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EFFECTS OF DIAGNOSTIC IRRADIATION
1003 altered ? " to account for the change of cellular composition. are
serum
and intra-
M.R.C. Tropical Metabolism Research Unit,
University College
of the West Indies, St. Mona, Andrew,
A. E. M. MCLEAN.
Jamaica.
EFFECTS OF DIAGNOSTIC IRRADIATION
SIR, The correspondence 1-4 since your leader5 has resulted in dropping the Harmful from the Effects of Diagnostic Irradiation ". No-one has contributed to this more than Dr. Alice Stewart, whose detailed studies have shown that the bulk of leukxmias cannot possibly be due to diagnostic radiology and that with the remainder it is only a possibility. There remains the genetic effect of radiation to cause anxiety in those requiring X-rays. The full genetic con"
"
"
sequence of X rays will not be manifested for thousands if not millions of years. It is therefore important to have a clear realisation of what these consequences will be. The effects of gene mutation can nowhere be better learnt than by studying the principal display in the main hall of the British Museum (Natural History), South Kensington, London. Here we learn any given gene mutates in about one in half a million individuals ".s Radiation, however, is not the only cause of gene mutation. "
"
Background radiation, the total is roughly O-lr per annum or about 3 per generation ",’ causes less than one-tenth of the number of naturally occurring gene mutations which require "between 30r and 80r".8 Background radiation therefore causes any given gene to mutate in about 1 in 5,000,000 individuals.
SPINAL-CORD DAMAGE FROM HYPEREXTENSION INJURIES IN CERVICAL SPONDYLOSIS SiR,—The association of cervical injury with rupture of the intervertebral disc was described 100 years ago,1
and that this is a common cause of spinal-cord damage in extension injury of the neck is well established. 2-6 Although it is true that this sort of injury is most often seen in the middle-aged and elderly, it is by no means exclusive to them, and it is found in young people who have had similar accidents. The spinal cord is at greater risk in the elderly, particularly in neck extension, because cervical spondylosis which narrows the spinal canal is more common in them. This has been described in many papers.5 7-11 Extension injuries are commoner in older people, because the elderly tumble more frequently, and it is doubtful if any of the three patients described by Dr. Hughes and Dr. Brownell (March 30) would have sustained their injury had they not been elderly and liable to fall. An injury to the neck in flexion must be forceful to cause spinal cord damage.2 12 In the nature of things young people tend to be involved in violent accidents, but they also may sustain severe cord damage due to extension of the neck in accidents of apparently trivial violence.7 13 14
Cervical spondylosis is only one element in the causation of cord damage from extension of the neck. The cord in the hyperextended neck is vulnerable at any age, and it is failure to realise this and that bony change may be absent or, if present, slight that leads to the misdiagnosis and of traumatic tetraplegia, and that caused mismanagement " me to state 1-4 the facility with which severe cervical-cord trauma may be sustained is only surpassed by the ease with which such damase can be overlooked ". Department of Neurology,
Pinderfields General Hospital, Wakefield.
only 14% of background radiation.The chance of diagnostic radiology causing a gene to mutate is therefore 1 in 35,000,000. If the birth-rate in Diagnostic radiology
Great Britain remains around 700,000 births per year, the probability that 1 baby will be born with such a mutation due to diagnostic radiology is once in fifty years. One baby in Great Britain each fifty years is, however, the effect on one gene only. As there are many genes the effect must be multiplied many times. No matter how much we multiply, however, the contribution of diagnostic radiology will not exceed 14% of the contribution of naturally occurring background radiation, or about 1 % of all gene mutations. It is known that the Atomic Bomb Casualty Commission " has found no evidence of genetic damage in the offspring of Japanese parents exposed to atomic radiation, even among those heavily irradiated ", and 1 mutated baby per gene every 50 years may not be considered very many, but can one tell what effect this will have if we are sufficiently lavish with time? Fortunately nature has made a grand experiment for us which gives us the answer. In different parts of Great Britain background radiation differs by 20%.10 In different parts of the world background radiation differs by 400%. This difference has been present since before life began without any detected detrimental influence to the population." The possibility of the 14% contribution of diagnostic radiology having an effect which may be called harmful is therefore most
unlikely.
Royal Infirmary, Edinburgh.
J. B. COOK.
amounts to
DAVID W. LINDSAY.
1. Burch, P. R. J. Lancet, Feb. 23, 1963, p. 441. 2. Lindsay, D. W. ibid. March 16, 1963, p. 602. 3. Rabinowitch, J. ibid. p. 603. 4. Stewart, A. ibid. March 30, 1963, p. 718. 5. Lancet, Feb. 2, 1963, p. 255. 6. British Museum (Natural History), London. Evolution; p. 15. 7. Hazard to Man of Nuclear and Allied Radiations; p. 45. H.M. Stationery Office, 1956. 8. ibid. p. 50. 9. Radiological Hazards to Patients; p. 84. H.M. Stationery Office, 1960. 10. Ross, S. E. J. Amer. med. Ass. 1963, 183, 721. 11. Brit. med. J. 1962, ii, 716.
EFFECT OF THALIDOMIDE ON SKIN-GRAFT SURVIVAL
SiR,—Two recent communications15 16 have pointed out similarity of action of tuberculin and of phytohæmagglutinin (P.H.A.) on cultures of human lymphocytes in
the
mitosis and transformation to large basophilic at a parallel with the cellular immune in vivo. response Among the substances that have been shown to inhibit the transformation caused by P.H.A. are prednisolone17 and thalidomide, 18 both of which produce some effect in concentrations comparable to those in the blood after an ordinary therapeutic dose. Since prednisolone is also known to delay the rejection of skin homografts and suppress the formation of large basophilic and pyroninophilic cells in the regional lymph-nodes,19 it was thought worth while to test thalidomide for this property.
inducing
cells, and hinted
Fifteen adult CBA female mice were given thalidomide 40 mg. daily (2000 mg. per kg.) orally in arachis oil for 35 days. 1. Butcher, R. G. H. Dublin J. med. Sci. 1853, 15, 383. 2. Barnes, R. J. Bone Jt Surg. 1948, 30B, 234. 3. Taylor, A. R., Blackwood, W. ibid. p. 245. 4. Kaplan, C. J. ibid. 1953, 35B, 97. 5. Birkin, C. R., Hirson, C. ibid. 1954, 36B, 57. 6. Cook, J. B. Proc. R. Soc. Med. 1959, 52, 799. 7. Symonds, C. Lancet, 1953, i, 451. 8. Crooks, F., Birkett, A. M. Brit. J. Surg. 1943, 31, 252. 9. Alexander, E., Davis, C. H., Field, C. H. Arch. Neurol. Psychiat. 1958, 79, 146. 10. Payne, E. E., Spillane, J. D. Brain, 1957, 80, 571. 11. Taylor, A. R. J. Bone Jt Surg. 1951, 33B, 543. 12. Jefferson, G. Brit. med. J. 1936, ii, 1126. 13. Wilson, P. D., Cochrane, W. A. Fractures and Dislocations. London, 1925.
Cook, J. B. in Scientific Aspects of Neurology (edited by H. G. Garland); p. 764. London, 1961. 15. Pearmain, G., Lycette, R. R., Fitzgerald, P. H. Lancet, March 23, 1963,
14.
p. 637.
16. 17. 18. 19.
Marshall, W. H., Roberts, K. B. ibid. April 6, 1963, p. 773. Nowell, P. C. Cancer Res. 1961, 21, 1518. Roath, S., Elves, M. W., Israels, M. C. G. Lancet, Feb. 2, 1963, p. 249. Scothorne, R. J. Ann. N.Y. Acad. Sci. 1957, 64, 1028.
serum
and intra-
M.R.C. Tropical Metabolism Research Unit,
University College
of the West Indies, St. Mona, Andrew,
A. E. M. MCLEAN.
Jamaica.
EFFECTS OF DIAGNOSTIC IRRADIATION
SIR, The correspondence 1-4 since your leader5 has resulted in dropping the Harmful from the Effects of Diagnostic Irradiation ". No-one has contributed to this more than Dr. Alice Stewart, whose detailed studies have shown that the bulk of leukxmias cannot possibly be due to diagnostic radiology and that with the remainder it is only a possibility. There remains the genetic effect of radiation to cause anxiety in those requiring X-rays. The full genetic con"
"
"
sequence of X rays will not be manifested for thousands if not millions of years. It is therefore important to have a clear realisation of what these consequences will be. The effects of gene mutation can nowhere be better learnt than by studying the principal display in the main hall of the British Museum (Natural History), South Kensington, London. Here we learn any given gene mutates in about one in half a million individuals ".s Radiation, however, is not the only cause of gene mutation. "
"
Background radiation, the total is roughly O-lr per annum or about 3 per generation ",’ causes less than one-tenth of the number of naturally occurring gene mutations which require "between 30r and 80r".8 Background radiation therefore causes any given gene to mutate in about 1 in 5,000,000 individuals.
SPINAL-CORD DAMAGE FROM HYPEREXTENSION INJURIES IN CERVICAL SPONDYLOSIS SiR,—The association of cervical injury with rupture of the intervertebral disc was described 100 years ago,1
and that this is a common cause of spinal-cord damage in extension injury of the neck is well established. 2-6 Although it is true that this sort of injury is most often seen in the middle-aged and elderly, it is by no means exclusive to them, and it is found in young people who have had similar accidents. The spinal cord is at greater risk in the elderly, particularly in neck extension, because cervical spondylosis which narrows the spinal canal is more common in them. This has been described in many papers.5 7-11 Extension injuries are commoner in older people, because the elderly tumble more frequently, and it is doubtful if any of the three patients described by Dr. Hughes and Dr. Brownell (March 30) would have sustained their injury had they not been elderly and liable to fall. An injury to the neck in flexion must be forceful to cause spinal cord damage.2 12 In the nature of things young people tend to be involved in violent accidents, but they also may sustain severe cord damage due to extension of the neck in accidents of apparently trivial violence.7 13 14
Cervical spondylosis is only one element in the causation of cord damage from extension of the neck. The cord in the hyperextended neck is vulnerable at any age, and it is failure to realise this and that bony change may be absent or, if present, slight that leads to the misdiagnosis and of traumatic tetraplegia, and that caused mismanagement " me to state 1-4 the facility with which severe cervical-cord trauma may be sustained is only surpassed by the ease with which such damase can be overlooked ". Department of Neurology,
Pinderfields General Hospital, Wakefield.
only 14% of background radiation.The chance of diagnostic radiology causing a gene to mutate is therefore 1 in 35,000,000. If the birth-rate in Diagnostic radiology
Great Britain remains around 700,000 births per year, the probability that 1 baby will be born with such a mutation due to diagnostic radiology is once in fifty years. One baby in Great Britain each fifty years is, however, the effect on one gene only. As there are many genes the effect must be multiplied many times. No matter how much we multiply, however, the contribution of diagnostic radiology will not exceed 14% of the contribution of naturally occurring background radiation, or about 1 % of all gene mutations. It is known that the Atomic Bomb Casualty Commission " has found no evidence of genetic damage in the offspring of Japanese parents exposed to atomic radiation, even among those heavily irradiated ", and 1 mutated baby per gene every 50 years may not be considered very many, but can one tell what effect this will have if we are sufficiently lavish with time? Fortunately nature has made a grand experiment for us which gives us the answer. In different parts of Great Britain background radiation differs by 20%.10 In different parts of the world background radiation differs by 400%. This difference has been present since before life began without any detected detrimental influence to the population." The possibility of the 14% contribution of diagnostic radiology having an effect which may be called harmful is therefore most
unlikely.
Royal Infirmary, Edinburgh.
J. B. COOK.
amounts to
DAVID W. LINDSAY.
1. Burch, P. R. J. Lancet, Feb. 23, 1963, p. 441. 2. Lindsay, D. W. ibid. March 16, 1963, p. 602. 3. Rabinowitch, J. ibid. p. 603. 4. Stewart, A. ibid. March 30, 1963, p. 718. 5. Lancet, Feb. 2, 1963, p. 255. 6. British Museum (Natural History), London. Evolution; p. 15. 7. Hazard to Man of Nuclear and Allied Radiations; p. 45. H.M. Stationery Office, 1956. 8. ibid. p. 50. 9. Radiological Hazards to Patients; p. 84. H.M. Stationery Office, 1960. 10. Ross, S. E. J. Amer. med. Ass. 1963, 183, 721. 11. Brit. med. J. 1962, ii, 716.
EFFECT OF THALIDOMIDE ON SKIN-GRAFT SURVIVAL
SiR,—Two recent communications15 16 have pointed out similarity of action of tuberculin and of phytohæmagglutinin (P.H.A.) on cultures of human lymphocytes in
the
mitosis and transformation to large basophilic at a parallel with the cellular immune in vivo. response Among the substances that have been shown to inhibit the transformation caused by P.H.A. are prednisolone17 and thalidomide, 18 both of which produce some effect in concentrations comparable to those in the blood after an ordinary therapeutic dose. Since prednisolone is also known to delay the rejection of skin homografts and suppress the formation of large basophilic and pyroninophilic cells in the regional lymph-nodes,19 it was thought worth while to test thalidomide for this property.
inducing
cells, and hinted
Fifteen adult CBA female mice were given thalidomide 40 mg. daily (2000 mg. per kg.) orally in arachis oil for 35 days. 1. Butcher, R. G. H. Dublin J. med. Sci. 1853, 15, 383. 2. Barnes, R. J. Bone Jt Surg. 1948, 30B, 234. 3. Taylor, A. R., Blackwood, W. ibid. p. 245. 4. Kaplan, C. J. ibid. 1953, 35B, 97. 5. Birkin, C. R., Hirson, C. ibid. 1954, 36B, 57. 6. Cook, J. B. Proc. R. Soc. Med. 1959, 52, 799. 7. Symonds, C. Lancet, 1953, i, 451. 8. Crooks, F., Birkett, A. M. Brit. J. Surg. 1943, 31, 252. 9. Alexander, E., Davis, C. H., Field, C. H. Arch. Neurol. Psychiat. 1958, 79, 146. 10. Payne, E. E., Spillane, J. D. Brain, 1957, 80, 571. 11. Taylor, A. R. J. Bone Jt Surg. 1951, 33B, 543. 12. Jefferson, G. Brit. med. J. 1936, ii, 1126. 13. Wilson, P. D., Cochrane, W. A. Fractures and Dislocations. London, 1925.
Cook, J. B. in Scientific Aspects of Neurology (edited by H. G. Garland); p. 764. London, 1961. 15. Pearmain, G., Lycette, R. R., Fitzgerald, P. H. Lancet, March 23, 1963,
14.
p. 637.
16. 17. 18. 19.
Marshall, W. H., Roberts, K. B. ibid. April 6, 1963, p. 773. Nowell, P. C. Cancer Res. 1961, 21, 1518. Roath, S., Elves, M. W., Israels, M. C. G. Lancet, Feb. 2, 1963, p. 249. Scothorne, R. J. Ann. N.Y. Acad. Sci. 1957, 64, 1028.