Enhanced Pulmonary Inflammatory Response to Ozone During Lactation in Rats: Evaluation of the Influence of Inhaled Dose

Abstract

We previously demonstrated that rats in a late stage of pregnancy and throughout lactation were more susceptible to pulmonary inflammation induced by exposure to 1 ppm ozone than were age-matched virgin females or rats following lactation. The purpose of the study reported here was to extend the comparison of ozone-induced pulmonary inflammation in lactating and postlactating rats to lower concentrations of ozone and to investigate the hypothesis that the enhanced response demonstrated by lactating rats is attributable to a greater inhaled ozone dose. During pregnancy and lactation the metabolic demands on the female are substantially increased above prepregnancy levels. In response to this metabolic demand, it was shown in this study that the minute volume of air-breathing postpartum rats on day 13 of lactation increased to approximately 150% of that of age-matched postlactating rats with the same lung size. Heightened ventilation in lactating rats was maintained during exposure to 0.3, 0.5, and 1.0 ppm ozone for 6 h, resulting in greater inhaled ozone doses in lactating rats compared to postlactating rats exposed identically. The pulmonary inflammatory response to ozone was assessed in the same rats 18 h after exposure by comparison of protein concentration and polymorphonuclear cell (PMN) numbers in bronchoalveolar lavage fluid (BALF). Both of these parameters were significantly greater in lactating than postlactating rats at 0.3, 0.5, and 1.0 ppm ozone. Statistical analysis indicated that most or all of the greater BALF protein in lactating rats could be accounted for by their greater inhaled dose, whereas a significant portion of the enhanced PMN influx in lactating rats remained unexplained by inhaled ozone dose.