Many inhaled pollutants adversely affect the integrity and function of the respiratory tract. Experimental data collected to assess the impact of these pollutants have generally been obtained from healthy subjects who are more resistant than are sensitive subpopulations.

We identified pregnant and lactating rats as a subpopulation that is highly susceptible, relative to male, prepregnant, or postlactating rats, to the inflammatory effects of certain irritants. Using ozone, an ubiquitous photochemical oxidant air pollutant, as a model inflammatory agent, we demonstrated that acute exposure of lactating rats induced significantly greater protein and neutrophil influx into the airspace than did identical exposure of postlactating rats. Owing to the increased metabolic demands of lactation, however, lactating rats also exhibited greater ventilation of the lungs and thus received a greater ozone dose. The greater inhaled ozone dose accounted for only a portion of the enhanced inflammatory response, indicating that the physiological state of lactation is inherently more sensitive to ozone than are nonpregnant/nonlactating states.

More recent studies reveal that the epithelial lining fluid (ELF) of the lung of lactating rats contains a lower concentration of the antioxidant ascorbic acid than does the ELF of prepregnant rats. This relative deficiency may contribute to the greater sensitivitiy of lactating rats to ozone. We are currently investigating additional hypotheses that might account for the inherent sensitivity of lactating (and pregnant) rats to ozone and other inflammatory agents to determine if this phenomenon may pertain to analogous human populations.