Environmentally persistent free radicals decrease cardiac function and increase pulmonary artery pressure

Abstract

Epidemiological studies have consistently linked inhalation of particulate matter (PM) to increased cardiac morbidity and mortality, especially in at risk populations. However, few studies have examined the effect of PM on baseline cardiac function in otherwise healthy individuals. In addition, airborne PM contain environmentally persistent free radicals (EPFR) capable of redox cycling in biological systems. The purpose of this study was to determine whether nose-only inhalation of EPFRs (20 min/day for 7 days) could decrease baseline left ventricular function in healthy male Sprague-Dawley rats. The model EPFR tested was 1,2-dichlorobenzene chemisorbed to 0.2-μm-diameter silica/CuO particles at 230°C (DCB230). Inhalation of vehicle or silica particles served as controls. Twenty-four hours after the last exposure, rats were anesthetized (isoflurane) and ventilated (3 l/min), and left ventricular function was assessed using pressure-volume catheters. Compared with controls, inhalation of DCB230 significantly decreased baseline stroke volume, cardiac output, and stroke work. End-diastolic volume and end-diastolic pressure were also significantly reduced; however, ventricular contractility and relaxation were not changed. DCB230 also significantly increased pulmonary arterial pressure and produced hyperplasia in small pulmonary arteries. Plasma levels of C-reactive protein were significantly increased by exposure to DCB230, as were levels of heme oxygenase-1 and SOD2 in the left ventricle. Together, these data show that inhalation of EPFRs, but not silica particles, decreases baseline cardiac function in healthy rats by decreasing cardiac filling, secondary to increased pulmonary resistance. These EPFRs also produced systemic inflammation and increased oxidative stress markers in the left ventricle.

Tar Balls from Deep Water Horizon Oil Spill: Environmentally Persistent Free Radicals (EPFR) Formation During Crude Weathering

“…37 Though the large tar balls do not pose a direct threat for inhalation or ingestion, small sand particles exposed to crude oil can also contain oil-born radical species. These small sand particles can be windblown, become airborne, inhaled, or digested.…”

Ambient and household air pollution: complex triggers of disease

“…At multiple locations in the deployment environment, PM 10 and PM 2.5 levels have been shown to consistently exceed occupational and military exposure guidelines (51). In fact, levels of PM 2.5 are ϳ10-fold greater in the deployment environment than those observed at rural and urban monitoring sites in the United States (51). Geological dust, smoke from burning trash (i.e., "burn pits"), and industrial processing facilities were identified as the primary air pollution sources.…”

“…Mahne et al (51) explored the link between exposures to environmentally persistent free radicals (EPFR), a component of PM, and decreased cardiac function. Their study used healthy male Sprague-Dawley rats to demonstrate that inhalation 1,2-dichlorobenzene (an EPFR) was asociated with a decrease in stroke volume, cardiac output, and stroke work, three components of left ventricular function.…”

Environmentally Persistent Free Radicals Cause Apoptosis in HL-1 Cardiomyocytes

“…Inhalation and intratracheal instillation of EPFRs also reduces cardiac left ventricular function in otherwise healthy adult rats and attenuates the heart’s ability to compensate for ischemia reperfusion injury (7-9). These cardiac deficits are associated with systemic inflammation, oxidative stress in ventricular tissue and increased pulmonary arterial pressure (7, 8). Diesel exhaust particles (DEP), which contain EPFRs, produce endothelial damage and accelerate atherosclerotic disease in mice (10).…”