Short-term PM exposure and social stress cause pulmonary and cardiac dysfunction

Abstract

Ambient particulate matter (PM) exposure increases risk for cardiopulmonary health problems which may be exacerbated in a stressful environment. Co-exposure to PM and stress characterizes the experience of many deployed military personnel and first responders but has not been thoroughly investigated. This is especially relevant to military personnel who have been exposed to high PM levels in conjunction with stressful military conflict situations. To understand the mechanisms and time-course of the health consequences following burn pit exposure, we exposed mice to moderate levels of ambient PM less than 2.5 μM in diameter (PM2.5) alone or in combination with psychological stress. We found male mice exposed to PM2.5 alone or in combination with stress had significantly reduced pulmonary function when subjected to methacholine, indicating increased airway hyperreactivity. These mice experienced increased goblet cell hyperplasia in their lungs, with no change in alveolar density. Mice exposed to PM2.5 and/or stress also exhibited reduced cardiac contractility, right ventricular (RV) output, and changes in RV capillary density and cardiac inflammatory markers. Taken together, these data indicate that short-term exposure to PM2.5 with or without stress causes a clear reduction in pulmonary and cardiac function. We believe that this model is well-suited for the study of military and other occupational exposures, and future work will identify potential mechanisms, including the inflammatory progression of these co-exposures.