Divergent Electrocardiographic Responses to Whole and Particle-Free Diesel Exhaust Inhalation in Spontaneously Hypertensive Rats

Abstract

Diesel exhaust (DE) is a major contributor to traffic-related fine particulate matter (PM)(2.5). Although inroads have been made in understanding the mechanisms of PM-related health effects, DE's complex mixture of PM, gases, and volatile organics makes it difficult to determine how the constituents contribute to DE's effects. We hypothesized that exposure to particle-filtered DE (fDE; gases alone) will elicit less cardiac effects than whole DE (wDE; particles plus gases). In addition, we hypothesized that spontaneously hypertensive (SH) rats will be more sensitive to the electrocardiographic effects of DE exposure than Wistar Kyoto rats (WKY; background strain with normal blood pressure). SH and WKY rats, implanted with telemeters to monitor electrocardiogram and heart rate (HR), were exposed once for 4 h to 150 μg/m(3) or 500 μg/m(3) of wDE (gases plus PM) or fDE (gases alone) DE, or filtered air. Exposure to fDE, but not wDE, caused immediate electrocardiographic alterations in cardiac repolarization (ST depression) and atrioventricular conduction block (PR prolongation) as well as bradycardia in SH rats. Exposure to wDE, but not fDE, caused postexposure ST depression and increased sensitivity to the pulmonary C fiber agonist capsaicin in SH rats. The only notable effect of DE exposure in WKY rats was a decrease in HR. Taken together, hypertension may predispose to the potential cardiac effects of DE and components of DE may have divergent effects with some eliciting immediate irritant effects (e.g., gases), whereas others (e.g., PM) trigger delayed effects potentially via separate mechanisms.

Cardiovascular Depression in Rats Exposed to Inhaled Particulate Matter and Ozone: Effects of Diet-Induced Metabolic Syndrome

“…Similar ECG results have been reported with bradycardia during inhalation of diesel exhaust or metal-rich PM (Farraj et al 2011; Lamb et al 2012). Although we did not assess electrical conduction in the present study, exposures to O 3 , PM 2.5 , or O 3 + PM 2.5 may initiate ECG alterations that were further modified in HFrD rats to decrease heart rate.…”

“…Inhalation exposure–induced depression of HR in rodents has been documented for O 3 (Farraj et al 2012; Uchiyama and Yokoyama 1989), diesel exhaust (Lamb et al 2012), and ambient PM 2.5 (Kamal et al 2011). Furthermore, acute exposure of laboratory rodents to O 3 (Uchiyama and Yokoyama 1989) or ambient PM 2.5 (Cheng et al 2003) also triggers a drop in BP, suggesting that inhalation of a variety of airborne toxicants can lead to cardiovascular depression in laboratory animals.…”

PM2.5-induced cardiovascular dysregulation in rats is associated with elemental carbon and temperature-resolved carbon subfractions

“…It is notable, therefore, that the adverse cardiovascular responses we describe for EC and its subfractions are consistent with HR, HRV and BP responses reported during controlled exposures to whole diesel engine exhaust in the same SH strain of rats we used in the current study [27,28]. While major components of laboratory-generated diesel exhaust are gaseous inorganic compounds (nitrogen oxides, sulfur dioxide, and carbon monoxide), the minor components of particulate EC and of volatile and semivolatile organic compounds (OC) have been linked to stimulation of both sympathetic and parasympathetic cardiovascular effects in SH rats where exposures compared whole versus filtered exhaust [29,30]. A major difference in our field studies compared to laboratory-generated diesel engine exhaust is the atmospheric transformation of EC core particulates that might result in surface adherence of volatile organic hydrocarbons such as carbonyls, or in oxidative modifications that alter the particle’s toxicity [31,32].…”

Photochemically Altered Air Pollution Mixtures and Contractile Parameters in Isolated Murine Hearts before and after Ischemia

“…We have previously exposed cultured lung cells to similar multipollutant mixtures in the photochemical reaction chamber and showed that gaseous products elicited biological and biochemical responses in the absence of particles (Sexton et al 2004). Furthermore, animal studies have shown that spontaneously hypertensive and mildly cardiomyopathic rats exposed to filtered diesel exhaust exhibited either a similar degree or a greater magnitude of electrophysiological changes compared with exposure to whole diesel exhaust (Carll et al 2012; Lamb et al 2012), implying that gaseous components of air pollution might be driving the cardiovascular effects.…”