Document 3N4jvDGwmwOXRn3qjwL7o6423

' -'v^ :'\.Q' ^ -'' `5 . !>;; - - ' . i:v^' ---" ' ' r4-N';KihV`J7,.-w.V~:k-O.T.5^lLl;&^-?r2ggl^ To South African Medical Journal : Suid-Afrikaanse Tydskrif vir Geneeskunde Cape Town, i5 June 1963 Volume 37 No. 24 Deel 37 Kaapstad. 15 Jucie 1963 EDITORIAL : VAN' DIE REDAKSIE PULMONARY ASBESTOS IS Or all the pneumoconioses or dust diseases, asbestosis would appear to be the most serious from many points of view. It can foilow a relatively short exposure--months instead of years as ir. silicosis--and while the morbidity rate, as determined by racioiogicai means, has beer, much re duced by measures to lessen the inhalation of asbestos dust m factories. ;t can sull be very high--tu-5J. ip. asbestos workers with 20 or more years' exposure and 23;, in those with 10-15 years' exposure.1 The reduction in frequency of pulmonary tuberculosis in the post-war era. and the equally striking increase in lung cancer in most countries, makes it difficult to assess the increased iiability of present-day sufferers from asbes tosis to these two complications. Clearly the data obtained 29 or more years ago have little validity now. while bronchia! carcinoma has such a range of frequency in different countries that conclusions based on world aver ages are hardly acceptable. In the case of pulmonary tuber culosis. the British figure for the association of this disease with fatal cases of asbestosis in the years 1932 - 39 was 35*5?while in the same period the figure was 57-1% in fatal cases of silicosis.5 But in one part of Germany, Meissen, more recent findings published in I960 show that tuberculosis as a complication of silicosis was still very significant--34-6'/--while the association with asbestosis w'as only 4/., little more than twice the tuberculosis figure for the whole population in that region.5 The iung-cancer rate in silicosis is not appreciably higher than in the general population, but in asbestosis its frequency is estimated to be about ten times that of simi lar age groups, both in Britain1 and in Germany.1 In recenc years the matter has been extended by the tardy acceptance by most pathologists of malignant meso thelioma as an entity, and the even more tardy apprecia tion that mesothelioma of the pleura may be associated with asbestosis.15,5 In occupations where pneumoconiosis of mineral origin is a hazard, those affected are normally the miners and occasionally the workers handling the material in bulk. Thereafter there is no danger as a rule to those who deal with the manufactured goods containing the raw material concerned. With asbestos it is otherwise. In Canada, where almost three-quarters of the world's production of asbestos is mined, the miners would appear to suffer little asbestosis and show no significantly increased cancer of the lung.' but ir. South Africa at ieasc. the miners, and even those living in the vicinity of the mines, may develop as bestosis and pleura! mesothelioma. Most cases of asbestosis. however, result not from min ing. but from employment in asbestos factories. Today asbestos is used in so many industries and is a constituent of so many manufactured goods that the occupations where asbestos is a potential hazard are too many to enumerate here. Workers at risk include such unlikely ones as the garage worker employed in under-body car spraying," and more obvious ones such as those employed in lagging pipes with asbestos, or those concerned with the manufacture of asbestos cement, roof and floor tiles, ceding boards, etc., or with the use c: ahem, such as builders ar.d bunders' labourers. White the modern use of asbestos expands the field of potential inhalers of asbestos fibres, the risk of asbes tosis is limited, and it is unlikely that these occupations wiii lead to a marked increase in pulmonary asbestosis. The effect of the inhalation of a small quantity of asbestos fibres, insufficient to produce pulmonary asbestosis. but possible in many of the occupations indicated, has been put on quite a different footing by two recent papers by Thomson and his colleagues in this Journal.1:15 In the tirst paper11 Thomson described 6 cases of mesothelioma, pleural and peritoneal, where there was no diffuse pul monary asbestosis of the ordinary type, out only a few small foci of asbestosis at the bases of the lower lobes. It was stressed that this limited basal asbestosis produced no signs or symptoms and was likely to be overlooked at autopsy, unless sections from the lung bases were ex amined microscopically. In only one of these cases was there a history of exposure to asbestos. This paper was followed by what appears to be the first investigation into the extent to which urban dwellers are exposed to the inhalation of asbestos fibres. Thomson ct al.n examined the bases of lungs for asbestos bodies by a simple smear technique, and found that more than a quarter of the subjects over the age of 15 years in the autopsy services of the Groote Schuur Hospital. Cape Town, showed asbestos bodies, supporting their conten tion chat the inhalation of asbestos fibres was now an urban hazard. They did not find that it was a significant hazard today, and were more concerned with what might happen in the future. They emphasized that the world's production of asbestos is increasing at a staggering rate, and is now eight times what it was 35 years ago, and that today asbestos-containing products are . ubiquitous, especially in urban areas. Thomson et al.': also drew attention to a simple but important fact which seems to have been overlooked so far from the medical and public health points of view. This is that the very reason for the use of asbestos in in dustry--its resistance to heat. acid, alkali, oxidation and reduction; in fact, its urtuai indestructibility--is the reason why it may become progressively mors dangerous to man. Wind and water may disperse asbestos fibres, but they cannot destroy them. Asbestos is now accumulating on the surface of the earth, mainly in the cities, at the rate of 2.400.000 long cons per annum; motor vehicles are discharging asbestos dust from brake drums, dutches, silencers and under-body coatings, and modern buildings may contain asbestos products from the roof to the base ment. The indestructibility of asbestos makes this to some extent cumulative, and in effect we may be creating such 3 630 S.A. Medical Journal 15 June 1963 an aSbestos environment in cities that in the future basal asbestosis may become almost universal in urban dwellers and mesothelioma of the pleura and peritoneum may become common tumours. " These observations and opinions are new and we await confirmation of these findings from other countries: they rr.av well be confirmed as regards the frequency of asbestos bodies in the lungs of urban dwellers. It would seem a hard tun of fate that the avoidance of ordinary pul monary asbestosis might lead to an increased frequency of mesothelioma of the pleura or peritoneum, presumably because the patient lives longer and the carcinogenic action of asbestos has a longer time to act. We hope the fears for the future expressed by Thomson et u/.is are unjusti fied, but it may be desirable to pay heed to their warnings, at least to the extent of restricting some unnecessary and possibly dangerous uses of asbestos. 1. Hohti?. H.. Jacob. C. and Muller. H. (i960): Ore Asbruos* ,ier Limren Stuttgart: Thieme. ' Sutherland. C. L. C19-10): Lancet, t. $93. 3. Wirih. J. (I960): Op. c:/.1 4. Doll, ft. (!95j); Br;l. J. Industr. Med.. 12. si. 5. Cartier, p. 0950: Arch, Industr. Hys.. S. C$2. 6. Van der School. H. C. M. (1952): Ned. T. Ceneesk.. 102. ]|24. 7. Wagner. J. C,, Siergs, C. A. and Marchand. P. UV60): Snt. 1. Industr Med.. 17. 260. ' S. Sraun. O. and Train. P. Arch.Industr. Hyg..17. 9. Sleggs. C. A.. Marchand. P. and Wagner, J. C. 03$!;:S. Afr. Med. 10. BrugMli, H. G. and Bavley, H. 0561): New Hr.gl. J. Med., 265 379 11. Thomson. 1. G. 056:): S. Air. Med. 36. 759. ' 12. Thomson, y G., Kaschuia. ft. O C and MacDonald. R. R. 0963); /hr.J.. 37, 77. ' BAKTERIELE GENETIKA Daar was 'n tyd toe dit aanvaar was dat die klassieke genetiese wette en beginsels nie op mikro-organismes. en veral bakteriee, van toepassing was nie. Bakteriee reproduseer vegetatief en hul mikroskopiese grootte het hulie ongeskik vir sitologiese studies gemaak. Vir baie jare was dit aanvaar dat daar fundamentele verskille. beide geneties en fisioiogies, tussen hoer diere en mikro-organismes bestaan en dat die wette wat op die een van toepassing is, nie vir die ander geld nie. Maar, gesten in die lig van die moderne fundamentele eenvormigheid tussen alle biologiese wetenskappe. is dit duidelik dat hierdie opvatting verkeerd was. Gemeenskaplike grond is gevind deur die intensiewe studie van bakteriele ge.netika wat slegs in die laaste twee dekades op die voorgrond getree het. Vandag is hierdie vafc die brandpunt van die biologiese weten skappe en het al seifs sover gevorder dat dit amper die tergende vraag ,,wat is lewe?", kan verklaar. Jacob en Wollman1 verdecl die historiese ontwikkeiing van bakteriele genetika in sekere tydvakke: Gedurende die laaste helfte van die 19de eeu is mikrobioiogie as eksperimentele wetenskap ingestel en aandag is'hoofsaaklik bestee aan die isolasie en morfologiese beskrywing van nuwe spesies. Van 1900 tot 19-0 is 'n groot aantal variasies van bakteriee geldentifiseer. bestudeer en oeskrywe. en hieruit is die vak bakteriele genetika gebore. In die laaste tycvak. begir.nence 19-0. word bakteriele oorerwmg ontleea en gekoorcineer ir. die he van die klassieke genetiese teoriee. Klassieke genetika ontieed die aara van kompiekse. dikweis nie-essensieie. eicnskappe. In teensteiiin? caarm.ee anaiiseer bakterieie genetika op die moiekulere vlak en gee 'r beter begrip van 'oasiese seliuiere meganismes. Ook d:er. dit as n handige instrument waarmee die struktuur en runksie van bioiogiese sisteme cepaal kan word. Treffer.de bewys. cat daar 'n chemiese basis v>r oorerwinc bestaan. is geiewer toe 'r bakterieie eienskap omvorm is deur desoksieriborukieiensuur (D.N.S.i. '-vat viz 'r pneumckokkaie mutant1 cere: is. Soortgciyke ir.grypende waamemings is in die afgelops :0 ;aar met baktsrie csdoer. waarvoor verskeie faktore vsramwoordeiik is. Cm siecs 'r caar te r.oem: Baktene kan. weens hulie Cuseewenaarde vocrtpiantmgsnelneid :n n kort tyd tot er.crme cetaiie aangroei. Die bakterieie sei $e oorerwingsfaktore is vasgeie deur >. enkeie iiniere struktuur. die bakterieie chromcsoom. bestaande u:t D.N'.S. wat oie makxomolekuiere pacroon van die bakterium beheer. Bakterie se genetiese materiaal is reiatief onstabiei. Mutasies kom spontaan voor in `n gegewe gene in een uit elke honderd miljoen sel-verdelings. Eksperimente'e metodes in bakteriele genetika tref deur hul eenvoud, akkuraatheid en berekenbaarheid waarmee analiese uitgevoer kan word. Die fundamentele probieme.van genetika het hierdeur binne die bestek van die nie-genetikus geval. Van die merkwaardigste bydraes op hierdie gebied is inderdaad gemaak deur fisici en biochemici. In 1953 beskrywe Watson en Crick,1 Nooelpryswenners van 1962, die struktuur van D.N.S.. gebaseer op chemiese analiese en kristallografiese studies, wat ailerwee as 'n biochemiese triomf aanvaar is. Hiervolgens sou D.N.S. bestaan uit twee poli- nukleotied-kettings wat spiraalsgewyse rondom 'n sentrale as gedraai is. Die ruggraat van elke spiraal bestaan uit fosfodiester-bande. Die basisse, op 'n gegewe viak van die een ketting, word met behuip van waterstotbande gebind aan basisse cp die ooreenstemmende vlak van die ander ketting. Waterstofbindings kan. weens struktureie redes, net piaasvind tussen die basts-pare adenien-timien en guaniensitosien sodat die een ketting dan die spieelbeeld van die ander is. Dit is verbasend watter beiangrike bioiogiese gevolgtrekkinge van hierdie model gemaak kan word: Dit lewer bewys van D.N.S. se molekuiere repiikasie: die aaneeniopende Iiniere volgorde van basis-pare gee aan'eiding tot `n bepaaice genetiese kode en soesitisiteic. terwy! dit ook `n verklaring vir mutasies aan die hand gee. Hierdie model dien veroer as voorbeeid van 'n nuwe studicrigting. naamiik molekttierc bioiogie. wat daargeste! is hooisaakiik deur die toedoen van bakterieie en virus-genetika. Hoe ver ons reeds vandag gevorder het van die klassieke sitoiogie blvk uit die feit dat as die genetika van cieriike somatiese selie op hierdie grondslag ontwikkei moe: word. c:t can 'n direkte uitvloeise! van bakterieie en virus-genetika is. wat weer op hulie beurt buiie ontstaar. 3an uee:;-e!ku;:ure te canke het. Die se.ntraie pcsisir wat atcomfisika vandag in die fisiese wetenskappe bekiee. kan or.s vergsiyk met m.ciekuiere bioiogie in die bioiogiese V'etenskappe. Vandag se teorie is die prakivk van more. Ir. hoeverre bakterieie genetika die natuurwctte gaan beinvicec. hang af van die sukses waarmee die teoriee. wat sodamg verkry $. on ander bioiogiese sisteme toegepas kan word. 1. lcco$. r. Wollmsft. . L. -I56i:: S*x:is.'hv Ca;irnc. London. Acicemic Vrsss. Otner.c: ?" 2. Avsrv. O. T.. NIsLeoU. C. M. en McCarthy. M. -'1944.: J. =XP. Mca.. 70. " Watsor.. J. D en Crick. ? H. C. '!$.'.): Nature Lon,; 17t. I t I *7- 'Hb-:-"