American Thoracic Society Journal news tips for January (first issue)

December 31, 2002

SMOKING, AIRWAY NARROWING, AND SUDDEN INFANT DEATH SYNDROME

After studying airway and other tissues, together with autopsy data, from 32 infants who died of sudden infant death syndrome, Australian researchers have concluded that maternal smoking during pregnancy alters airway structure which can lead to excessive airway narrowing in exposed babies. The investigators said that alterations in airway structure from in utero cigarette smoke exposure are those likely to result in excessive airway narrowing in response to irritants encountered during the postnatal period. Such narrowing could account for the symptoms and abnormal lung function in exposed infants. The investigators believe that the level of change in the inner airway wall of the babies who were exposed in the womb may be dose-related, particularly in mothers who smoked more than 20 cigarettes per day. They also believe that smoking mothers tend to under-report the number of cigarettes they smoke. The research appears in the first issue for January 2003 of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine.

POTENTIAL LUNG THERAPY FOR PREMATURE INFANTS

Researchers working with premature baboons that represented an animal model for bronchopulmonary dysplasia (BPD), a serious illness of very low birth weight babies, treated the group of study animals with low molecular weight catalytic antioxidant. They believe this compound could represent a potential therapy to prevent this deadly evolving lung disease in human premature babies. BPD, common among premature newborns, involves lung injury caused by being on a ventilator and receiving oxygen, usually for more than 1 week. The researchers believe that the premature lung may be deficient in antioxidant enzymes. Reporting on the antioxidant infused in the premature baboons that were animal models of severe BPD, they presented data that showed the agent inhibits lung structure changes and inflammation in the baboons' lungs, damage that had been induced by 100 percent oxygen; reduced levels of proinflammatory peptides and a bronchoconstrictor; and lessened the number of pulmonary inflammatory cells which developed during an allergic reaction. An editorial in the same issue of the ATS journal points out that the authors' current research on premature baboon infants delivered even earlier at 125 days of gestation (69.4 percent of 180-day term) may be of "enormous clinical relevance" in potentially reducing further lung damage in extremely immature human infants. The research and editorial are published in the first issue for January 2003 of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine.

UPPER AIRWAY SIZE MUCH SMALLER IN CHILDREN WITH OBSTRUCTIVE SLEEP APNEA

Medical investigators used magnetic resonance imaging (MRI) on young children with obstructive sleep apnea (OSA) to reveal that the upper airway of the children with OSA is significantly smaller with respect to airway volume and cross-sectional area when compared with matched control subjects without OSA. The researchers used MRI to visualize and accurately measure the upper airway, various soft tissues, and the skeleton comprising this area in 20 children with OSA and 20 control subjects, who had an average age of less than 4 years. The investigators said that their findings suggested that the upper airway of children with OSA is restricted along the upper two-thirds of its length and predominately in the region where the adenoid and tonsils overlap. In sleep apnea, a sleeping person repeatedly stops breathing long enough to decrease the amount of oxygen in the blood and brain and to increase carbon dioxide. After more than 10 seconds, the person very briefly arouses and resumes breathing. This happens many times over during the night. OSA results from a blockage in the throat or upper airway, and is a common disorder in children, possibly involving 2 percent of that population. The research appears in the first issue for January 2003 of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine.
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For the complete text of these articles and editorial, please see the American Thoracic Society Online Web Site at http://www.atsjournals.org. For either contact information or to request a complimentary journalist subscription to ATS journals online, or if you would like to add your name to the Society's twice monthly journal news mailing list (please select either postal or electronic delivery), contact Cathy Carlomagno at (212) 315-6442, or by e-mail at ccarlomagno@thoracic.org.

American Thoracic Society

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