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ToxSci Advance Access published online on December 9, 2008
Toxicological Sciences, doi:10.1093/toxsci/kfn253
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© The Author 2008. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org

Age, strain, and gender as factors for increased sensitivity of the mouse lung to inhaled ozone

Elizabeth M. Vancza*, Karen Galdanes*, Al Gunnison*, Gary Hatch{dagger} and Terry Gordon*,1

* Department of Environmental Medicine, New York University School of Medicine, 57 Old Forge Road, Tuxedo, NY 10987 {dagger} Pulmonary Toxicology Branch, Experimental Toxicology Division, National Health Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711

1 Address correspondence to: Terry Gordon, Ph.D., New York University School of Medicine, Department of Environmental Medicine, 57 Old Forge Road, Tuxedo, NY 10987, Phone: (845) 731-3536, FAX: (845) 351-5472, E-mail: terry.gordon{at}nyumc.org

Received September 2, 2008; revision received December 2, 2008; accepted December 3, 2008


  Abstract

Ozone (O3) is a respiratory irritant that leads to airway inflammation and pulmonary dysfunction. Animal studies show that neonates are more sensitive to O3 inhalation than adults, and children represent a potentially susceptible population. This latter notion is not well established, and biological mechanisms underlying a predisposition to pollution-induced pulmonary effects are unknown. We examined age and strain as interactive factors affecting differential pulmonary responses to inhaled O3. Male and female adult mice (15wk old) and neonates (15 to 16d old) from 8 genetically diverse inbred strains were exposed to 0.8ppm O3 for 5h. Pulmonary injury and lung inflammation were quantified as total protein concentration and total polymorphonuclear neutrophil (PMN) number in lavage fluid recovered 24h post-exposure. Dose-response and time-course curves were generated using SJL/J pups, and 18O lung burden dose was assessed in additional mice. Inter-strain differences in response to O3 were seen in neonatal mice: Balb/cJ and SJL/J being most sensitive and A/J and 129x1/SvJ most resistant. The PMN response to O3 was greater in neonates than in adults, specifically for SJL/J and C3H/HeJ strains, and the heightened response was independent of dose. Small gender differences were also observed in adult mice. Variation in protein concentrations and PMN counts between adults and pups were strain-dependent, suggesting that genetic determinants do play a role in age-related sensitivity to O3. Further research will help to determine what genetic factors contribute to these heightened responses, and to quantify the relative contribution of genes vs. environment in O3-induced health effects.

Key Words: Children's health; Genetic susceptibility; Lung inflammation; Lung injury; Ozone.


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