Abstract
BackgroundEpidemiological studies have linked exposures to ambient fine particulate matter (PM2.5) and traffic with autonomic nervous system imbalance (ANS) and cardiac pathophysiology, especially in individuals with preexisting disease. It is unclear whether metabolic syndrome (MetS) increases susceptibility to the effects of PM2.5. We hypothesized that exposure to traffic-derived primary and secondary organic aerosols (P + SOA) at ambient levels would cause autonomic and cardiovascular dysfunction in rats exhibiting features of MetS. Male Sprague Dawley (SD) rats were fed a high-fructose diet (HFrD) to induce MetS, and exposed to P + SOA (20.4 ± 0.9 μg/m3) for 12 days with time-matched comparison to filtered-air (FA) exposed MetS rats; normal diet (ND) SD rats were separately exposed to FA or P + SOA (56.3 ± 1.2 μg/m3).ResultsIn MetS rats, P + SOA exposure decreased HRV, QTc, PR, and expiratory time overall (mean effect across the entirety of exposure), increased breathing rate overall, decreased baroreflex sensitivity (BRS) on three exposure days, and increased spontaneous atrioventricular (AV) block Mobitz Type II arrhythmia on exposure day 4 relative to FA-exposed animals receiving the same diet. Among ND rats, P + SOA decreased HRV only on day 1 and did not significantly alter BRS despite overall hypertensive responses relative to FA. Correlations between HRV, ECG, BRS, and breathing parameters suggested a role for autonomic imbalance in the pathophysiologic effects of P + SOA among MetS rats. Autonomic cardiovascular responses to P + SOA at ambient PM2.5 levels were pronounced among MetS rats and indicated blunted vagal influence over cardiovascular physiology.ConclusionsResults support epidemiologic findings that MetS increases susceptibility to the adverse cardiac effects of ambient-level PM2.5, potentially through ANS imbalance.
Highlights
Epidemiological studies have linked exposures to ambient fine particulate matter (PM2.5) and traffic with autonomic nervous system imbalance (ANS) and cardiac pathophysiology, especially in individuals with preexisting disease
To further explore whether metabolic syndrome (MetS) increases susceptibility to PM2.5, we investigated the pathophysiologic effects of repeated exposure to trafficderived PM2.5 at ambient levels in a rat model of MetS characterized by hypertension, hypertriglyceridemia, hyperglycemia, and insulin resistance induced by 8-week dietary fructose supplementation [6, 9, 10]
At the conclusion of the study, air-exposed MetS rats had hyperglycemia relative to a historic range for normal diet-fed male Sprague Dawley rats at a corresponding age of 20 weeks (50– 135 mg/dL), with no additional effect of P + primary and secondary organic aerosols (SOA)
Summary
Epidemiological studies have linked exposures to ambient fine particulate matter (PM2.5) and traffic with autonomic nervous system imbalance (ANS) and cardiac pathophysiology, especially in individuals with preexisting disease. It is unclear whether metabolic syndrome (MetS) increases susceptibility to the effects of PM2.5. We hypothesized that exposure to traffic-derived primary and secondary organic aerosols (P + SOA) at ambient levels would cause autonomic and cardiovascular dysfunction in rats exhibiting features of MetS. Preexisting cardiovascular disease and diabetes strengthen the link between PM2.5 exposure and acute cardiac events such as arrhythmia, cardiac arrest, and heart failure decompensation [1]. The dose-effect relationship for PM2.5-induced cardiac pathophysiology, its modifying factors, and the underlying mechanisms at real-world exposure levels remain unresolved. In MetS subjects researchers have found exaggerated cardiovascular inflammation [3] as well as increased BP and altered heart rate variability (HRV) in association with moderate increases in PM2.5, suggesting pathogenic sympathetic nervous system dominance, a state of enhanced sympathetic influence relative to opposing parasympathetic influences over the cardiovascular system [4, 5]
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