Small particles disrupt postnatal airway development.

Journal of Applied Physiology
DongYoub LeeJackie K W Chan

Abstract

Increasing numbers of epidemiologic studies associate air pollution exposure in children with decreased lung function development. The objective of this study was to examine the effects of exposure to combustion-generated fine [230 and 212 nm number mean aerodynamic particle diameter (NMAD)] to ultrafine (73 nm NMAD) particles differing in elemental (EC) and organic (OC) carbon content on postnatal airway development in rats. Neonatal Sprague-Dawley rats were exposed from postnatal day 7 through 25, and lung function and airway architecture were evaluated 81 days of age. In a separate group of rats, cell proliferation was examined after a single particle exposure at 7 days of age. Early life exposure to 73 nm high OC/EC particles altered distal airway architecture and resulted in subtle changes in lung mechanics. Early life exposure to 212 nm high OC/EC particles did not alter lung architecture but did alter lung mechanics in a manner suggestive of central airway changes. In contrast, early life exposure to 230 nm low OC/EC particles did not alter lung architecture or mechanics. A single 6-h exposure to 73 nm high OC/EC particle decreased airway cell proliferation, whereas 212 nm high OC/EC particles increased it and 230 nm low...Continue Reading

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Feb 25, 2011·Annals of Biomedical Engineering·DongYoub LeeAnthony S Wexler
Sep 15, 2011·Toxicological Sciences : an Official Journal of the Society of Toxicology·Jackie K W ChanLaura S Van Winkle
Dec 20, 2012·American Journal of Respiratory and Critical Care Medicine·Jonathan Grigg
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