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Susceptibility of the Developing Lung to Combustion Derived Ultrafine Particles

出版	University of California, Davis, 2012
ISBN	12679677149781267967718
URL	http://books.google.com.hk/books?id=ET0gnwEACAAJ&hl=&source=gbs_api

註釋Exposure to urban particulate matter (PM) has been epidemiologically correlated with multiple cardiopulmonary morbidities and mortalities, especially in susceptible populations such as young children. PM is currently divided into three fractions, separated by particle size. The coarse fraction, PM10 consists of particles less than 10 microns in diameters, while the fine PM2.5, and ultrafine PM0.1 fractions contains particles less than 2.5 and 0.1 microns, respectively. Although PM originates from both natural and anthropogenic sources, vehicle combustion exhaust is a major contributor to the PM2.5 and PM0.1 fractions. Vehicle exhaust is rich in polycyclic aromatic hydrocarbons (PAH) and reactive oxygen species (ROS) that have been epidemically shown to be correlated with deficits in lung growth and function in developing children. The lung is a heterogeneous organ that undergoes extensive growth and maturation phases postnatally, that may be adversely affected upon exposure to environmental pollutants such as PM. Current studies of ambient urban PM are confounded by the complex mixture of soot, metals, allergens and organic compounds present in addition to seasonal and temporal variance. To address this issue, we have developed a laboratory based ultrafine PM (PFP) that are comprised of mostly organic compounds, namely PAHs, and are devoid of metals and allergens to study biological effects on the developing lung. We used 7 day old postnatal and adult rats as a model for childhood development and exposed these animals to a single 6 hour exposure to PFP or filtered air and analyzed markers of lung cytotoxicity, xenobiotic metabolism, antioxidants and phase II detoxification enzymes. The developing neonates are more susceptible to PFP, and are substantially less adaptable compared to adults. Xenobiotic metabolizing cytochrome P450 enzymes are immature in the neonates, and induction is delayed following exposure. Furthermore, antioxidant levels such as glutathione, is severely depleted in the neonates, and resynthesis enzymes were not upregulated, unlike adult animals. Finally, phase II detoxification enzymes induction was also muted in neonates following PFP exposure. We conclude that the inability of neonates to sufficiently adapt in response to PFP may, in part, explain their susceptibility to PFP and urban ultrafine PM.