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THE LANCETThe Miners: A Special Case ?

To the miners’ weapon of an overtime ban, theGovernment has replied by taking emergency powersand imposing a three-day week throughout industry.The time is now ripe for suggestions of Govern-mental retreat with dignity, and a formula for thishas been devised by Dr ANTHONY FREEMAN in aletter to The Times.’ He proposes that the offer tothe miners could be increased, without violating theGovernment’s wages policy, by large increases in

compensation for the injuries and ill-health particu-larly associated with mining. These are indeedformidable. Risks of death from industrial injuryare 10 times greater than in manufacturing industry.Miners’ standardised mortality from all causes is now15% higher than the mean for all occupations,compared with 6% higher in 1931. Their wiveshave a 29% excess, showing that social factors, out-side the work itself but connected with the entiresocial milieu of coal mining, are an importantdeterminant of illness and its outcome. 2 Earningsfall with increasing age and experience, as the minersbecome less able to cope with the extremely arduousnature of work at the coalface. A collier on a fullymechanised face still has an average energy expendi-ture per shift of 1790 Kcal., compared with 1990 forhand-hewing,3 and in most pits there is still a greatdeal of shovelling, often from a kneeling position.Even on a "button job" a man may have severalmiles to walk underground, with steep gradients,over irregular ground, and often a low roof. In oneSouth Wales mining village, 25% of men aged 35-54, and 61% of those aged 55-64, were found onclinical assessment to have important chronic dis-abilities affecting employment. 4 The absence ofsuitable alternative work for the disabled in collierydistricts is notorious, and most are also areas of highunemployment where disability and middle age addup to permanent unemployment. Inception-rates forincapacity in miners are 182% and average days ofincapacity 217% of the England and Wales mean,5and general-practice consultation-rates are 124% ofthe mean. 6 These figures represent real disability;studies of the proneness of miners to complain ofrheumatic pain, compared with other manual workersand office workers, showed that miners had moreadvanced radiological joint damage at earlier ages,and that their consultation-rates, though high, wereproportional to the objective evidence of joint

1. Freeman, A. Times, Jan. 8, 1974.2. Hart, J. T. Lancet, 1972, i, 192.3. Davis, P. R., Knight, A. A. in Medicine in the Mining Industries

(edited by J. M. Rogan). London, 1972.4. Hart, J. T. J. R. Coll. Gen. Practnrs, 1971, 21, 517.5. Report of an Enquiry into the Incidence of Incapacity for Work.

H.M. Stationery Office, 1965.6. Logan, W. P. D., Cushion, A. A. Morbidity Statistics from General

Practice; vol. I. H.M. Stationery Office, 1958.

disease. 7 No association was found between psycho-metric test scores and rheumatic symptoms. 8

Turning to specific diseases, there are the vexedquestions of disability from pneumoconiosis, and thecontribution of coal dust to bronchitis. Simplepneumoconiosis seldom causes severe disability, butevaluation of lesser degrees of disability is difficultbecause of the crude nature of tests of respiratoryfunction normally available, with ranges of normalthat vary widely between individuals. Even moredifficult is any attempt to estimate disability chieflyfrom radiological change alone, and it may beunfortunate that discussion of the subject has beenso dominated by this sometimes deceptive variable.Necropsy studies correlating morbid anatomical

change at a histological level with previous radiologi-cal category and tests of respiratory function haveconfirmed that function may be impaired in simplepneumoconiosis and that this impairment maycorrelate better with histological change than withradiological category.9 9 American work has suggestedthat evaluation of respiratory function in simplepneumoconiosis is difficult without assessment of gasexchange. 10 In most disabilities the patient’sreported symptoms are a more sensitive indicationof departure from his own normal state than anyobjective tests, and the elimination of subjective datain compensation situations is an important handicapin accurate diagnosis; colliers rightly fear pneumo-coniosis, and there is no evidence that they seek thediagnosis on any substantial scale. Complicatedpneumoconiosis (progressive massive fibrosis) is

beyond any doubt a crippling disease, and the B andC categories cause the same prolonged and verydistressing terminal illness as do other obstructive

respiratory diseases, with cor pulmonale and a fightfor each breath that may last for years. It is nowrare in young men, and in the elderly it grosslyimpairs life without very greatly shortening it, sothat (as in bronchitis) mortality studies are of littlevalue. CocHxNE’s claim that category A does notshorten or seriously impair life 11 conflicts with a

great deal of clinical experience, and has beencriticised on methodological grounds.12Miners have a 56% excess mortality from bron-

chitis.13 The inhalation of dusts is one of the manycauses of mucus hypersecretion-the initiatingchange in chronic bronchitis-but the MedicalResearch Council’s subcommittee on the relationbetween occupation and bronchitis 14 concluded thatcoal dust is uniquely lacking in this effect. The

capacity of coal dust to do good, or at least not to

7. Lawrence, J. S., Aitken-Swan, J. Br. J. ind. Med. 1952, 9, 1.8. Heron, A., Braithwaite, D. ibid. 1953, 10, 27.9. Lyons, J. P., Ryder, R., Campbell, H., Gough, J. Br. med. J. 1972,

i, 713.10. Rasmussen, D. L., Nelson, C. W. Am. Rev. resp. Dis. 1971, 103, 240.11. Cochrane, A. L. Br. med. J. 1973, iii, 532.12. Curry, B. ibid. p. 633.13. Registrar General’s Decennial Supplement, England & Wales, 1961;

Occupational Mortality Tables. H.M. Stationery Office, 1971.14. Br. med. J. 1966, i, 101.

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do harm, has been asserted many times by expertsat a safe distance from the coalface; and betweenthe wars, when the introduction of mechanisationwithout dust control created gross disease on a mass

scale, the complacency of experts, including theMedical Research Council’s committees, delayedeffective dust suppression for a whole generation.15It has even been suggested that the miners’ 20%deficit in deaths from lung cancer can be attributedto a protective effect of coal dust, rather than toreduced cigarette smoking 16; the latter interpreta-tion would, of course, increase the occupationalfactor in miners’ bronchitis. Particularly importantis GouGH’s hypothesis that there may be an inverserelation between bronchitis and retained dust in the

lungs, the dust being removed by mucus hyper-secretion which in susceptible subjects it has induced;those without bronchitis would thus be more prone to

pneumoconiosis.17 All particle sizes would be import-ant in this respect (not only those below 2 micronsthat enter the alveoli, which are the only ones mea-sured by the existing techniques of dust sampling).There is overwhelming evidence that coal mining

still uses up men and discards them to an exceptionalextent. And there are still anomalies in compensationthat should be put right-in respect, particularly, ofdisability from bronchitis, of social disabilities in

colliery districts, and of planned alternative workfor the middle-aged. Action here, as Dr FREEMANsuggests, might be a way out of the deadlock. Butof course it would be a short-term answer only. Theminers are not, in fact, asking for special treatment;and they might agree that lower-paid workers-hos-pital auxiliaries, for instance-have an even better casefor a high award. High wages have not been to blamefor the leaping costs of food and housing.

Hepatitis VirusesEVER since the discovery of the association of

Australia antigen, or HBAg, with serum or B-typehepatitis there has been hope that there wouldbe a similar advance with hepatitis A. Work with

HBAg led to rapid advances in knowledge of serumhepatitis: carriage of antigen can be detected easilyand accurately with passive hasmagglutination or

radioimmunometric assay.l8 The virus is almost

certainly the 42 nm. particle described by DANE etal. 19; and this particle contains an inner structurewhich looks like a picornavirus-the so-called core,clearly identified and shown to be serologicallydistinct from the HBAg by ALMEIDA et a1.20 So farefforts at growing the virus have been unsuccessful,although it can be transmitted to chimpanzees 21; but

15. Meicklejohn, A. Br. J. ind. Med. 1954, 11, 198.16. Ashley, D. J. B. Br. J. Cancer, 1967, 21, 243.17. Gough, J. Industr. Med. Surg. 1960, 29, 283.18. Reesink, H. W., Duimel, W. J., Brummelhuis, H. G. J. Lancet,

1973, ii, 135.19. Dane, A. S., Cameron, C. H., Briggs, M. ibid. 1970, i, 659.20. Almeida, J. A., Rubenstein, D., Stott, E. J. ibid. 1971, ii, 1225.21. Barker, L. W., et al. J. infect. Dis. 1972, 127, 648.

serum hepatitis can be spread orally as well as

parenterally, 22, 23 and this week’s report by Dr HEATH-COTE and her colleagues of HBAg in saliva and semenis a further clue to the mode of spread. Theseworkers used a particularly sensitive and accurate

radioimmunoassay technique, and they confirmed thespecificity of the results by subsequently subtypingthe positive samples.The realisation that hepatitis B associated with

HBAg is a not uncommon cause of jaundice evenwhen there is no history of contact with blood

products (for example, in a survey of 681 patients5% had no such history 24), and the evidence forspread by other than parenteral routes, have ledsome workers to doubt the distinction between serumand infectious hepatitis. But clinical evidencefavours the distinction 25 and immunological evidencesolidly supports it. Thus hepatitis A or MS1

protects against reinfection with the same virus, andnormal pools of human gamma-globulin protectagainst hepatitis A; hepatitis B or MS2 can be

produced in volunteers who have previously hadhepatitis A virus. Similarly, hepatitis B protectsagainst itself but not against hepatitis A.

Efforts to identify hepatitis A and to grow it havemet with little success. The virus seems to betransmissible to marmosets, but the work is verydifficult to carry out and to control and -is of moretheoretical interest than of practical application. 26,27There is clear evidence that virus must be present instools and that antibodies are present in convalescentserum, and FERRis and his colleagues 28 havedescribed antigen in faeces. Now from the N.I.H.comes new evidence for the existence of virus instools. FEINSTONE et al.,29 using immune electronmicroscopy,30 have identified a virus in the stools ofpatients with hepatitis A. These investigators hadMS1 hepatitis-A pools and acute and convalescentsera, and in coded studies they identified a 27 nm.virus, morphologically of the picornavirus family.Antibodies to the virus appeared in all of 6 patientswho had had experimental MS1 hepatitis and in 6out of 6 patients with natural hepatitis-A infections.2 patients with hepatitis-B-virus infections and 2with experimental non-bacterial enteritis discoveredby similar techniques 31 had no antibody to the

hepatitis-A virus. The virus was not antigenicallyrelated to HBAg nor to the core of the Dane particle.These new findings should be capable of speedy22. Krugman, S., Giles, J. P. J. Am. med. Ass. 1970, 212, 1019.23. Goldby, S. Lancet, 1971, i, 749.24. Public Health Laboratory Service. Br. med. J. 1973, iv, 746.25. Lancet, 1973, ii, 1007.26. Deinhardt, F., Holmes, A. W., Capps, R. B., Popper, H. J. exp.

Med. 1967, 125, 673.27. Provost, P. J., Hensohn, O. L., Villarejos, V. M., Arguedas, J. A.,

Hilleman, M. R. Proc. Soc. exp. Biol. Med. 1973, 142, 1257.28. Cross, G. F., Waugh, M., Ferris, A. A., Gust, P. D., Kaldor, J.

Austr. J. exp. Biol. med. Sci. 1971, 49, 1.29. Feinstone, S. M., Kapikian, A. Z., Purcell, R. H. Science, 1973,

182, 1026.30. Almeida, J. D., Waterson, A. P. Adv. Virus Res. 1969, 15, 307.31. Kapikian, A. Z., Wyatt, R. G., Dolin, R., Thornhill, T. S., Kalica,

A. K., Chanock, R. M. J. Virol. 1972, 10, 1075.