O-3-induced inflammation in prepregnant, pregnant, and lactating rats correlates with O-3 dose estimated by O-18

Previous studies have shown that rats late in pregnancy and throughout lact ation are more susceptible to ozone (O-3)-induced pulmonary inflammation th an are prepregnant (virgin) or postlactating rats. The major aim of the pre sent study was to determine whether these differences in response intensity could be accounted for by the O-3 dose to the lower region of the lung. Th e relative O-3 dose to the lower lung of groups of pregnant, lactating, and virgin female rats was estimated by measuring the incorporation of the O-1 8 isotope into low-speed (cells) and high-speed (surfactant) pellets of bro nchoalveolar lavage fluid immediately after acute exposure to 0.5-1.1 parts /million O-18(3). The polymorphonuclear leukocyte (PMN) and protein inflamm atory responses were established 20 h after acute exposure of identical phy siological groups to 0.5-1.1 parts/million O-16(3) (common isotope). A sing le regression of PMN inflammation data against surfactant O-18 concentratio n for all physiological groups gave a linear relationship, indicating direc t proportionality of PMN inflammation with this estimate of relative dose t o the lower lung regardless of physiological status. This implies that the chemical species that react with surfactant molecules, i.e., O-3 or its met abolites, are the same as or proportional to those chemical species respons ible for initiating PMN inflammation. Additional experiments showed that lu ng tissue ascorbic acid concentration was significantly lower in pregnant a nd lactating rats than in virgin female rats. Although a causative relation ship cannot be assumed, the deficit in tissue ascorbic acid concentration i n pregnant and lactating rats compared with virgin female rats is consisten t with their greater responsiveness and higher relative surfactant O-3 dose .