Supplementary oxygen and risk of childhood lymphatic leukaemia

Naumburg, Estelle; Bellocco, Rino; Cnattingius, Sven; Jonzon, Anders; Ekbom, Anders

doi:10.1080/08035250216105

Cited by 79 publications

(75 citation statements)

References 24 publications

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“…15%, in all animals. MAP decreased to a nadir of 14 (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) mm Hg in 17 animals and to 32 mm Hg in one. HR decreased to 64 (30 -96) bpm.…”

Section: Resultsmentioning

confidence: 99%

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High Brain Tissue Oxygen Tension During Ventilation With 100% Oxygen After Fetal Asphyxia in Newborn Sheep

et al. 2009

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ABSTRACT:The optimal inhaled oxygen fraction for newborn resuscitation is still not settled. We hypothesized that short-lasting oxygen ventilation after intrauterine asphyxia would not cause arterial or cerebral hyperoxia, and therefore be innocuous. The umbilical cord of fetal sheep was clamped and 10 min later, after delivery, ventilation with air (n ϭ 7) or with 100% oxygen for 3 (n ϭ 6) or 30 min (n ϭ 5), followed by air, was started. Among the 11 lambs given 100% oxygen, oxygen tension (P O2 ) was 10.7 (1.8 -56) kPa [median (range)] in arterial samples taken after 2.5 min of ventilation. In those ventilated with 100% oxygen for 30 min, brain tissue P O2 (Pbt O2 ) increased from less than 0.1 kPa in each lamb to individual maxima of 56 (30 -61) kPa, whereas in those given oxygen for just 3 min, Pbt O2 peaked at 4.2 (2.9 -46) kPa. The maximal Pbt O2 in airventilated lambs was 2.9 (0.8 -5.4) kPa. Heart rate and blood pressure increased equally fast in the three groups. Thus, prolonged ventilation with 100% oxygen caused an increase in Pbt O2 of a magnitude previously only reported under hyperbaric conditions. Reducing the time of 100% oxygen ventilation to 3 min did not consistently avert systemic hyperoxia. (Pediatr Res 65: 57-61, 2009) C urrent guidelines from the International Liaison Committee on Resuscitation breathe considerable uncertainty as to how much supplementary oxygen should be given during resuscitation of newborn asphyxiated infants (1). Previous recommendations were to be generous with oxygen, but recent guidelines from a number of countries, e.g. Australia, Canada, Finland, the Netherlands, Sweden, and the United Kingdom recommend initial ventilation with air, because of the results from several experimental (2-5) and clinical (6 -13) studies indicating that resuscitation with 100% oxygen is harmful. In the clinical studies, the time of exposure to 100% oxygen was typically 5-7 min (8,13), whereas only one animal study (5) has investigated an exposure time to oxygen less than 15 min.We speculated that very short times of exposure might not allow systemic hyperoxia to develop and so be harmless to the newborn infant, except for a possible negative effect on the lungs. In fact, the pulse oximetric saturation at 3 min after birth is usually below 80% (14,15) in the normal air-breathing infant, suggesting the presence of cardiac or pulmonary rightto-left shunts. One might expect that such shunts would delay the appearance of arterial hyperoxemia in the infant breathing pure oxygen. However, this has been studied neither in normal nor in asphyxiated subjects.We used a sheep model of term intrauterine asphyxia with postnatal resuscitation, and hypothesized that hyperoxia of arterial blood and of brain tissue could be prevented by limiting the period of ventilation with 100% oxygen to 3 min. We also investigated whether the speed of circulatory recovery, as reflected by the heart rate (HR) and mean arterial blood pressure (MAP) responses, and the speed of recovery of brain oxygenation, as reflected ...

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“…15%, in all animals. MAP decreased to a nadir of 14 (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) mm Hg in 17 animals and to 32 mm Hg in one. HR decreased to 64 (30 -96) bpm.…”

Section: Resultsmentioning

confidence: 99%

“…Gene transcripts were quantified using real-time PCR on ABI PRISM ® 7000 sequence detection system (Applied Biosystems, Foster City, CA) as described previously (10). The quantitative value of each sample was normalized to the corresponding value of beta-actin and results expressed as relative values.…”

Section: Methodsmentioning

confidence: 99%

High Brain Tissue Oxygen Tension During Ventilation With 100% Oxygen After Fetal Asphyxia in Newborn Sheep

et al. 2009

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“…Neonatal exposure to oxidant molecules is not limited to peroxides from TPN, as many babies receive short periods of oxygen supplementation at delivery. A short period of neonatal oxygen supplementation has been shown to have serious consequences later in life (22,49). Further translational studies will need to investigate the combined effect of both of these clinical relevant sources of oxidants that have been shown to induce different responses in other experimental conditions (50,51).…”

Section: Discussionmentioning

confidence: 99%

Neonatal Exposure to Oxidants Induces Later in Life a Metabolic Response Associated to a Phenotype of Energy Deficiency in an Animal Model of Total Parenteral Nutrition

et al. 2010

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Failure to protect total parenteral nutrition (TPN) from ambient light exacerbates the generation of peroxides, which affects blood glucose and plasma triacylglyceride (TG) in neonates. Based on the concept that the origin of adult diseases can be traced back to perinatal life, it was hypothesized that neonatal exposure to peroxides may affect energy availability later in life. Three-day-old guinea pigs, fitted with a jugular catheter, were fed regular chow (sham) Ϯ i. T he association between oxidative stress and characteristic features of the metabolic syndrome, such as diabetes, hypertension, and dyslipidemia, is well documented (1-6). Human (7) and animal studies (8,9) suggest that the origin of the metabolic syndrome can be traced back to perinatal life, a time when newborn infants are at greater risk of oxidative stress caused by weak antioxidant defenses (10 -12) or exposure to an oxidative environment or both (13-18). Several reports suggest that, in neonates, oxidative stress triggers the events that lead to programming of adult diseases (19 -22).Total parenteral nutrition (TPN) represents a source of oxidants in the form of peroxides that can be calibrated either by applying or not photoprotecting. The peroxides are derived from interactions between dissolved oxygen and electron donors such as lipid, amino acid, or ascorbic acid (23,24). The reaction is catalyzed by photoexcited riboflavin (24). Therefore, the main active agents participating in the generation of peroxides in TPN are ambient light [(ϩ)L] and multivitamin preparations (MVP) (23,24). Photoprotection [(Ϫ)L] of TPN reduces the levels of peroxides by close to 50% (23,25,26). Absence of photoprotection of TPN is associated in preterm newborn infants with higher urinary peroxide concentrations (16), higher blood pressure in girl babies (15), and greater blood glucose and plasma triacylglycerol concentrations (13). Hence, peroxides contaminating TPN solutions are not completely quenched by newborns infants and are thought to be an agent initiating metabolic perturbations. We questioned whether these peroxides are linked to metabolic consequences later in life.Based on the concept that neonatal oxidative stress may interfere with metabolic programming (27), we hypothesized that neonatal exposure to peroxides such as those generated in solutions of parenteral nutrition, induces a permanent modification in lipid and glucose metabolism especially lipogenesis and/or glycolysis. Perturbations in lipid and glucose metabolism, which are fuels for energy production, could have longterm consequences on growth and physical activity, thereby affecting global development. The aim of this study was to measure in adult guinea pigs metabolic responses and spontaneous physical activity after a brief neonatal exposure to i.v. oxidant molecules limited to the first wk of life. A second objective was to assess if these modifications were related to the infusion of peroxides. MATERIALS AND METHODSExperimental design. The metabolic response and the levels...

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“…4,5 In addition, there is an epidemiologic association with higher risk for childhood leukemia and cancer in neonates who are resuscitated with 100% O 2 at birth. 27,28 The deleterious effect of hyperoxia is not only relevant during the NICU stay but also in the first minutes of life. In the delivery room, hyperoxia may not only cause initial oxidative injury but it could trigger a cascade of events that may be impossible to stop despite excellent NICU care.…”

Section: Discussionmentioning

confidence: 99%

Avoiding hyperoxia in infants ⩽1250?g is associated with improved short- and long-term outcomes

et al. 2006

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Supplementary oxygen and risk of childhood lymphatic leukaemia

Abstract: Resuscitation with 100% oxygen immediately postpartum is associated with childhood lymphatic leukaemia, but further studies are warranted to confirm the findings.

Cited by 79 publications

References 24 publications

High Brain Tissue Oxygen Tension During Ventilation With 100% Oxygen After Fetal Asphyxia in Newborn Sheep

High Brain Tissue Oxygen Tension During Ventilation With 100% Oxygen After Fetal Asphyxia in Newborn Sheep

Neonatal Exposure to Oxidants Induces Later in Life a Metabolic Response Associated to a Phenotype of Energy Deficiency in an Animal Model of Total Parenteral Nutrition

Avoiding hyperoxia in infants ⩽1250?g is associated with improved short- and long-term outcomes

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