DEVELOPMENTAL M E D I C I N E A N D C H I L D N E U R O L O G Y . 1982, 24

The wide variations in estimates of tooth-lead levels are due to factors additional t o irregularities of analytical performance. Apparently it is not enough to reduce variability by restriction to one type of tooth, to a limited age-range, or to teeth in which root resorption is minimal. Substantial differences sometimes can be observed between lead levels in teeth of the same type from the upper and lowerjaw of the same subject, and even from contralateral teeth of the same type in the same jaw!

Nevertheless, within the limits imposed by such sampling considerations, estimates of tooth-lead' levels may be deemed acceptable to reflect lead uptake during the years of formation of deciduous and permanent teeth'. Thereafter, in permanent teeth, recourse may be made to the isolation and analysis of circumpulpal dentine, which reflects lead uptake after formation has been completed. Typical increases of lead in bulk tooth substance of up to Ipg per gram per annum are observable.

MRC Dental Unit, The Dental School, Lower Maudlin Street, Bristol BSI 2LY.

MAURICE STACK

REFERENCES 1. Stack, M. V., Delves, H. T. (1982) 'Tooth-lead analysis: a n inter-laboratory survey.' In Proceedings

of the International Symposium on Harmonisation of Collaborative Analytical Studies. Helsinki, 20th-21st August 1981. ( I n press.)

2. Rutter, M. (1980) 'Raised lead levels and impaired cognitive behavioural functioning: a review of the evidence.' Developmental Medicine and Child Neurology, 22, Suppl. 42.

Lead and Brain Function

SIR-The important paper on lead and brain function by Yule and his colleagues ( D M C N , 23, 567), like the closely similar earlier study of David et a/.' (which they omit to mention), may fall far short of that unattainable perfection which some claim to desire before they are prepared to take the matter seriously; but it adds to thegrowing list ofreports which suggest that 'normal' body burdens of lead are actively pathogenic for mental development and function in children. Since present-day body burdens are authoritatively claimed to be some 100 to 1000 times greater than the natural levels against which Man evolved as a species2, and since the range of blood lead levels in urban children (7 to60pg/dl in the report by Yule et a/.) approaches and often exceeds levels at which symptoms of clinical poisoning can appear in sensitive children ( > 4 0 ~ g / d l ) ~ , and mental symptoms in adult males (ca. 30pg/dIj4, the findings of Yule and colleagues are, in a broad sense, to be expected apriori. In contrast, your Editorial in the same issue seems to suggest that admitting an influence of lead on children's problems could distract attention from the conventional social factors such as parental attitudes, and in the last sentence tries t o play the matter down. This response is more political than scientific, and seems inappropriate in a medical and scientific journal. The lead factor merely adds another important dimension to our understanding of behavioural and educational problems, and is not seen by any workers known to us in the field as a full alternative to the conventional soFial influences on child development*.

The problem o f measuring children's exposure (0 lead by analysing their blood is clearly revealed in this pilot study by Yule ('t ul. In addition to the time lapse between lead analysis and educational testing (not in itself necessarily a seriously confounding factor). there is a n * I am glad t o hear i t . I/nri~pi,ntont /?/itor, / )M( 'N.

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LETTERS

apparent decline in blood lead with age, which is markedly more rapid than that in any other study so far reported’. It is indeed notable that Yule and colleagues were able to correlate blood lead level with tests of ability after controlling for such a large confounding variable. Furthermore, the controlled interval spans a possible transition period in cognitive development; an active period in physiological growth occurring between the ages of six and eight years, preceded and followed by two-year plateaux when little growth occurs6. It may be that differential cognitive development during this critical period could explain why mathematical ability was apparently not sensitive to Iead exposure.

The key question of whether we are dealing with a fortuitous association between lead and mentation or a cause-and-effect relationship is largely answered by the favourable intellectual and behavioural responses to detoxification evinced by many children3, ’, ’, and by the detailed and extensive evidence from animal studies4 that behavioural changes can be induced by ‘low level’ lead exposure, down t o a blood lead level of ra. 5pg/d14. Some, a t least, of the biochemical correlates of these behavioural changes have been identified4. In the light of these findings, any unsupported suggestion that some unknown factor fortuitously associated with increased lead absorption in children may really be responsible for their impaired abilities should be regarded more as a bow to current orthodoxy than a scientifically justified reservation.

Department of Chemistry, University of Reading, Whiteknights, Reading RG6 2AD. *Department of Chemistry, University of Birmingham, Birmingham B 15 2TT.

D. BRYCE-SMITH R. STEPHENS*

REFERENCES 1 . David, 0. J., Hoffman, S., Kagey, B. (1979) ‘Sub-clinical lead levels and behaviour in children’.

Trace Suhsrances in Environmental Health, 13, 52-58. 2. United States National Academy of Sciences (1980) Lead in the Human Environmenr. Washington,

D.C.: National Academy Press. 3. Moncrieff, A. A., Koumides, 0. P., Clayton, B. E., Patrick, A. D., Renwick, A. G. C., Roberts, G. E.

(1964) ‘Lead poisoning in children’. Archives qfDi.sease in Childhood, 39, 1-13. 4. Bryce-Smith, D., Stephens, R. (1980) Lead or Heafth-a Revieu qf Contemporary Lead Pollution.

London: Conservation Society. 5. Great Britain: Department of the Environment (1981) European Community Screening Programme.for

I.rad: United Kingdom Results for 1979-80. Pollution Report No. 10, Fig. 16. 6. Cookson, C. (198 1) ‘Learning is linked t o spurts in development of brain’. Times EducationalSupplement.

15th May, p. 16. 7. David, 0. J., Hoffman, S. , Sverd, J., Clark, J., Voeller, K. (1976) ‘Lead and hyperactivity. Behavioural

response to chelation: a pilot study’. American Journal qf Psychiatry. 133, 1155-1 158. 8. David, 0. J. (1978) ‘Sub-clinical effects of lead o n children’. Proceedings of the Conference ‘Lead

Pollurion-Healrh <ffecr.r’. London: Conservation Society.

Infantile Spasms

SIR-Curatolo et a/. (DMCN, 23, 449) are quite correct in recommending a careful opthalmoscopic examination ,of infants with infantile spasms. One would be remiss in not doing so.

The finding of normal retinae should not be used as an argument against a CAT scan. Information about structural abnormalities and brain atrophy is necessary to predict

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