title: Small particles disrupt postnatal airway development.
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 OC/EC particles did not. The early life exposure to ultrafine, high OC/EC particles results in persistent alterations in distal airway architecture that is characterized by an initial decrease in airway cell proliferation.
authors.affiliation: Department of Mechanical and Aerospace Engineering, Univ. of California, Davis, CA 95616, USA.
authors.forename: DongYoub
authors.initials: D
authors.lastname: Lee
authors.forename: Chris
authors.initials: C
authors.lastname: Wallis
authors.forename: Anthony S
authors.initials: AS
authors.lastname: Wexler
authors.forename: Edward S
authors.initials: ES
authors.lastname: Schelegle
authors.forename: Laura S
authors.initials: LS
authors.lastname: Van Winkle
authors.forename: Charles G
authors.initials: CG
authors.lastname: Plopper
authors.forename: Michelle V
authors.initials: MV
authors.lastname: Fanucchi
authors.forename: Ben
authors.initials: B
authors.lastname: Kumfer
authors.forename: Ian M
authors.initials: IM
authors.lastname: Kennedy
authors.forename: Jackie K W
authors.initials: JK
authors.lastname: Chan
mesh_terms: D000367:Age Factors; D000818:Animals; D000831:Animals, Newborn; D001985:Bronchial Provocation Tests; D016084:Bronchoconstriction / Q000187:drug effects; D002244:Carbon / Q000633:toxicity*; D049109:Cell Proliferation / Q000187:drug effects; D007150:Immunohistochemistry; D019570:Inhalation Exposure; D008168:Lung / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000254:growth & development / Q000378:metabolism; D010316:Particle Size; D052638:Particulate Matter / Q000633:toxicity*; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015656:Respiratory Mechanics / Q000187:drug effects; D055114:X-Ray Microtomography
chemical_list: D052638:Particulate Matter; D018809:Proliferating Cell Nuclear Antigen; D002244:Carbon