![]() ![]() Children who exercise outdoors in areas with high levels of air pollution have a greater risk of developing asthma ( 15, 44). Elevated particulate pollution has also been associated with increased medication use and hospital admission in children and adults. Epidemiologic studies suggest that these health effects can begin at birth chronic exposure to air pollution is associated with reduced lung function growth in humans ( 2, 13, 14, 16, 22, 27, 42, 45, 51). 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.Īir pollutants, including particulate matter and ozone, have been shown to adversely affect human health. 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. In contrast, early life exposure to 230 nm low OC/EC particles did not alter lung architecture or 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. Early life exposure to 73 nm high OC/EC particles altered distal airway architecture and resulted in subtle changes in lung mechanics. In a separate group of rats, cell proliferation was examined after a single particle exposure at 7 days of age. Neonatal Sprague-Dawley rats were exposed from postnatal day 7 through 25, and lung function and airway architecture were evaluated 81 days of age. The objective of this study was to examine the effects of exposure to combustion-generated fine to ultrafine (73 nm NMAD) particles differing in elemental (EC) and organic (OC) carbon content on postnatal airway development in rats. Increasing numbers of epidemiologic studies associate air pollution exposure in children with decreased lung function development. ![]()
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