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

Abstract

BackgroundWe tested the hypothesis that cardiovascular responses to PM2.5 exposure will be enhanced in hypertensive rats and linked to specific carbonaceous pollutants in an urban industrial setting.MethodsSpontaneously hypertensive rats were exposed by inhalation to concentrated PM2.5 in an industrial area of Dearborn, Michigan, for four consecutive summer days. Blood pressure (BP), heart rate (HR) and HR variability (HRV) metrics (SDNN, RMSSD) were assessed by radiotelemetry and compared to 1 h- and 8 h-averaged fluctuations in PM2.5 composition, with a focus on elemental and organic carbon (EC and OC, respectively), and temperature-resolved subfractions (EC1-EC5, PC (pyrolized carbon), and OC1-OC4), as well as other major and minor PM components.ResultsMean HR and BP were increased, while HRV was decreased over 4 days of exposure. Using 1 h averages, EC (1 μg/m3 increase) was associated with increased HR of 11-32 bpm (4-11% increase), 1.2-1.5 ms (22-27%) decreases in SDNN, 3-14 mmHg (1.5-8%) increases in systolic BP, and 5-12 mmHg (4-9%) increases in diastolic BP. By comparison, associations with OC were negligible. Using 8 h averages, EC subfractions were linked with increased heart rate (EC1: 13 bpm; EC2, EC3, PC: <5 bpm) and SDNN (EC1> > EC2 > EC3, EC4, PC), but with decreased RMSSD (EC2, EC5 > EC3, EC4). Minimal effects were associated with OC and OC1. Associations between carbon subfractions and BP were negligible. Associations with non-carbonaceous components and trace elements were generally non-significant or of negligible effect size.ConclusionsThese findings are the first to describe associations between acute cardiovascular responses and thermally resolved carbon subfractions. We report that cardiovascular responses to PM2.5 carbonaceous materials appear to be driven by EC and its EC1 fraction.

Long‐Term Exposure of Fine Particulate Matter Causes Hypertension by Impaired Renal D 1 Receptor–Mediated Sodium Excretion via Upregulation of G‐Protein–Coupled Receptor Kinase Type 4 Expression in Sprague‐Dawley Rats

“…Epidemiological studies have shown that traffic or household PM 2.5 exposure can increase blood pressure in both the short‐ and long‐term. Many animal experimental studies have validated the view of the above‐mentioned evidence‐based‐studies . In this study, PM 2.5 was confirmed to be associated with increased blood pressure, and the blood pressure was positively correlated with the exposure dose within a certain range.…”

“…Many animal experimental studies have validated the view of the above-mentioned evidence-based-studies. 8,31,[52][53][54] In this study, PM 2.5 was confirmed to be associated with increased blood pressure, and the blood pressure was positively correlated with the exposure dose within a certain range. Even a lower concentration of PM 2.5 exposure can cause an increased blood pressure.…”

Ambient Air Pollution and Risk of Gestational Hypertension

“…to PM 2.5 exposure is driven mostly by elemental carbon and its fractions (28). In addition, concentrated dust-storm particles induce adverse cardiovascular effects on spontaneously hypertensive rats, suggesting its toxic nature (29).…”

Mitochondrial damage: An important mechanism of ambient PM2.5 exposure-induced acute heart injury in rats

“…The care and use of the animals reported in this study was approved by the Institutional Animal Care and Use Committee of Shanxi University. 5 …”

“…People are widely exposed to PM 2.5 mostly originated from coal combustion, vehicle exhaust, construction and agricultural pollution [1]. Recently, epidemiological studies have demonstrated that short-and long-term exposures to PM 2.5 are associated with cardiovascular diseases [2][3][4], while laboratory investigations have showed that PM 2.5 may induce mammal cardiovascular dysregulation and heart failure [5][6].…”