Cardiac and Thermoregulatory Toxicity of Residual Oil Fly Ash in Cardiopulmonary-Compromised Rats

Campen, Matthew J.; Costa, Daniel L.; Watkinson, William P.

doi:10.1080/08958370050029743

Cited by 16 publications

(14 citation statements)

References 20 publications

(33 reference statements)

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“…A possible mechanism, which has gained attention in the last few years, is that particulate matter alters the autonomic control of the heart [3]. Animal studies have shown that exposure to combustion particles can produce a reduction in heart rate variability, which reflects alterations in cardiac autonomic function that are considered a risk factor for sudden death and death from arrhythmia [36][37][38]. These data have been confirmed in humans.…”

Section: Potential Mechanismssupporting

confidence: 63%

Short‐term effects of air pollution on cardiovascular diseases: outcomes and mechanisms

Franchini¹,

Mannucci

2007

Journal of Thrombosis and Haemostasis

120

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Summary. The effects of air pollution on health have been intensively studied in recent years. Acute exposure to environmental pollutants such as particulate and gaseous matters (carbon monoxide, nitrogen oxides, sulphur dioxide and ozone) was associated with an increased rate of events and mortality because of cardiovascular diseases. These effects were investigated in short‐term studies, which related day‐to‐day variations in air pollution to disease, and in long‐term studies, which have followed cohorts of exposed individuals over time. The evidence from the literature on the short‐term cardiovascular effects of air pollutants is discussed from clinical and mechanistic points of view.

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Section: Potential Mechanismssupporting

confidence: 63%

Short‐term effects of air pollution on cardiovascular diseases: outcomes and mechanisms

Franchini¹,

Mannucci

2007

Journal of Thrombosis and Haemostasis

120

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“…A similar association has been observed in a controlled exposure study in humans (Gong et al, 2004) and in animals exposed to residual oil fly ash, a component of PM 2.5 (Campen et al, 2000;Watkinson et al, 1998;Wellenius et al, 2002).…”

supporting

confidence: 71%

Effects of Ambient Particles and Carbon Monoxide on Supraventricular Arrhythmias in a Rat Model of Myocardial Infarction

Wellenius

Coull

Batalha³

et al. 2006

Inhalation Toxicology

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The association between short-term increases in particulate air pollution and increased cardiovascular morbidity and mortality is well documented. Recent studies suggest an association between particulate matter with aerodynamic diameter < 2.5 microm (PM2.5) and supraventricular arrhythmias (SVA), but the results have been inconsistent. We evaluated this hypothesis in a rat model of acute myocardial infarction (AMI). Diazepam-sedated Sprague-Dawley rats with AMI were exposed (1 h) to either filtered air (n = 16), concentrated ambient fine particles (CAPS; mean = 645.7 microg/m3; n = 23), carbon monoxide (CO; 35 ppm; n = 19), or CAPs and CO (n = 24). Each exposure was immediately preceded and followed by a 1-h exposure to filtered air (baseline and postexposure periods, respectively). Surface electrocardiograms were recorded and the frequency of supraventricular premature beats was quantified. Among rats in the CAPS group, the probability of observing any SVA decreased from baseline to the exposure and postexposure periods. This pattern was significantly different than that observed for the filtered air group during the exposure period (p = .048) only. In the subset of rats with one or more SVA during the baseline period, the change in SVA rate from baseline to exposure period was significantly lower in the CAPS (p = .04) and CO (p = .007) groups only, as compared to the filtered air group. No significant effects were observed in the group simultaneously exposed to CAPS and CO. Thus, the results of this study do not support the hypothesis that exposure to ambient air pollution increases the risk or frequency of supraventricular arrhythmias.

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“…Healthy SD rats instilled with the highest dose (2.5 mg) of ROFA (19) demonstrated an initial 50-bpm decrease in HR, in conjunction with a 2.0°C decrease in T co (Figure 3). These Changes in core temperature in healthy mice exposed to O 3 while maintained at normal ambient temperature.…”

Section: Particulate Matter/metals Instillationmentioning

confidence: 99%

“…Healthy rats exposed via IT procedures to ROFA and other PM demonstrated significant biphasic, dose-related responses consisting of both acute (0-6 hr post-IT) and delayed (12-72 hr post-IT) bradycardia and hypothermia, accompanied by a high incidence of cardiac arrhythmias and substantial pulmonary inflammation (13,14,(17)(18)(19). Healthy SD rats instilled with the highest dose (2.5 mg) of ROFA (19) demonstrated an initial 50-bpm decrease in HR, in conjunction with a 2.0°C decrease in T co (Figure 3).…”

Section: Particulate Matter/metals Instillationmentioning

confidence: 99%

Cardiovascular and Systemic Responses to Inhaled Pollutants in Rodents: Effects of Ozone and Particulate Matter

Watkinson¹,

Campen²,

Nolan³

et al. 2001

Environmental Health Perspectives

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539Over the past decade our laboratory has been investigating the nature and extent of specific extrapulmonary responses observed in rodents following exposure to ambient pollutants and other xenobiotic agents. These responses are characterized by primary decreases in important indices of cardiac and thermoregulatory functions, along with secondary decreases in associated parameters. The summation of these effects, termed the hypothermic response (1), has both physiological and behavioral components, appears to be most pronounced in (and possibly unique to) the rodent, and may significantly impact the interpretation of experimental data and its subsequent extrapolation to the human situation. Typically, healthy adult rats may exhibit decreases in heart rate (HR) of 50-100 beats per minute (bpm) and decreases in core temperature (T co ) of 1.5-2.5°C following routine exposures to moderate levels of ambient pollutants, such as ozone (O 3 ) or particulate matter (PM). In addition, there appear to be similar, albeit related, decreases in other functional parameters, including metabolism, minute ventilation, blood pressure, and cardiac output. Furthermore, it has been demonstrated that the magnitudes of these observed decreases may be significantly modulated by changes in experimental conditions. For example, experimental stresses related to exercise, restraint, and handling, as well as the imposition of changes in ambient temperature (T a ), have all been shown to have profound effects on these responses. Finally, it has been proposed that a moderate hypothermic response may afford protection and improve survivability following toxic exposures, whereas a more severe response may actually potentiate the toxicity. Although the underlying mechanisms of the hypothermic response are still largely unexplored and unknown, preliminary experimental evidence suggests that these effects may be mediated, at least partly, via components of the parasympathetic nervous system. O 3 is a ubiquitous ambient pollutant and a known pulmonary irritant (2). In a series of earlier studies from our laboratory (3-6), we investigated both the pulmonary and systemic consequences of O 3 exposures (0.25-2.0 ppm) in rodents. With respect to nonpulmonary end points, these studies used radiotelemetry procedures to examine HR, T co , and electrocardiographic changes in rats and mice over a variety of experimental conditions. These studies were among the first to report consistent, robust concentration-related decreases in the abovementioned parameters in rodents following exposure to routine experimental levels of O 3 .More recently, the putative toxicity of PM has attracted considerable attention, and numerous epidemiological studies published over the last few years have reported a slight but consistent association between the concentration of ambient PM and the incidence of adverse health effects in man (7-12). Despite limited supporting experimental evidence, there is a growing consensus that higher levels of PM in the air are associated with in...

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Cardiac and Thermoregulatory Toxicity of Residual Oil Fly Ash in Cardiopulmonary-Compromised Rats

Cited by 16 publications

References 20 publications

Short‐term effects of air pollution on cardiovascular diseases: outcomes and mechanisms

Short‐term effects of air pollution on cardiovascular diseases: outcomes and mechanisms

Effects of Ambient Particles and Carbon Monoxide on Supraventricular Arrhythmias in a Rat Model of Myocardial Infarction

Cardiovascular and Systemic Responses to Inhaled Pollutants in Rodents: Effects of Ozone and Particulate Matter

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