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Erythropoietin production during flights with pressurised aircrafts
THE LANCET 1 2 3
James PB. Jet “leg”, pulmonary embolism, and hypoxia. Lancet 1996; 347: 1697. Tardy B, Page Y, Zeni F, et al. Thrombosis in land travellers. Presse Med 1993; 22: 811–14. Nicholson AN. Low humidity: dehydration, dipsosia or just dryness? RAF School of Aviation Medicine Report no 01/96. Farnborough, May, 1996.
SIR—James1 emphasises the importance of hypoxia as a risk factor for older passengers engaged in long-haul air travel. A cabin altitude of 8000 ft (2438 m), which is equivalent to a cabin ambient pressure of 75·8 kPa, is regarded as the maximum acceptable cabin altitude of modern airliners cruising at altitudes up to 43 000 ft (13 106 m). We have measured oxygen saturation of haemoglobin (SaO2; ear pulse-oximetry) in 15 resting healthy individuals seated in a hypobaric chamber with an inside ambient pressure of 75·8 kPa. Mean SaO2 was 90% (SD 1·9; range 85–93) after 30 min of exposure.2 There is considerable interindividual variation in the responses to a lowered partial O2 pressure. Responses to hypoxic hypoxia include an increase in pulmonary ventilation, which is evident even at 6600 ft (2012 m).3 However, immobility, cramped seating conditions, and drowsiness might hinder proper respiratory activities. Moreover, the lower ambient pressure in the cabin leads to gastrointestinal distension, which might limit downward movements of the diaphragm. In those who were dozing off in our hypobaric chamber we found much lower SaO2 levels (80%) at cabin altitudes of 8000 ft (2438 m). when they were stimulated to respire properly, SaO2 levels increased substantially. Therefore, if airlines’ advice on routine in-flight exercise were also to address proper pulmonary ventilation, both important hypoxia and venous thrombosis might be prevented. For older people, these exercises should not be too strenuous, because strenuous activities might lower their SaO2 even further. Airlines’ advice should also include recommendations on adequate fluid intake, because the low relative humidity in the cabin could lead to dehydration. The cabin relative humidity from outside fresh air is less than 1%. Moisture from passengers and crew will cause it to increase, depending on the passenger load factor, ventilation rate, temperature, and pressure. During 16 long-haul flights (Boeing 747–400) we found cabin values ranged between 7 and 14% (mean 10%), which is in accord with studies in other types of aircraft,4 We undertook a pilot study, in which six healthy people were exposed for 8 h to a simulated altitude of 8000 ft and relative humidity of 8–10% and were instructed to drink 2 L in that time. Compared with the control condition (sea level; relative humidity 30–40%), we found an increase of mean plasma osmolality, mean urine osmolality, and urine specific gravity, indicating dehydration. Because dehydration is a risk factor in long-haul air travel, airlines should instruct passengers to take adequate fluids, while avoiding alcohol (diuretic action, cellular dehydration, drowsiness) and carbonated beverages (gastrointestinal distension). *Ries Simons, Jan Krol Netherlands Aerospace Medical Centre, PO Box 22, 3769 AZ Soesterberg, Netherlands
1 2 3
4
James PB. Jet “leg”, pulmonary embolism, and hypoxia. Lancet 1996; 347: 1697 Harinck E, Hutter PA, Hoorntje TM, et al. Air travel in adults with cyanotic congenital heart disease. Circulation 1996; 93: 272–76. Lagica P, Koller EA. Respiratory, circulatory, and ECG changes during acute exposure to high altitude. J Appl Physiol 1976; 41: 159–67. Hawkins FH. Human factors in flight. Aldershot: Gower Technical Press, 1987: 286.
416
Erythropoietin production during flights with pressurised aircrafts SIR—Erythropoietin (EPO) production and release from the renal cortex is regulated by the relative amount of oxygen available to the tissues involved in its production.1 For medical and technical reasons, pressurised aircraft usually maintain cabin pressure equivalent to altitudes at or below 8000 ft (2438 m) which results, in healthy people, in an arterial oxygen saturation of at least 90%.2 Since it is known from studies in the Alps that EPO concentrations increase at an altitude of 2300 m,3 we investigated the influence of prolonged flight at a cabin pressure equivalent to 2438 m altitude on serum concentrations of EPO. Seven men (mean age 33·4, SD 3·4, years) were studied during a routine military flight lasting 8 h. Blood samples were taken 2 h before, during (1, 4, and 7 h after take-off), and 8 h after landing. Serum was analysed for EPO by ELISA (IBL, Hamburg, Germany). At baseline before take-off, crew members had normal EPO concentrations for sedentary men (10·4 [SD 4·4] mU/mL), which increased significantly during the flight (1 h 12·4 [3·6] mU/mL, p<0·086; 4 h, 15·2 [3·7] mU/mL, p<0·005; 7 h 23·1 [7·3] mU/mL, p<0·026); and returned to baseline values 8 h after landing (15·0 [10·3] mU/mL, p<0·140). The reduced cabin pressure inside aircraft leads to an increase in EPO concentrations during long-distance flights. It is not known whether this has long-term effects on erythropoiesis in flight crews or frequent travellers who are exposed to this type of intermittent hypoxic stress. This research was supported by grant No 50 WB 9377 from the Bundesministerium für Bildung, Wissenschaft, Forschung und Technologie (BMBF), Deutsche Agentur für Raumfahrtangelegenheiten.
*Hanns-Christian Gunga, Michael Frommhold, Wulf Hildebrandt, Karl Kirsch, Lothar Röcker *Department of Physiology, Benjamin Franklin Medical Centre, Free University of Berlin, Germany; Sporthochschule Köln, Physiologisches Institut, Köln; E-3a Component, NATO Airbase, Geilenkirchen; and Institut für Sport und Leistungsmedizin, Heidelberg
1 2 3
Jelkmann W. Erythropoietin: structure, control of production, and function. Physiol Rev 1992; 72: 449–89. Auerbach PS, ed. Wilderness medicine. St Louis: Mosby, 1995. Gunga H-C, Kirsch K, Röcker L, et al. Time course of erythropoietin, triiodothyronine, thyroxine, and thyroid-stimulating hormone at 2315 m. J Appl Physiol 1994; 73: 1068–72.
DEPARTMENT OF ERROR Manganese toxicity and parenteral nutrition—In the final paragraph of this letter by Beath and colleagues (June 22, p 1773–74), the third sentence should have read “We support the recommendation that plasma concentrations of manganese should be monitored . . .” Effect of d-sotalol on mortality in patients with left ventricular dysfunction after recent and remote myocardial infarction—In this article by Waldo and colleagues (July 6, p 7), the incidence of torsade de pointes under the placebo column in table 3 should read 0 (0), not 2 (2). In Figure 2, LVEP should read LVEF, the unit following QTc should be millisecond, and under relative risk, the second vertical line (corresponding to effect of drug on mortality in full sample) should have appeared dashed, rather than solid. Fall-related factors and risk of hip fracture: the EPIDOS prospective study —In this article (July 20, p 145) the following acknowledgment was omitted: EPIDOS study was supported by INSERM-MSD-Chibret. Comparison of non-chlorofluorocarbon-containing salbutamol and conventional inhaler—In this letter by Desager and colleagues (July 20, p 200), 44 patients were randomly allocated to receive either chlorofluorocarbon-containing (CFC) salbutamol or CFC-free salbutamol.
Vol 348 • August 10, 1996
James PB. Jet “leg”, pulmonary embolism, and hypoxia. Lancet 1996; 347: 1697. Tardy B, Page Y, Zeni F, et al. Thrombosis in land travellers. Presse Med 1993; 22: 811–14. Nicholson AN. Low humidity: dehydration, dipsosia or just dryness? RAF School of Aviation Medicine Report no 01/96. Farnborough, May, 1996.
SIR—James1 emphasises the importance of hypoxia as a risk factor for older passengers engaged in long-haul air travel. A cabin altitude of 8000 ft (2438 m), which is equivalent to a cabin ambient pressure of 75·8 kPa, is regarded as the maximum acceptable cabin altitude of modern airliners cruising at altitudes up to 43 000 ft (13 106 m). We have measured oxygen saturation of haemoglobin (SaO2; ear pulse-oximetry) in 15 resting healthy individuals seated in a hypobaric chamber with an inside ambient pressure of 75·8 kPa. Mean SaO2 was 90% (SD 1·9; range 85–93) after 30 min of exposure.2 There is considerable interindividual variation in the responses to a lowered partial O2 pressure. Responses to hypoxic hypoxia include an increase in pulmonary ventilation, which is evident even at 6600 ft (2012 m).3 However, immobility, cramped seating conditions, and drowsiness might hinder proper respiratory activities. Moreover, the lower ambient pressure in the cabin leads to gastrointestinal distension, which might limit downward movements of the diaphragm. In those who were dozing off in our hypobaric chamber we found much lower SaO2 levels (80%) at cabin altitudes of 8000 ft (2438 m). when they were stimulated to respire properly, SaO2 levels increased substantially. Therefore, if airlines’ advice on routine in-flight exercise were also to address proper pulmonary ventilation, both important hypoxia and venous thrombosis might be prevented. For older people, these exercises should not be too strenuous, because strenuous activities might lower their SaO2 even further. Airlines’ advice should also include recommendations on adequate fluid intake, because the low relative humidity in the cabin could lead to dehydration. The cabin relative humidity from outside fresh air is less than 1%. Moisture from passengers and crew will cause it to increase, depending on the passenger load factor, ventilation rate, temperature, and pressure. During 16 long-haul flights (Boeing 747–400) we found cabin values ranged between 7 and 14% (mean 10%), which is in accord with studies in other types of aircraft,4 We undertook a pilot study, in which six healthy people were exposed for 8 h to a simulated altitude of 8000 ft and relative humidity of 8–10% and were instructed to drink 2 L in that time. Compared with the control condition (sea level; relative humidity 30–40%), we found an increase of mean plasma osmolality, mean urine osmolality, and urine specific gravity, indicating dehydration. Because dehydration is a risk factor in long-haul air travel, airlines should instruct passengers to take adequate fluids, while avoiding alcohol (diuretic action, cellular dehydration, drowsiness) and carbonated beverages (gastrointestinal distension). *Ries Simons, Jan Krol Netherlands Aerospace Medical Centre, PO Box 22, 3769 AZ Soesterberg, Netherlands
1 2 3
4
James PB. Jet “leg”, pulmonary embolism, and hypoxia. Lancet 1996; 347: 1697 Harinck E, Hutter PA, Hoorntje TM, et al. Air travel in adults with cyanotic congenital heart disease. Circulation 1996; 93: 272–76. Lagica P, Koller EA. Respiratory, circulatory, and ECG changes during acute exposure to high altitude. J Appl Physiol 1976; 41: 159–67. Hawkins FH. Human factors in flight. Aldershot: Gower Technical Press, 1987: 286.
416
Erythropoietin production during flights with pressurised aircrafts SIR—Erythropoietin (EPO) production and release from the renal cortex is regulated by the relative amount of oxygen available to the tissues involved in its production.1 For medical and technical reasons, pressurised aircraft usually maintain cabin pressure equivalent to altitudes at or below 8000 ft (2438 m) which results, in healthy people, in an arterial oxygen saturation of at least 90%.2 Since it is known from studies in the Alps that EPO concentrations increase at an altitude of 2300 m,3 we investigated the influence of prolonged flight at a cabin pressure equivalent to 2438 m altitude on serum concentrations of EPO. Seven men (mean age 33·4, SD 3·4, years) were studied during a routine military flight lasting 8 h. Blood samples were taken 2 h before, during (1, 4, and 7 h after take-off), and 8 h after landing. Serum was analysed for EPO by ELISA (IBL, Hamburg, Germany). At baseline before take-off, crew members had normal EPO concentrations for sedentary men (10·4 [SD 4·4] mU/mL), which increased significantly during the flight (1 h 12·4 [3·6] mU/mL, p<0·086; 4 h, 15·2 [3·7] mU/mL, p<0·005; 7 h 23·1 [7·3] mU/mL, p<0·026); and returned to baseline values 8 h after landing (15·0 [10·3] mU/mL, p<0·140). The reduced cabin pressure inside aircraft leads to an increase in EPO concentrations during long-distance flights. It is not known whether this has long-term effects on erythropoiesis in flight crews or frequent travellers who are exposed to this type of intermittent hypoxic stress. This research was supported by grant No 50 WB 9377 from the Bundesministerium für Bildung, Wissenschaft, Forschung und Technologie (BMBF), Deutsche Agentur für Raumfahrtangelegenheiten.
*Hanns-Christian Gunga, Michael Frommhold, Wulf Hildebrandt, Karl Kirsch, Lothar Röcker *Department of Physiology, Benjamin Franklin Medical Centre, Free University of Berlin, Germany; Sporthochschule Köln, Physiologisches Institut, Köln; E-3a Component, NATO Airbase, Geilenkirchen; and Institut für Sport und Leistungsmedizin, Heidelberg
1 2 3
Jelkmann W. Erythropoietin: structure, control of production, and function. Physiol Rev 1992; 72: 449–89. Auerbach PS, ed. Wilderness medicine. St Louis: Mosby, 1995. Gunga H-C, Kirsch K, Röcker L, et al. Time course of erythropoietin, triiodothyronine, thyroxine, and thyroid-stimulating hormone at 2315 m. J Appl Physiol 1994; 73: 1068–72.
DEPARTMENT OF ERROR Manganese toxicity and parenteral nutrition—In the final paragraph of this letter by Beath and colleagues (June 22, p 1773–74), the third sentence should have read “We support the recommendation that plasma concentrations of manganese should be monitored . . .” Effect of d-sotalol on mortality in patients with left ventricular dysfunction after recent and remote myocardial infarction—In this article by Waldo and colleagues (July 6, p 7), the incidence of torsade de pointes under the placebo column in table 3 should read 0 (0), not 2 (2). In Figure 2, LVEP should read LVEF, the unit following QTc should be millisecond, and under relative risk, the second vertical line (corresponding to effect of drug on mortality in full sample) should have appeared dashed, rather than solid. Fall-related factors and risk of hip fracture: the EPIDOS prospective study —In this article (July 20, p 145) the following acknowledgment was omitted: EPIDOS study was supported by INSERM-MSD-Chibret. Comparison of non-chlorofluorocarbon-containing salbutamol and conventional inhaler—In this letter by Desager and colleagues (July 20, p 200), 44 patients were randomly allocated to receive either chlorofluorocarbon-containing (CFC) salbutamol or CFC-free salbutamol.
Vol 348 • August 10, 1996