Abstract
Studies from this laboratory have shown that lactating rats exhibit a greater inflammatory response to inhaled ozone than age-matched nulligravidous or postlactating rats. One factor contributing to this enhanced response by lactating rats is their greater ventilation, which results in a higher inhaled dose rate. In the study reported here, we investigate the concept that lactating rats are predisposed to ozone-induced inflammation, not only because of their higher ventilation but also because of the inherently greater sensitivity of their tissues. We found that the airways of naive, 13-day postpartum lactating Sprague-Dawley rats have significantly greater numbers of polymorphonuclear leukocytes (PMNs), a higher protein concentration, and a lower concentration of the antioxidant ascorbic acid than do the airways of virgin females. Lactating rats also have a higher PMN concentration in their circulating blood. These differences in the steady state condition of lactating rats, particularly the airways of the respiratory tract, suggest that predisposition of lactating rats to pulmonary inflammation induced by ozone may be due in part to changes in immunological status during lactation and to the greater propensity of the respiratory tract tissues of lactating rats to respond to stimulation by ozone. We compared the kinetics of airway inflammatory changes detected in bronchoalveolar lavage fluid following acute exposure of lactating and virgin female rats to 0.3 and 0.5 ppm ozone for 6 h, and observed an earlier onset and greater intensity and persistence of the inflammatory response in the lactating animals.