Short‐term PM exposure and social defeat cause reduction in pulmonary and right ventricle function

Abstract

Military members, first responders, and various other occupations are exposed to environments containing high levels of air pollution and psychological distress. While much is known about the effects of particulate matter (PM) and stress on cardiac and lung function, we investigated the interaction of these factors and whether the combination of prolonged PM and stress exposures exacerbate cardiac and lung function in a mouse model. Male C57Bl/6 mice were exposed to filtered air (FA) or PM at concentrations of 137.7 ± 70.76 (daily mean ± standard deviation) for five days/week for three weeks. A subset of each group was stressed by exposing them to a retired male aggressor for two hours/day, 3-5 nights/week (FA-stress and PM-stress groups). Echocardiography of the mice showed no changes in left ventricle (LV) systolic or diastolic indices, but a significant reduction in right ventricle (RV) stroke volume and cardiac output in the PM, FA-stress and PM-stress groups (P<0.05via two-way ANOVA) compared to FA. Pressure-volume loops found a reduction in contractility as the PM and PM-stress groups, but not FA-stress, had significantly reduced end-systolic elastance (Ees, P<0.05 via two-way ANOVA) compared to FA. Data on respiratory mechanics was acquired using the flexiVent FX2 (SCIREQ Inc.) system. With an increasing dose of methacholine, PM exposure caused an increase in lung resistance (Rrs), central airway resistance (Rn), and tissue damping (G) (area under the curve [AUC], P<0.05 via two-way ANOVA) compared to FA. The FA-stress and PM-stress groups had significantly increased lung elastance (Ers), Rrs, Rn, and G (AUC P<0.05 via two-way ANOVA) compared to FA. Tail-vein blood pressure measurements in these mice found that an increased diastolic, but not systolic pressure was induced by PM exposure, but not by stress (P<0.05via two-way ANOVA). Taken together, short-term exposure to PM with and without psychological distress impairs respiratory mechanics and RV function. These results suggest that even short-term exposure to PM, such as in occupational settings, causes notable dysfunction in cardiopulmonary function equal to stress.