year following awakening to ‘lead-consciousness’.12

When physicians are thus alerted to the possibility of an unsuspected high prevalence of lead poisoning the difficulty in establishing a clinical diagnosis, and the extreme importance of removal from lead environment and early institution of treatment in these cases, the diagnosis of plumbism is entertained in almost every toddler with vague ill-health. In areas of the United States where lead poisoning is known to be endemic, the relevant diagnostic investigations are often done on many hospital outpatients every day. These tests include blood-lead determinations, semi-quantitative urinary coproporphyrin estimations,2 and X-ray examinations of the abdomen for radio-opaque material and the epiphyses for lines of increased density. In this way many cases of increased lead absorption are diagnosed which would have escaped detection on clinical criteria alone.

Once the diagnosis of increased lead absorption has been made it is of paramount importance to prevent re-exposure to lead, either by removing the source of lead or by re-housing the family. Siblings of affected children should always have their blood-lead levels estimated, since they will often be found to have increased lead absorption, even though they have no symptoms.

PHILIP BENSON

REFERENCES 1. Benson, P. F. (1962) ‘Influence of climatic factors on blood levels in children with pica.’ Guy’s Hosp.

2. - Chisolm, J. J. (1960) ‘A reliable qualitative urine coproporphyrin test for lead intoxication in

3. Bradley, J. E., Powell, A. E., Niermann, W., McGrady, K. R., Kaplan, E. (1956) ‘The incidence of

4. Byers, R. K. (1959) ‘Lead poisoning.’ Pediatrics, 23, 585. 5. Chisolm, J. J., Harrison, H. E. (1956a) ‘The exposure of children to lead.’ Pediatrics, 18,943. 6. - - (19566) ‘Quantitative urinary coproporphyrin excretion and its relation to edathamil calcium

Rep., 111, 306.

young children.’ J. Pediat., 56,759.

abnormal blood levels of lead in a metropolitan pediatric clinic.’ J. Pediut., 49, 1.

disodium administration in children with acute lead intoxication.’ J. din. Invest., 35, 1131.

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ANNOTATIONS

7. Emmerson, B. T., Thiele, B. R. (1960) ‘Calcium versenate in the diagnosis of chronic lead nephro-

8. Greengard, J., Adams, B., Berman, E. (1965) ‘Acute lead encephalopathy in young children.’ J. Pediat.,

9. Griggs, R. C., Sunshine, I., Newill, V. A., Newton, B. W., Buchanan, S., Rasch, C. A. (1964) ‘Environ-

10. Henderson, D. A. (1958) ‘The aetiology of chronic nephritis in Queensland.’ Med. J . Ausr., 45, 377. 11. McLaughlin, M. C. (1956) ‘Lead poisoning in children in New York City, 1950-1954; an epidemio-

12. Mellins, R. B., Jenkins, C. D. (1955) ‘Epidemiological and psychological study of lead poisoning in

13. Moncrieff, A. A., Koumides, 0. P., Clayton, B. E., Patrick, A. D., Renwick, A. G. C., Roberts, G . E.

14. Smith, H. D., King, L. R., Margolin, E. G. (1965) ‘Treatment of lead encephalopathy.’ Amer. J. Dis.

15. Tepper, L. B. (1963) ‘Renal function subsequent to childhood plumbism.’ Arch. environ. HZrh. (Chic.),

16. Woods, G. E., Walters, R. M. (1964) ‘Lead poisoning in mentally subnormal children.’ Lancet, ii, 592.

pathy.’ Med. J. Aust., 47, 243.

66,707.

mental factors in childhood lead poisoning.’ J. Amzr. med. Ass., 187, 703.

logical study.’ New York J. Med., 56,3711.

children.’ J. Amer. med. ,Ass., 158, 15.

(1964) ‘Lead poisoning in children.’ Arch. Dis. Childh., 39, 1 .

Child., 109, 322.

7,76.

THE MEANINGS OF ‘AGGRESSION’ ‘IF there is a problem, science can solve it.’ Perhaps this assumption was the origin of a symposium on ‘aggression’, held by the Institute of Biology in 1963. The proceedings, now published’, ranged from conflict among social insects to the hostile behaviour of people in small groups. The contributors represented zoology, psychology, psychiatry and sociology.

They begin a long way away from man. JAMES FISHER, on conflict between birds of different species, will interest zoologists but-despite a reference to human ‘sub-species’- has only a tenuous relevance to the rest of the book. The main theme of the first five chapters is the analysis of conflict within animal species-its characteristics, precisely described, and its causes. D. I. WALLIS shows how ‘aggressive’ behaviour keeps the colonies of social insects, such as ants and bees, separate. Members of a colony are distinguished by their odour; strangers are driven off. L. H. MATTHEWS describes how he sought authentic examples of fighting to the death among mammals, and failed to do so, though a few-such as hippo- potamus and elephant seals-are quite severely gashed during violent encounters. K. R. L. HALL gives further detail on the relationships of dominance and submission which evidently confer stability on groups of monkeys and apes.

What is the modern zoological attitude to so-called aggressive behaviour ? No general account emerges from these contributions. The present picture depends on an analysis of standard social stimuli (signals) and highly predictable patterns of movements, characteristic of each species. Every social species has a repertoire of signals-sights, sounds, odours and contacts : they include the gorgeous colours of birds and tropical fish, the sounds-raucous or musical-of birds and mammals in spring, the stench of a tom cat in rut. Each often seems to evoke a highly specific response in other members of the same species. Sometimes this response is flight or withdrawal; sometimes it is ‘attack’, usually consisting of gestures or displays which induce withdrawal. An injurious clash is quite exceptional. Commonly, the result of an encounter depends on which animal is occupying its own territory (or defended region): as in football, the home team starts with a big advantage. Withdrawal is not the only way in which clashes are averted: there are ‘submissive’ or ‘appeasing’ signals which seem to prevent attack; these are obviously crucial in colonial species, for members of one group must not come into severe conflict. These inhibiting signals may play a part in forming a status system (or peck order) within each group.

G 57 1