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Age-related differences in pulmonary effects of acute and subchronic episodic ozone exposures in Brown Norway rats
Citation:
Snow, S., C. Gordon, V. Bass, M. Schladweiler, A. Ledbetter, K. Jarema, P. Phillips, A. Johnstone, AND U. Kodavanti. Age-related differences in pulmonary effects of acute and subchronic episodic ozone exposures in Brown Norway rats. INHALATION TOXICOLOGY. Informa Healthcare USA, New York, NY, 28(7):313-23, (2016).
Impact/Purpose:
In this susceptibility to ozone induced pulmonary injury and inflammation were assessed in rats of 4 age groups. We demonstrate that while juvenile and adolescent rats are more susceptible to acute and subchronic changes in breathing frequency, minute volume, or enhanced pause, the recovery from reduced relaxation time is impaired only in senescent rats. Likewise, while rats of all ages are susceptible to acute pulmonary protein leakage, the lung cell injury and neutrophilic inflammation occurs only in the juvenile and adolescent animals.
Description:
Ozone (O3) is known to induce adverse pulmonary and systemic health effects. Importantly, children and older persons are considered at-risk populations for O3-induced dysfunction, yet the mechanisms accounting for the age-related pulmonary responses to O3 are uncertain. In this study, we examined age-related susceptibility to O3 using 1 mo (adolescent), 4 mo (young adult), 12 mo (adult) and 24 mo (senescent) male Brown Norway rats exposed to filtered air or O3 (0.25and 1.00 ppm), 6 h/day, two days/week for 1 week (acute) or 13 weeks (subchronic). Ventilatory function, assessed by whole-body plethysmography, and bronchoalveolar lavage fluid (BALF) biomarkers of injury and inflammation were used to examine O3-induced pulmonary effects.Relaxation time declined in all ages following the weekly exposures; however, this effect persisted only in the 24 mo rats following a five days recovery, demonstrating an inability to induce adaptation commonly seen with repeated O3 exposures. PenH was increased in all groups with an augmented response in the 4 mo rats following the subchronic O3 exposures. O3 led to increased breathing frequency and minute volume in the 1 and 4 mo animals. Markers ofpulmonary permeability were increased in all age groups. Elevations in BALF γ-glutamyl transferase activity and lung inflammation following an acute O3 exposure were noted in only the 1 and 4 mo rats, which likely received an increased effective O3 dose. These data demonstrate that adolescent and young adult animals are more susceptible to changes in ventilation and pulmonary injury/inflammation caused by acute and episodic O3 exposure.
