pathways mediating the diving reflex may evoke serious fatal arrhythmias, 10. 11 and there is ample evidence that in certain circumstances the manoeuvre can also be dangerous in normal individuals. 12,13

SIR,-We apologise for

any ambiguity which may have omission of the word "annual" in the senthrough tence referring to risk of leukxmia in the latter part of our paper (May 13, p. 1032). However, throughout the rest of the paper it was made clear that we were speaking solely of annual risk. We agree entirely with Professor Lindop’s calculations (May 27, p. 1155) and draw her attention to table ti(A) of our paper which clearly shows that the risk of radiation-induced leukasmia can be an appreciable proportion of the natural risk of this disease. Our paper was, as indicated, an abridged version of one presented at the International Symposium on the Late Biological Effects of Radiation held in Vienna in March, 1978. The complete version will be published in the proceedings of the symposium ; it contains a detailed discussion on the risk of radiation-induced leukaemia in relation to the naturally occurring risk. Up to age 75 a man’s total risk of death from malignant dis ease is about 1 in 4, his natural risk of fatal leukaemia being, as Lindop points out, about 1 in 200. Also, as Lindop suggests, the risk ofleuka*mia incurred as a result of exposure to 10 mSv per year from age 20 to age 65 is about one-seventh of the natural risk. This relatively large increase is a reflection of the low natural incidence of the disease; the point we are making is that the absolute risk of leuka:mia, both naturally occurring and radiation induced, is small. The total mortality risk from any malignancy incurred as a result of such an irradiation history is about 1 in 370, just over 1% of the total natural risk. These calculations are made once again on the basis of I.C.R.P. risk factors and the risk-time relationship used pre-





Department of Diagnostic Radiology, Hammersmith Hospital,




SiR,-Two papers in The Lancet have brought to attention the bile-salt binding property of aluminium hydroxide and demonstrated its efficacy in the treatment of cholereic’ and pl-st-vagotomy2 diarrhoea. However, bile salts and their metabolites have long been implicated as carcinogens or cocarcinogens in human colon cancer,3.4 and the finding of higher fascal bile acid levels in colon cancer patients than in patients with other intestinal diseases, provides clinical support for this contention.s There is, therefore, the theoretical possibility that aluminium hydroxide, by increasing the delivery of bile salts to the large intestine, may indirectly promote cancer of the colon. In rats, bile salts promote experimental colon cancer.6 Cholestyramine, a bile-salt-binding agent, promotes colon tumours induced in rats by dimethylhydrazine (D.M.H.)’ and, because in-vitro studies have now shown aluminium hydroxide to have bile-salt binding properties comparable to those of cholestyramine,8 we decided to test the prediction that aluminium hydroxide would similarly promote D.M.H.-induced colon cancer.

groups of 10 Wistar rats we gave 20 weekly subcuinjections of D.M.H. (20 mg/kg) with or without weekly gastric instillation of ’Aludrox’ at a dose equivalent to 5 ml for an adult human (i.e., 22 mg/kg). A further 10 rats were given saline injections and instillations. Animals deemed terminal9 To

viously. We thank Professor table i of our paper.


London W12 0HS



Lindop for pointing out

Nuclear Health and Safety Department and Berkeley Nuclear Laboratories, Central Electricity Generating Board, London EC4P 4EB




killed and examined at necropsy. weeks of observation 6 animals receiving D.M.H. plus aludrox were dead compared with 1 animal receiving All the control animals were carcinogen alone (r

Paroxysmal atrial tachycardia and the diving reflex.

1261 pathways mediating the diving reflex may evoke serious fatal arrhythmias, 10. 11 and there is ample evidence that in certain circumstances the m...
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