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Articles in PresS, published online ahead of print October 22, 2001
J Appl Physiol, 10.1152/jap.00381.2001
Submitted on April 20, 2001
Accepted on October 22, 2001
1 Environmental Health, Harvard School of Public Health, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: sshore{at}hsph.harvard.edu.
During ozone (O3) exposure, adult mice decrease their minute ventilation (VE). To determine whether there are age-related differences in the ventilatory response to O3, A/J mice aged 2, 4, 8, or 12 weeks, were exposed to O3 (0.3, 0.5, 1.0, 2.0 or 3.0 ppm for 3 h) in nose-only exposure plethysmographs. Baseline VE normalized for body weight decreased with age from 4.94±0.26 ml/min/g in 2 week old mice to 1.87±0.07 ml/min/g in 12 week old mice, consistent with the higher metabolic rates of younger animals. O3 caused a concentration related decrease in VE in mice of all ages, but the response was significantly less in the 2 wk old than in the older mice. The decrease in VE was the result of decreases in both tidal volume and breathing frequency. The increased baseline VE/g and the smaller decrements in VE induced by O3 in the immature mice resulted in an inhaled dose of O3 normalized for body weight that was 3-4 times higher than in adult mice. To determine whether these differences in O3 dose lead to age-related differences in the ability of O3 to induce airway hyperresponsiveness (AHR) or inflammation, we measured airway responsiveness to inhaled aerosolized methacholine by whole body plethysmography before and 3 hours after cessation of O3. We also performed bronchoalveolar lavage (BAL). O3 exposure caused a dose related increase in airway responsiveness in 8 and 12 wk old mice, but did not cause AHR at any dose in either 2 or 4 wk old mice, even though higher inhaled doses of O3 normalized for body weight were delivered to these younger animals. O3-induced BAL IL-6 and MIP-2 were also increased in 8 week compared to 2 week old mice. The results suggest that immature mice are less sensitive than adult mice to O3, at least in terms of its ability of 03 to induce AHR and promote release of certain cytokines.
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