CIGARETTE-SMOKING AND CADMIUM

CIGARETTE-SMOKING AND CADMIUM

491 seem to depend on the disintegration of tablets. Adherence to drug control is emphasised. Not only must the active ingredient be carefully assayed...

164KB Sizes 2 Downloads 264 Views

491 seem to depend on the disintegration of tablets. Adherence to drug control is emphasised. Not only must the active ingredient be carefully assayed but also the entire pharmaceutical preparation. Changing the pharmaceutical properties, and thereby also perhaps the biological availability, of the present preparations without notifying the

differences in bioavailability

some

TREATMENT AFTER EXPOSURE TO COLD

rate of the

physicians

may be hazardous.

Wihuri Research Institute, Helsinki 14, and

Department of Medicine, University of Helsinki, Helsinki 29, Finland.

First

VESA MANNINEN

JOHN MELIN PENTTI REISSEL.

CIGARETTE-SMOKING AND CADMIUM SIR,-We read with great interest the finding by Dr. Lewis and his colleagues (Feb. 5, p. 291) that cadmium accumulates in human tissues with increasing age and cigarette-smokers accumulate more cadmium in their organs than non-smokers.

Leucocyte and plasma ascorbic-acid concentrations decrease with increasing age.1 Leucocyte and plasma ascorbic-acid concentrations are consistently lower in cigarette-smokers than non-smokers.2,3The reason for the lower tissue-ascorbic-acid of smokers is unknown. Smoking is associated with atherosclerosis4 and is a risk factor in the development of coronary heart-disease.5 Ascorbic acid is 6 necessary for the mobilisation of cholesterol and is implicated in the pathogenesis of atherosclerosis in manand in animals.S The accumulation of cadmium in organs and the severe anxmia associated with cadmium toxicity are prevented by dietary ascorbic-acid supplements.9 The accumulation of cadmium increases with age and cigarette-smoking. This is associated with a decrease in tissue-ascorbic-acid conIt is possible that the low ascorbic-acid centrations. concentrations of smokers is related to the need of the vitamin to detoxify the accumulation of cadmium from

cigarette-smoking. The leucocyte-counts

are higher in smokers than in non-smokers. 10-12 The ascorbic-acid concentration in leucocytes is inversely proportional to the total leucocytecount. 13 It might therefore be suggested that the low ascorbic-acid concentrations in smokers are due to leucocytosis. This is unlikely, since the leucocyte-ascorbic-acid concentration is a measure of the availability of the vitamin for storage and does not reflect tissue utilisation of the vitamin.14 In smokers, both the leucocyte and plasma ascorbic-acid concentrations are low, indicating that tissueascorbic-acid is low. Smokers given ascorbic-acid supplements excrete 40% less ascorbic acid than non-smokers, indicating a greater metabolic demand for the vitamin in smokers. 15

Department of Pharmacology, University of Dublin, Trinity College, Dublin 2. 1. 2. 3. 4. 5.

H. S. LOH C. W. M. WILSON.

Loh, H. S., Wilson, C. W. M. Int. J. Vit. Nutr. Res. 1971, 41, 259. Pelletier, O. Am. J. clin. Nutr. 1968, 21, 1259. Brook, M., Grimshaw, J. J. ibid. p. 1254. Kershbaum, A., Bellet, S. Geriatrics, 1966, 21, 155. Smoking and Health Now: A report of the Royal College of Physicians. London, 1971. 6. Spittle, C. R. Lancet, 1971, ii, 1280. 7. Schaffer, C. F. Am. J. clin. Nutr. 1970, 23, 27. 8. Ginter, E., Bobek, P., Babala, J., Barbierikova, E. Cor Vasa, 1969, 11, 65. 9. Spivey Fox, M. R., Fry, B. E. Science, 1970, 169, 989. 10. Howell, R. W. Lancet, 1970, ii, 152. 11. Corne, F., Lellouch, J., Schwartz, D. ibid. 1971, ii, 632. 12. Banks, D. C. ibid. p. 815. 13. Loh, H. S., Wilson, C. W. M. Int. J. Vit. Nutr. Res. 1971, 41, 253. 14. Loh, H. S., Wilson, C. W. M. Br. med. J. 1971, iii, 733. 15. Pelletier, O. Am. J. clin. Nutr. 1970, 23, 520.

SIR,-Your editorial (Jan. 29, 1972)

hypothermia contained leading.

some

on severe

comments

which

accidental are mis-

reported by Niazi and Lewis1 was revived by simple rewarming is not borne out by the case-report. The first heat was supplied by wet packs at 45 °C applied over the chest-i.e., near the heart. Once the heart resumed beating, active rewarming was continued by wrapping the whole body in wet packs, and once the core temperature had reached 20 °C active rewarming was continued in a bath at 45 °C. Throughout cooling and rewarming intermittent positive-pressure ventilation was The statement that the

case

used.

Though immersion of a hypothermic patient in a bath 45 °C is undoubtedly the most rapid method of rewarming, it has disadvantages in that it is unsuitable in the presence of major injuries, effective cardiorespiratory resuscitation cannot be performed, and there is a risk in the manhandling involved since there is a serious danger of cardiac arrest or cerebral hypoxia if the patient is moved awkwardly.2 Also, there is the problem of maintaining the airway of an unconscious patient while in the bath. Endotracheal intubation would be an answer and I have intubated patients down to 25-5°C under electrocardiographic monitoring without causing any arrhythmia. Any bradycardia is mediated via the vagus, and this should be blocked by intravenous atropine as is used for intubation at normothermia. At normothermia hypoxia aggravates arrhythmias due to intubation, and inflation with oxygen is recommended before passage of the endotracheal tube.3 All the hypothermic patients I have intubated have been breathing 100 % oxygen for some minutes before intubation, and this may be the reason why arrhythmias have not been a problem. If ventricular fibrillation does supervene, the experience of Linton and Ledingham 4 would suggest that electrical defibrillation is unlikely to be successful with a cardiac temperature below 28 °C, and mouth-to-mouth ventilation and efficient external cardiac massage might buy time until the cardiac temperature can be raised-e.g., during rapid transport to a hospital5 or while heating equipment is at

being prepared. 6 Though rapid rewarming after prolonged hypothermia may cause severe arterial hypotension in the spontaneously ventilating patient, the reason is still in doubt. The case reported by Talbott et al .7 died with profound circulatory collapse with cyanosis, respiration which was gasping and shallow, and an absence of pulses. They state that the mechanism of vasomotor collapse occurring during rewarming is different fron the mechanism in surgical or medical shock. Their conclusion is that: " In retrospect it is thought that sudden vasodilatation was responsible for the cardiovascular breakdown ". This conclusion is strange in view of the clinical features and post-mortem findings of congestion of the lungs. In rewarming hypothermic rabbits, oedema of the lungs associated with congestion and watery serous exudates in the tissues and air S passages was described by Walther as a terminal effect.8 These findings, as well as the clinical reports of acute pulmonary oedema developing during rewarming,9 would Niazi, S. A., Lewis, F. J. Ann. Surg. 1958, 147, 264. Freeman, J., Pugh, L. G. C. E. Int. Anesthesiol. clin. 1969, 7, 997. Lee, J. A. Synopsis of Anæsthesia. Bristol, 1959. Linton, A. L., Ledingham, I. McA. Lancet, 1966, i, 24. Krittingen, R. O., Naess, A. Br. med. J. 1963, i, 1315. Kügler-Podelleck, I., Rodewald, G., Horatz, K., Kuegler, S., Mueller-Brunotte P. Dt. med. Wschr. 1965, 90, 74. 7. Talbott, J. M., Consolazio, W. V., Percora, L. J. Archs intern. Med. 1941, 68, 1120. 8. Walther, A. Virchows Arch. path. Anat. Physiol. 1862, 25, 414. 9. Bloch, M. Br. med. J. 1967, i, 376.

1. 2. 3. 4. 5. 6.