Ozone co-exposure modifies cardiac responses to fine and ultrafine ambient particulate matter in mice: concordance of electrocardiogram and mechanical responses

Abstract

BackgroundStudies have shown a relationship between air pollution and increased risk of cardiovascular morbidity and mortality. Due to the complexity of ambient air pollution composition, recent studies have examined the effects of co-exposure, particularly particulate matter (PM) and gas, to determine whether pollutant interactions alter (e.g. synergistically, antagonistically) the health response. This study examines the independent effects of fine (FCAPs) and ultrafine (UFCAPs) concentrated ambient particles on cardiac function, and determine the impact of ozone (O3) co-exposure on the response. We hypothesized that UFCAPs would cause greater decrement in mechanical function and electrical dysfunction than FCAPs, and that O3 co-exposure would enhance the effects of both particle-types.MethodsConscious/unrestrained radiotelemetered mice were exposed once whole-body to either 190 μg/m3 FCAPs or 140 μg/m3 UFCAPs with/without 0.3 ppm O3; separate groups were exposed to either filtered air (FA) or O3 alone. Heart rate (HR) and electrocardiogram (ECG) were recorded continuously before, during and after exposure, and cardiac mechanical function was assessed using a Langendorff perfusion preparation 24 hrs post-exposure.ResultsFCAPs alone caused a significant decrease in baseline left ventricular developed pressure (LVDP) and contractility, whereas UFCAPs did not; neither FCAPs nor UFCAPs alone caused any ECG changes. O3 co-exposure with FCAPs caused a significant decrease in heart rate variability when compared to FA but also blocked the decrement in cardiac function. On the other hand, O3 co-exposure with UFCAPs significantly increased QRS-interval, QTc and non-conducted P-wave arrhythmias, and decreased LVDP, rate of contractility and relaxation when compared to controls.ConclusionsThese data suggest that particle size and gaseous interactions may play a role in cardiac function decrements one day after exposure. Although FCAPs + O3 only altered autonomic balance, UFCAPs + O3 appeared to be more serious by increasing cardiac arrhythmias and causing mechanical decrements. As such, O3 appears to interact differently with FCAPs and UFCAPs, resulting in varied cardiac changes, which suggests that the cardiovascular effects of particle-gas co-exposures are not simply additive or even generalizable. Additionally, the mode of toxicity underlying this effect may be subtle given none of the exposures described here impaired post-ischemia recovery.Electronic supplementary materialThe online version of this article (doi:10.1186/s12989-014-0054-4) contains supplementary material, which is available to authorized users.

TRPA1 mediates changes in heart rate variability and cardiac mechanical function in mice exposed to acrolein

“…The data presented here also suggests that a single exposure to gaseous irritant pollutants causes not only cardiac electrical disturbances, which are commonly observed in humans (Peters et al, 2000), but acute, nearly imperceptible changes in cardiac mechanical function as well; these findings corroborate not only our previous work (Kurhanewicz et al, 2014) but the work of others (Tong et al, 2010). More importantly, the current study confirms that gaseous air pollutants have effects beyond the respiratory system affecting not only cardiac function but also the homeostatic control of the cardiovascular system as indicated by changes in HRV.…”

“…Acrolein produced abnormal modulation of autonomic balance and an increased incidence of arrhythmia through TRPA1, which also mediated an increase in LVDP. In contrast, exposure to ozone did not appear to cause any significant effects despite the fact that mild cardiovascular effects of ozone at similar levels have been documented by our lab in the past and by others (Barath et al, 2013; Farraj et al, 2012; Farraj et al, 2015; Kurhanewicz et al, 2014; Wang et al, 2013; Wu et al, 2010). …”

Inhalation of printer-emitted particles impairs cardiac conduction, hemodynamics, and autonomic regulation and induces arrhythmia and electrical remodeling in rats

“…Thus, declines in both EjeT and CtrI suggested that PEPs exposure may impair contractility despite HRV indicating enhanced sympathetic influence. These findings accord with the negative inotropic effects of exposures at > 2-fold higher PM concentrations of carbon black [33,34], diesel exhaust [31], or concentrated ambient PM [69], which may decrease cardiac output while inducing catecholamine surges to provoke hypertension, pulmonary edema, and intracellular signaling toward cardiac remodeling [65]. Accordingly, PEPs impaired contractility indices during exposure especially on day 21, but these effects rapidly dissipated immediately after exposure when systolic pressure increased-potentially through neurohormonal compensation.…”

Effect of Vitamin E and Omega-3 Fatty Acids on Protecting Ambient PM2.5-Induced Inflammatory Response and Oxidative Stress in Vascular Endothelial Cells

“…Air pollutants, especially ambient PM 2.5 , have become important risk factor in the development of cardiovascular diseases. Epidemiological survey has confirmed an association between PM 2.5 and increased risk of cardiovascular morbidity and mortality [ 16 ]. Recent study has reported that ambient PM 2.5 exposures independently induced acute systemic inflammatory responses [ 17 ].…”