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safety were instilled during the last year at school, theindustrial safety officer would then have become a

familiar figure to all before they start work.As in the two preceding years a separate, report on

industrial health 9 has been published at the same time.For the fourth year in succession no deaths were reportedfrom lead poisoning. Of six cases of mercury poisoning,two (including one death) were reported from poisoningby organo-mercury compounds-the first such cases tobe notified in Great Britain for some years.

Five more cases of beryllium poisoning came to thenotice of the inspectorate during 1960; and five cases ofcadmium poisoning (including one death) were dis-covered. These and a number of other diseases are

prescribed under the National Insurance (IndustrialInjuries) Act, 1946, and since 1959 details of claims

accepted under this Act have been notified to the medicalinspectors in whose division the cases occurred. This

arrangement provides medical inspectors with a widerknowledge of the incidence of industrial diseases over andabove the fourteen diseases notifiable under the FactoriesAct, 1937.

9. Annual Report of the Chief Inspector of Factories on Industrial Health,1960. Cmnd 1478. H.M. Stationery Office. Pp. 63. 3s. 6d.

10. Hamman, L., Rich, A. R. Bull. Johns Hopk. Hosp. 1944, 74, 177.11. Grant, I. W. B., Hillis, B. R., Davidson, J. Amer. Rev. Tuberc. 1956,

74, 485.12. Rubin, E. L., Lubliner, R. Medicine, Baltimore. 1957, 36, 397.13. Lancet, 1958, i, 730.14. Scadding, J. G. Brit. med. J. 1960, i, 443.15. Nicholson, H. in Progress in Clinical Medicine (edited by R. Daley and

H. Miller); p. 207. London, 1961.16. Read, J. J. Path. Bact. 1958, 76, 403.17. Read, J. Med. J. Aust. 1961, ii, 241.18. Nicholson, H. in Progress in Clinical Medicine (edited by R. Daley and

H. Miller); p. 209. London, 1961.19. Livingstone, J. L., Jefferson, K., Reid, L. Unpublished.20. Read, J. Amer. Rev. Tuberc. 1958, 78, 353.

DIFFUSE PULMONARY FIBROSIS

DIFFUSE interstitial pulmonary fibrosis is a bafflingdisease. Since 1944, when Hamman and Rich 10 firstdescribed what now seems to have been an acute type ofthis condition, many workers have recorded their experi-ences of it,1112 but little progress has been made towardsunderstanding its aetiology.l3Recent contributions include those of Scadding,14

Nicholson,15 and Read.16 17 Scadding, reviewing 26 cases,made a plea for the use of the purely descriptive, ifrather cumbersome, title of chronic diffuse interstitialpulmonary fibrosis of undetermined xtiology in prefer-ence to the more popular one of Hamman-Rich syndromeor disease; the latter title may erroneously imply that allcases are due to the same agent. Nicholson remarks thatthe clinical course varies widely; and when it is slow amistaken diagnosis is especially likely. The chest radio-graph may be helpful, but the appearances also varywidely. Though the shadows are commonly streaky andlinear, sometimes they are nodular; and Nicholson 18reports an unpublished series of Livingstone, Jefferson,and Reid 19 in which three-quarters of the chest radio-graphs showed fine mottling.Read 20 noted that in the diffuse pulmonary fibrosis of

Hamman and Rich the essential lesion is diffuse thicken-

ing of most or all alveolar walls throughout the lung,making the lung less distensible than normal and inter-fering with oxygen transfer across the alveolar capillarymembrane. This process is not of course specific to thiscondition. Many possible astiological agents have beensuggested. These have included chemical irritants,syphilis, interference by chemotherapy leading to incom-

plete resolution of pneumonic exudate, viral infections,allergy, and collagen disorders. None of these has beenestablished. Attention has become focused on the histo-

logical changes; and lung biopsy promises to yield furtherinformation about the progressive changes.An attempt to reproduce the changes in animals was

made by Read,16 who administered rabbit anti-rat-lungserum to rats by various routes and found that intra-tracheal, but not intravenous or intraperitoneal, adminis-tration led to distinctive lung changes which he describedas pneumotoxic pneumonia. The lesions either resolvedor proceeded to fibrosis of the alveolar septa. Read iscautious about inferring from these experiments that

pulmonary fibrosis in man develops in the same sort ofway. Impetus might be given to further such workif the clinical picture were to be correlated more exactlywith radiographic, histological, and physiological changes.Meanwhile the condition remains ill understood and itstreatment, even with corticosteroids, unsatisfactory.

1. Education and Physical Growth: Implications of the study of children’sgrowth for educational theory and practice. By J. M. TANNER, M.D.,D.SC., reader in growth and development of children, Institute of ChildHealth, University of London. London. University of London Press.1961. Pp. 144. 12s. 6d.

AGE AND EDUCATION

AT school and elsewhere children are nearly alwaysclassified according to chronological age. This method,though it has the merit of simplicity, has drawbacks whichare becoming increasingly evident. Dr. J. M. Tanner,who is widely known for his work on the physical growthand development of children, has written a book in whichhe discusses the educational implications of physicalgrowth and development. 1Tanner points out that children differ widely in many

aspects of physical maturation-in height and weight, inthe development of the nervous structures underlying theability to walk or to control micturition, in the time atwhich their endocrine glands bring about the changes ofadolescence, and probably in the development of the brain.There is reason to suppose that advancement in physicaldevelopment (as represented by skeletal age) is signifi-cantly, though not closely, associated with advancementin mental ability. At present tests of intelligence fail todifferentiate between advancement and actual ability.Most of the variations between children, says Tanner,

are biological and hereditary in origin. Although low liv-ing standards and poor nutrition retard development, evenif everybody lived under optimal conditions the normalrange of physical development would probably be reducedby less than a year. No social steps could significantlyreduce the range of individual differences in speed ofphysical maturation, even if this were desirable. It there-fore behoves us to fit our educational system, in theory andin practice, to these biological facts.A fast-maturing boy will have a somewhat greater

chance of passing any age-bound examination than will aslow-maturing boy of the same chronological age, even ifthe examination tests abilities largely independent ofsocial and emotional attitudes. If the examination is to befair either developmental age should be estimated and thisfactor allowed for, or else (and this is more practicable)the late maturer should be given opportunities to catch up." It is no good his increasing his intellectual capacity at atime when there is nobody there, so to speak, to see him.If the usual ’bus has left by the time he arrives, othersshould be following after."