1337LEADING ARTICLES

Cigarettes

1. Lambe, W. Additional Reports on the Effects of a PeculiarRegimen in Cases of Cancer, Scrofula, Consumption, Asthma,and other Chronic Diseases. London, 1815.

2. Annual report by Tobacco Manufacturers’ Standing Committee.See Lancet, June 22, 1957, p. 1306.

" We are constantly deluded by language. We say a

person dies of a cancer ... The truth must be that a persondies of the causes of cancer ; and the cancer is not thecause, but the mode of dying."—WILLIAM LAMBE, 1815.1THE evidence that heavy cigarette-smoking causes

cancer and hence death has become increasinglydifficult to ignore. The Medical Research Council’sstatement set out on p. 1345 summarises the facts

clearly and concisely, and concludes with the importantstatement that " In the opinion of the Council, themost reasonable interpretation of this evidence is thatthe relationship is one of direct cause and effect."This conclusion accords with the view of most whoare familiar with the mass of detailed evidence accumu-lated in the past seven years, not least through thecareful and convincing studies of Prof. A. BRADFORDHILL, F.R.S., and Dr. RICHARD DOLL. The unhurriedverdict of an impartial scientific body such as theM.R.C. cannot but command respect and must makeevery thoughtful person reconsider the criticisms

by the Tobacco Manufacturers’ Standing Committee. 2This committee discounts the suggestion of causeand effect because it derives from observationsrather than from strictly controlled human experi-mentation on randomly selected population groupsand because, so far, no very convincing supporthas come from the laboratory. The limitationsof observational data have long been well knownto epidemiologists ; but should SNOW have waitedfor the discovery of the cholera vibrio before per-suading Londoners not to drink their own sewage ?As the tobacco manufacturers have implied, atmo-spheric pollution may be a factor in the causation ofcancer of the lung ; but its incrimination, like theassociation of genotype and disease, rests equally onobserved correlations. In the urgent defence of thepublic health we should base action on the bestevidence currently available.Whatever the reaction to the evidence we already

have, all will agree that more would be welcome. In1954 the British Tobacco Manufacturers’ Associationgave £ 250,000 to the Medical Research Council, ofwhich £ 69,000 had been spent by the end of lastOctober. This may seem a comparatively smallamount for such an important subject. The work ofthe council is, however, increasing, as its latest annualreport, published this week, makes clear. It hasprovided, with the help of the fund, laboratoryfacilities and staff (in the University of Exeter) for anew carcinogenic-substances research group and has

set up other research groups concerned with atmo-

spheric pollution (at St. Bartholomew’s Hospital) andwith epidemiological research in respiratory diseases(in the University of Sheffield). In addition, grantshave been made to individuals in universities, hospitals,and elsewhere.

It would be unreasonable to expect the people orthe Government to take kindly to the idea of reducingcigarette-smoking; for this is both a widespreadpleasure and the source of immense State revenueand of an important element in international trade.It may reasonably be argued that the citizen shouldbe free to engage in the pleasures he chooses, providedhe does not harm others ; but all smokers and

potential smokers should at least be aware of theextent of the risk in smoking cigarettes heavily, andthis information can be conveyed best (and perhapsonly) with the Government’s help. Measures aimedat direct control of smoking, even were this desirable,would have little chance of success. No such measurecould succeed without the approval of a large majorityof the people, and it seems unlikely that approvalon this scale would be forthcoming. (Almost to aman, the large smoking public has more than onceshrugged off indirect control applied through steeprises in the tax on tobacco.) Yet the responsibility ofGovernment and people, whether smokers or not,cannot end with subsidising -research and publicisinghazards : it should extend to discouraging youngpeople from taking up the habit of smoking cigarettes.A middle-aged cigarette-smoker with a chronic coughmay be moved by the fear of cancer to reduce hissmoking or give it up ; but we cannot expect a youngperson to be deterred by a risk that is apparently soremote, and among adolescents smoking seems infact to be lamentably common .3 4 Youngsters areunlikely to be influenced so much by lectures, pamph-lets, and the advice of adults as by fashion amongthose to whom they look for an example. Smoking isvery much a matter of fashion, and if the large loss oflife due to cigarettes is to be reduced the fashion,especially among young people, must be changed.Such a change (as is clear from the article on p. 1348of this issue) does not necessarily require legislation ;and closer study of the social history of tobacco mightbe rewarding. In any event it is doubtful whethertobacco habits can be changed rapidly so long as thereformer’s modest voice has to be pitted against thepower of modern advertisements ; but organisations,such as the British Broadcasting Corporation, that donot depend on advertising revenue could do much tocounter commercial propaganda, and the cinema

might shape tobacco habits just as it shapes hairstyles. In addition, fuller use should be made of

existing legislation : the law against selling tobaccoto young people is often administered with theutmost laxity.

It would be unrealistic as well as arrogant to supposethat cigarette-smoking can or should be forbidden :the aim should rather be to influence the heavysmoker to modify his habit. This modificationmight take two forms : first, replacement of the

cigarette by the less dangerous pipe or cigar ; and,secondly, reduction in the amount of tobacco

3. Jones, A. P. Ibid, March 23, 1957, p. 631.4. Raven, R. W. Ibid, June 1, 1957, p. 1139 ; Roy. Soc. Hlth J.

1957, 77, 250.

1338

used. The evidence suggests that the temperatecigarette-smoker, who confines himself to, say, oneafter each meal or to two or three in the evening, runsan appreciably lower risk. Two hundred years ago"

drunkenness was the acknowledged national vice ofEnglishmen of all classes." 5 Today, to drink whiskyfrom a hip-flask in a suburban train on the way towork is socially unacceptable. Maybe to smoke acigarette at such a time will in due course also bedeemed a social impropriety. If so, the communitywill be the healthier.

5. Trevelyan, G. M. English Social History. London, 1942.6. Barcroft, J. Researches on Pre-natal Life. Oxford, 1946.7. Acheson, G. H., Dawes, G. S., Mott, J. C. J. Physiol. 1957,

135, 623.8. Walker, J. J. Obstet. Gynœc., Brit. Emp. 1954, 61, 162.9. MacKay, R. B. Ibid, 1957, 64, 185.

10. Randall, C. L. Amer. J. Obstet. Gynec. 1957, 73, 931.

The Newborn Infant’s Oxygen-supplyTHE newborn infant, deprived of the placental

circulation, will die unless by his own efforts he canproduce and maintain a higher level of oxygenationthan prevailed in the later phases of intra-uterinelife. The immediate adjustments of post-natal lifeare directed to this end and are primarily concernedwith establishing adequate pulmonary ventilation andensuring that the brain, rather than the liver, receivesthe best-oxygenated blood.The fundamental work of BARCROFT 6 showed that

in pre-natal life the foetus elaborates the centralnervous organisation required for breathing, whichnormally is inhibited until required for pulmonaryrespiration. Release from inhibition occurs eitherbecause of the inflow of new sensory stimuli at birthor by hypoxic depression of the inhibitory centres.AcgESOrr et al.’ have extended this work using, likeBARCROFT, the sheep. In a study of oxygen con-sumption in foetal and newborn sheep they haveshown that there exists a remarkable, but limited,capacity to adjust the oxygen need in relation to thesupply. In the latter half of pregnancy adequateoxygenation can be maintained only by great increasesin umbilical blood-flow. If the placenta is insufficientor the compensatory mechanisms in the foetus fail,the survival of the foetus depends entirely on itstolerance to anoxia. That similar mechanisms

operate in human pregnancy seems likely from thework of WALKER s and RACHEL MACKAY, who haveshown a progressive fall in oxygen saturation of theumbilical-cord blood as pregnancy proceeds to termand, especially, beyond. A similar fall is found whenpregnancy is complicated by pre-eclamptic toxaemia.Some of the clinical facets of placental insufficiencyhave been discussed by RANDALL.LO

Placental circulatory failure with decompensationof the foetus will cause, in severe cases, intra-uterinedeath. Lesser degrees of hypoxia may initiate intra-uterine gasping movements which, if associated withmeconium-stained liquor amnii, produce asphyxiaand meconium pneumonitis. The anoxic infant isborn with an inadequate oxygen reserve and a

depressed nervous system-two factors which greatlydecrease its ability to attain adequate pulmonaryventilation. More acute lowering of foetal oxygenationis found in cases of abnormal delivery ; interruptionsof placental blood-flow, as in placenta praevia andprolapsed cord ; and interference with the oxygen-

supply to the placenta by general or spinal anaesthesia.HENDERSON et al.11 point out that, while all thesefactors produce a measurable lowering of umbilical-vein oxygen saturation, this is not necessarily a goodguide to the clinical state of the infant. Some infantsat birth may survive with extremely low cord-oxygensaturations, whereas others with mildly reduced oxygensaturations are severely asphyxiated. This is to be

expected in view of the limited value of a singlesampling of cord blood and the many traumatic andchemical factors which influence the first hours of ababy’s life.

After birth the majority of infants rapidly attaina near-adult arterial oxygen saturation.12 2 SHIELDSand TAYLOR 13 have shown that infants born aftercomplications of pregnancy, heavy maternal analgesia,or operative delivery are considerably slower in achiev-ing a normal saturation, determined by a contin.uous-recording ear oximeter. Further studies on the linesof those reported by CROSS et al.14 are needed in orderto elucidate the special metabolism of the newbornand its powers of survival in low oxygen levels.

Possibly other factors are more important than

oxygen saturation in determining the clinical con-

dition of the newborn and the eventual prognosis.One of the other factors is the circulatory status of thenewborn. The neonatal circulation plays an importantpart in producing lung expansion and also ensurespreferential oxygenation of the brain. ADAMS andLiND,15 by cardiac catheterisation, have demonstrateddirectly the persistence of a patent ductus arteriosuswith a predominantly left-to-right shunt in the firstfew days of life. Dr. GUNTHER 16 has attempted torelate the complicated circulatory adjustments afterbirth with the changes in blood-volume consequenton occlusion of the cord and the later development ofpulmonary syndrome. Early clamping of the cord orelevation of the infant while the cord is still attachedto an atonic uterus will deprive the infant of much ofhis blood-volume. This will be of greatest importancein premature babies, who have a relatively largerproportion of blood in the placenta, and in babiesdelivered by caesarean section. It is just these twoclasses of infants that are susceptible to pulmonarysyndrome or, as it is better known, hyaline membranedisease. BROWN 17 has already drawn attention tothe possible connection between early clamping of thecord and the onset of hyaline membrane disease. Sofar, the arguments for this association are largelytheoretical. Dr. BONHAM CARTER,18 summarisingrecent advances in this field, has ingeniously relatedthe changes immediately after birth with the respira-tory difficulties of early neonatal life. It should notbe difficult to devise a controlled study to demonstratethis relationship. It is now generally, although notuniversally, accepted that hyaline membranes are

formed from pulmonary exudate, probably as a resultof pulmonary congestion or hypertension.19 Early11. Henderson, H., Mosher, R., Bittrich, N. M. Ibid, p. 664.12. Smith, C. A., Kaplan, E. Amer. J. Dis. Child. 1942, 64, 843.13. Shields, L. V., Taylor, E. S. Amer. J. Obstet. Gynec. 1957,

73, 1011.14. Cross, K. W., Tizard, J. P. M., Trythall, D. A. H. Acta pœdiat.,

Stockh. 1957, 46, 265.15. Adams, F. H., Lind, J. Pediatrics, 1957, 19, 431.16. Gunther, M. Lancet, June 22, 1957, p. 1277.17. Brown, R. J. K. Ibid, Jan. 19, 1957, p. 163.18. Bonham Carter, R. E. Ibid, June 22, 1957, p. 1292.19. Gitlin, D., Craig, J. M. Pediatrics, 1956, 17, 64.