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EXAMINATION OF EVACUEES

THE LANCET

LONDON: SATURDAY, 1V19.RCH 23, 1940

THE Minister of Health has promised that ifschool-children have to be evacuated again he willensure that they are medically examined beforethey reach their billets. Householders in the

reception areas have not forgotten the disclosuresof the last evacuation and this time will justlyinsist that children who are dirty in person orhabits are housed elsewhere. The Minister hasnow set out his plans for medical examination ina circular to local authorities, whose duty it willbe to put them into effect. The closing date forthe registration of children who want to beevacuated is March 30, and the circular recom-mends that within three weeks of that date allthe children registered should be examined byschool medical officers in the evacuation areas andtreatment instituted " for any condition whichwould render them unsuitable for billeting onprivate householders." Children whose conditionis not altogether satisfactory are to be re-examinedat intervals of not more than a month, and thosewho have had scabies or " severe " pediculosis atshorter intervals. Parents are to be told that theymust keep their children clean and that the

presence of scabies or impetigo will disqualifythem from private billeting. So much for the

preliminaries. Over and above these, localauthorities must arrange for a further medicalexamination of the children in the evacuation areaon the day that evacuation takes place or the

preceding day and still another on their arrivalin the reception area. The circular remarks thatchildren going to distant places will arrive latein the evening, but urges that they should bedistributed to their billets with a minimum of

delay.With the Ministry’s preliminary plans no-one

will quarrel. These are but a tightening up ofthe measures that have always been taken inschools to ensure cleanliness and freedom fromminor infections. Last time, however, we weretold that some at least of the nits and acari werethere because the children had been on holidaybefore the evacuation took place. Regular super-vision must therefore continue in the holidaysand urgent steps should be taken to cleanse thehomes from which verminous children come. Butthe arrangements made for inspection whenevacuation comes seem to be framed with thesole purpose of meeting the letter of the Minister’spromises. Under what conditions will the secondevacuation take place? If Herr Hitler is con-

siderate and the Ministry can give their promised36 hours notice the scheme may work in a modi-fied form, always presuming that raids do not

come before April 20, when the preliminaryexaminations will be finished. But we are toldthat evacuation will be ordered " only if air-raidsdevelop on a scale involving serious and continu-ing perils to civilian population " and it is at leastpossible that it will not be ordered until raidshave begun. Local authorities are to arrange forthe examination of 400 children an hour, whichwould need 20 doctors at the rate of one childper three minutes. Where are these to be foundwhen raids are on? Certainly not in improvisedminor-ailment clinics at railway stations in theevacuation areas. And what examination of anyvalue is-likely to be made by tired medical officerslate at night with children and helpers clamour-ing to go to their billets?

If preliminary examination and treatment arecarried out thoroughly all the most particularhouseholder will ask is to be assured that thechildren are free from obvious pediculi and acuteinfections. This means that the child’s head andbody must be examined for parasites and skineruptions, its throat for obvious inflammation, andits temperature must be taken. Such an exam-ination will rule out all but the more obscureinfections, and it can well be carried out by schoolnurses and health visitors, school-teachers, or

indeed by any intelligent helper with a little .

instruction. These people will have the advan-tage of knowing the children they were examining-a great help in diagnosis-and if they travelwith the children they can make their inspectioneither at the despatching or receiving end as seemsconvenient, but need not make it at both. And

finally, this modified examination can be plannedin detail in advance, with some certainty that itcan be put into operation even under air-raidconditions.

MORE ABOUT SILICOSISSINCE HALDANE and COLLIS2 wrote their two

classic summaries of existing knowledge or

silicosis in 1914 and 1915 there has been animmense amount of both clinical and experi-mental work on the subject. The experimentalinvestigations have mostly aimed at deciding,first what is the causative agent in disease-pro-ducing dust, and secondly what measures can beused to neutralise the harmful dust. The hard-ness and sharpness of the dust particles was thefirst reason suggested for the pathogenicity ofindustrial dust, and this mechanical theory sur-vived for many years. But GARDNER’S failureto produce silicotic lesions with carborundum dust,and KETTLE’S 4 convincing experiment in whichiron-coated quartz failed to bring about the resultobtained with the original quartz brought the

theory of "

microscopic trauma " into final dis-repute. To take its place a chemical theory wasevolved. This supposed that a soluble toxic sub-stance, liberated from the dust particles, irritatedthe surrounding tissue to produce a fibrous

1. Haldane, J. S. Second Report of Royal Commission onMetalliferous Mines and Quarries, London, 1914.

2. Collis, E. L. Pub. Hlth 1915, 28, 252 : 29, 11, 37.3. Gardner, L. V. Amer. Rev. Tuberc. 1923, 7, 344.4. Kettle, E. H. J. Path. Bact. 1932, 35, 395.

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response. The toxic substance was thought to besilicic acid-dissolved Si02. Experimental sup-port was given to the toxic theory by GYE andKETTLE,5 who produced " almost a specific "lesion by subcutaneous injections of fine silicaparticles, and by GYE and PURDy6 who found livernecrosis in animals which had been injected withcolloidally dispersed silicic acid. Thus silicic acidcame to be regarded as the immediate cause ofthe fibrosis in silicosis. But the question of whatconstituents of mineral dusts would produce thetoxic substance, and hence cause the disease,remained in dispute. Industrial experience pointedto those dusts containing a large proportion offree silica-quartz and flint-as being the mostdangerous, and most good experimental work withanimals, such as that of Gardener, supportedthat conclusion. But a great body of other evi-dence has arisen, much of it seemingly contradic-tory, and much of it invalidated through faultyobservation or improperly controlled experimentswhich has prevented universal agreement beingreached as to which dusts are dangerous andwhich harmless.In addition to supplying much of our clinical

knowledge of silicosis and keeping it up to datewith their periodic reports the South Africanmedical workers in the gold-mining district havecontributed many of the most trustworthy experi-mental studies. In these they have the advan-tage of close cooperation with experts in manyfields. Thus, with the cooperation of theChamber of Mines, SIMSON and STRACHAN,9 ofthe South African Institute of Medical Research,have secured authentic mineral specimens whosemineralogical and chemical characterisation mustcommand confidence. These were sillimanite,orthoclase, muscovite, quartz, rutile, glass, a

dust residue from human silicotic lung, andseveral mine dusts-all mineral materials of indus-trial interest whose silicosis-producing propertieshad hitherto been in doubt. The size distributionof the dust particles, which was estimated byPATTERSON, was very uniform in the severalminerals, and corresponded closely with thatfound in the air breathed by mine workers."Several small spaced doses of suspensions of thedusts were injected intravenously into rabbits, thedust being left to act on the tissue for periods upto 700 days. Most of the animals survived formore than a year. The tissues chiefly affectedwere those of the liver, spleen, lymph-nodes andbone-marrow-that is, those provided with an

active reticulo-endothelial system related toabundant sinusoid tissue. Quartz, the minedusts, and the lung residue were active. In allorgans, particularly in the liver, there was a

definite series of events culminating in densefibrosis. The spleens were greatly enlarged, thelymph-glands were either " firm and rubber-like

"

5. Gye, W. E. and Kettle, E. H. Brit. J. exp. Path. 1922, 3, 241.6. Gye, W. and Purdy, W. J. Ibid, 1924, 5, 238.7. Gardner, L. V. J. indust. Hyg. 1932, 14, 18.8. Irvine, L. G. Report on Miners’ Phthisis Medical Bureau,

Union of South Africa, 1939.9. Simson, F. W. and Strachan, A. S. Pub. S. Afr. Inst. med.

Res. 1940, 9, 95.10. Patterson, H. S. Bull. Inst. Min. Met. June, 1939.

or "

densely hard as a result of hyaline fibrosisand calcification," and there was " discretefibrous nodulation " of the bone-marrow. Theinactive dusts-sillimanite, orthoclase, rutile,muscovite (of which sericite is a variety) and pow-dered glass-were seen as

" accumulations ofdust, apparently enclosed within a limiting mem-brane. " There was no true chronic inflammatoryreaction and no fibrosis. These experimentsshould mark the end of the suspicions attachedto these minerals as causative agents in silicosis.They will confirm the current belief that quartz,flint, and other forms of free silica are the noxiouselements of industrial dust, and SIMSON andSTRACHAN maintain a close relation of their animalresults to the human disease.

In the South African experiments the presenceof coaldust with quartz in the proportion of 3 to 2seems to have increased rather than prevented theaction of silica. In Stockholm, NAESLUND 11 hasbeen investigating in rabbits and guineapigs thepossibility of preventing silicosis by specific dustinhalation, and the question of the risk of sili-cosis being increased by inhaling mixed dust.Coal seemed to have no influence on the effectof quartz. On the other hand, the effect wasdelayed by mixing quartz with cement when amilder silicosis resulted. The admixture of limewith quartz made little difference, so that if thereis a neutralising agent for quartz in cement itdoes not appear to be the lime. There is a wide-

spread belief that simultaneous inhalation of freesilica and of alkali (e.g., soap powder) resultsin a rapidly developing silicosis. Various alkalis,with and without quartz, have been tried out inthe Swedish experiments. The alkalis producednecrosis, cedema and cell proliferation in the

lungs, and when they were mixed with quartzthe same result was obtained. The effect in bothcases could in fact have been directly due to theirritation of the alkali. The inhalation of alkalinedusts also rendered the animals very susceptibleto infection, so that many of the examples ofthis type of

"

acute silicosis " recorded may havebeen cases of acute infection in alkali-damagedlungs.We have already commented in these columns

on the work of DENNY, ROBSON and IRWIN 12 ofToronto on the prevention of experimental silicosiswith aluminium. This work rested on the find-ing that finely divided metallic aluminium wouldalmost abolish the solubility of quartz. Simul-taneous inhalation of quartz and aluminium dustby rabbits failed to produce the lesions seen whenquartz alone was breathed. The close associationof the aluminium with the quartz resulted in thelatter becoming coated with a thin layer ofhydrated aluminium hydroxide, which effectivelyprevented the quartz from going into solution.It was held that the development of the silicoticlesions could be prevented in this way. This

startling claim was not without some supportfrom industrial experience. It had been advo-

11. Naeslund, C. J. indust. Hyg. 1940, 22, 1.12. Denny, J. J., Robson, W. D. and Irwin, D. A. Canad. med.

Ass. J. 1937, 37, 1 ; 1939, 40, 213 ; see Lancet, 1937, 2,271 ; and 1939, 1, 882.

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cated by HALDANE 13 that the dust of certainshales could act as a natural antidote to theharmful dust of other rocks, and the belief hadlong been held that the practice of

" stone-dust-

ing" in coal-mines had certainly not increasedthe silicosis hazard, and may even have lessenedit. Lately it has been shown by WIIITEHOUSE 14and KING 15 that these shale dusts exert the samedepressing effect as aluminium, though to a lesserdegree, on the solubility of quartz and flint.NAESLUND agrees with DENNY and his colleaguesthat metallic aluminium is the most effectivematerial for depressing the solution of silica, buthis success in preventing silicosis was not as

complete as theirs; there are not yet grounds forintroducing aluminium dust as a prophylacticmeans against silicosis. MIDDLETON’S 16 case

of an aluminium-paint worker whose lungs con-tained lesions which could only be ascribed to thealuminium particles seems to lend support to thisview. In the meantime, the results of clinicaltrials now being carried out in Canada will beawaited with interest.

TRAUMATIC SHOCK AND THESUPRARENAL CORTEX

THERE is much to suggest that the suprarenalcortex plays a part in the defence of the bodyagainst the effects of injury. The patient withAddison’s disease is notoriously unable to tolerateeven mild surgical operations and the animaldeprived of its suprarenal glands in a few daysbecomes highly susceptible to many differentnoxious agents. The histopathological features ofthe " alarm-reaction, " which has been studied forseveral years by SELYE and his collaborators atMontreal, include hyperplasia of the suprarenalcortex, and it has lately been observed that

patients after surgical operations excrete a con-siderable quantity of adrenal cortical substancein the urine. The condition of suprarenal corticalinsufficiency closely resembles that of traumaticshock. Shock, however, develops within a fewhours while the effects of complete extirpation ofthe suprarenals in mammals do not appear forseveral days. It is evident from experiments bySWINGLE and others 11 that the normal animal hasreserves of cortical hormone which enable it toresist the milder degrees of trauma. In theseexperiments adrenalectomised dogs which weremaintained in apparently normal health and

activity by small doses of cortical hormone couldbe reduced to a condition of profound shock bytrauma which had no deleterious action on normaldogs, and this shock was successfully treated withlarge doses of cortin.We cannot assume that traumatic shock is

caused by inhibition of the functional activity ofthe suprarenal cortex, but it is possible thatcertain changes which take place during traumatic

13. Haldane, J. S. Trans. Inst. min. Eng. 1917, 55, 264 1931,80, 415.

14. Whitehouse, A. G. R. J. indust. Hyg. 1938, 20, 556.15. King, E. J. Biochem. J. 1938, 32, 2283.16. Middleton, E. L. Bull. Inst. Min. Met. April, 1939.17. Swingle, W. W., Parkins, W. M., Taylor, A. R. and Hays,

H. W. Amer. J. Physiol. 1938, 124, 22.

shock call for supplies of cortical hormone inexcess of the available stores. For example, thealterations in serum electrolytes and corpuscularconcentration after experimental scalds 18, are

almost identical with those in cortical insufficiencyand these alterations are rapidly corrected byadministration of the synthetic hormone desoxy-corticosterone. These experiments suggest thatthe blood changes after scalds may be a result ofaltered permeability of cell membranes whichhave been damaged by excessive heat. There is,nevertheless, no good evidence that blood changesin themselves are responsible for the circulatoryfailure of tramatic shock. In fact the shock pro-duced in SWINGLE’S experiments was not accom-panied by electrolyte changes, corpuscular con-centration or disturbance of water distribution,but was attributed rather to altered capillary toneand permeability.

VARANGOT 19 has urged, and Dr. PoLLAK supportshim in a letter on another page, that there is aclear case for the trial of cortical hormone in dif-ferent forms of shock. Hitherto extensive trialhas been handi.capped by the expense of corticalextract, but the synthesis of desoxycorticosteroneacetate by STEiGER and REICHSTEIN 20 has madesuch treatment a practical proposition. In thiscountry the synthetic hormone has been tested byWiLSON and STEWART 21 on a small scale in thesecondary shock of burns and scalds and someother forms of circulatory failure. While theyreport some benefit in burn shock and intestinalobstruction the effects seem to be neither constantnor very dramatic. Certainly in profound shockthe hormone is incapable by itself of raising theblood-pressure. Further investigation may, how-ever, show that it is useful if only as an adjuvantto established methods of therapy.

AN EASTER APPEAL

THERE are in Great Britain and Northern Ireland1095 organisations which come under the heading ofvoluntary hospitals. On Easter Sunday at 8.40 P.M.they will make a joint broadcast appeal, having chosenas their spokesman an officer of the merchant servicewho was lately one of their patients. The combinedstreet collections which the London hospitals have beenmaking for the past few years have shown the valueof coordinated effort, and on Christmas Eve their firstjoint broadcast appeal was made. Its results wereencouraging and the B.B.C. and the hospitals havenow arranged to hold three combined broadcastappeals this year of which this Easter talk will bethe second. Contributors may if they wish earmarktheir gifts for any particular hospital in which theyare interested. The committee arranging the appealmay be addressed at 10, Old Jewry, London, E.C.2.

Dr. CHARLES SLATER, consulting bacteriologist toSt. George’s Hospital and formerly reader inbacteriology to the University of London, died at

Tunbridge Wells on March 15 in his 84th year.

18. Lowdon, A. G. R., McKail, R. A., Rae, S. L., Stewart, C. P.and Wilson, W. C. J. Physiol., 1939, 96, 27 P.

19. Varangot, J. Pr. méd. Jan. 31, 1940, p. 103.20. Steiger, M. and Reichstein T. Helv. chim. Acta, 1937, 20,

1164 ; Ibid, 1938, 21, 171.21. Wilson, W. C. and Stewart C. P. Edinb. med. J. 1939, 46,

(Transactions) 153.