On the pulmonary toxicity of oxygen : III. The induction of oxygen dependency by oxygen use

Author Posting. © The Author(s), 2010. This is the author's version of the work. It is posted here by permission of Elsevier B.V. for personal use, not for redistribution. The definitive version was published in Experimental and Molecular Pathology 89 (2010): 36-45, doi:10.1016/j.yexmp.2010.05.004.Oxygen is central to the development of neonatal lung injury. The increase in oxygen exposure of the neonatal lung during the onset of extrauterine air breathing is an order of magnitude, from a range of 10-12 to 110-120 Torr. The contributions of oxygen and the volume and pressure relationships of ventilatory support to lung injury are not easily distinguished in the clinical setting. Sequential changes in inspired air or 100% oxygen were studied in 536 newborn rabbits without ventilatory support. Bilateral cervical vagotomies (BCV) were performed at 24 hours post natal to induce ventilatory distress which eventuates in hyaline membrane disease. The sequences applied yielded evidence for an induced state of oxygen dependency from oxygen use which was reflected in differences in survival and the extent of pulmonary injury. The median survival for animals kept in air throughout was 3 hours. Oxygen before vagotomy or during the first 3 hours afterwards extended the survival significantly but produced more extensive, more severe, and more rapid lung lesions. Returning animals to air after prior oxygen exposure reduced the number of survivors past 10 hours and shortened the maximum survival in those groups. These features indicate the development of a dependency of the defense mechanisms on the availability of oxygen at the higher level for metabolic and possibly other aspects of the pulmonary and systemic response to injury, beyond the usual physiological need. Subset analysis revealed additive and latent effects of oxygen and demonstrated a remarkable rapidity in onset of severe lesions under some circumstances, illustrating the toxicity of oxygen per se.John A. Hartford Foundation, New York, N.Y. 10022-171

A review of the epidemiological evidence on tea, flavonoids, and lung cancer

Tea and its main bioactive ingredients, the flavonoids, have been associated with human cancer for several decades. In this article, an overview is provided of observational epidemiological studies of lung cancer incidence in relation to intake of green tea, black tea, flavonols/flavones, and catechins. A PubMed search was conducted in September 2007. Articles were selected if they provided risk ratios (relative risk or odds ratio) for lung cancer and were of observational design (cohort, case-control, or case-cohort). Three of 12 studies reported a significantly lower risk of lung cancer with a high intake of flavonoids, whereas 1 study reported a significantly increased risk. After stratification by type of flavonoid, catechin intake was no longer associated with lung cancer risk in 3 of 4 studies available. For tea, 4 of 20 studies reported significantly reduced risks with high intake. Two studies found significantly increased risk ratios, but both were older studies. Findings were similar for green and black tea but became more significant when only methodologically sounder cohort studies were considered. When tea intake and lung cancer were studied among never- or former smokers to eliminate the confounding effect of smoking, 4 of 7 reported associations were significantly protective. In general, the studies on tea, flavonoids, and lung cancer risk indicate a small beneficial association, particularly among never-smokers. More well-designed cohort studies, in particular for catechins, are needed to strengthen the evidence on effects of long-term exposure to physiological doses of dietary flavonoids