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1 Center for Comparative Respiratory Biology and Medicine, California National Primate Research Center, University of California, Davis, Davis, California, United States
* To whom correspondence should be addressed. E-mail: mvfanucchi{at}ucdavis.edu.
Inner city children exposed to high levels of ozone suffer from an increased prevalence of respiratory diseases. Lung development in children is a long term process, and there is a significant period of time during development when children growing up in urban areas are exposed to oxidant air pollution. This study was designed to test whether repeating cycles of injury and repair caused by episodes of ozone exposure lead to chronic airway disease and decreased lung function by altering normal lung maturation. We evaluated postnatal lung morphogenesis and function of infant monkeys following 5 months of episodic exposure of 0.5 parts per million ozone beginning at one-month of age. Non-human primates were chosen because their airway structure and postnatal lung development is similar to humans. Airway morphology and structure were evaluated at the end of the five month exposure period. Compared to control infants, ozone exposed animals had four fewer non-alveolarized airway generations, hyperplastic bronchiolar epithelium, and altered smooth muscle bundle orientation in terminal and respiratory bronchioles. These results suggest that episodic exposure to environmental ozone compromises postnatal morphogenesis of tracheobronchial airways.
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