Citation:

Martin, B., L. Thompson, Y. Kim, C. King, S. Snow, Mette C. Schladweiler, Najwa Haykal Coates, I. George, Ian Gilmour, U. Kodavanti, M. Hazari, AND A. Farraj. Peat Smoke Inhalation Alters Blood Pressure, Baroreflex Sensitivity and Cardiac Arrhythmia Risk in Rats. JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH - PART A: CURRENT ISSUES. Taylor & Francis, Inc., Philadelphia, PA, 83(23-24):748-763, (2020). https://doi.org/10.1080/15287394.2020.1826375

Impact/Purpose:

This report describes a study that examined the concentration-dependent cardiovascular impacts of exposure to peat smoke, an important wildland fire air pollution source. Measures of blood pressure, heart rate, cardiac arrhythmogenic risk, and systemic inflammation were combined with assessment of baroreceptor function, a measure of homeostatic control of blood pressure. Exposure to peat smoke caused significant changes in heart rate, systolic and diastolic blood pressure, sensitivity to aconitine-induced cardiac arrhythmia, and systemic mediators of inflammation and injury. Importantly, some of these effects were accompanied by increased baroreceptor gain, indicating dysregulation of the baroreflex and a potential role for autonomic modulation in mediating such responses. In addition, exposure to low peat caused cardiovascular responses that were qualitatively distinct from effects with high peat, effects likely driven by differences in particle size and composition among exposure concentrations. Increased understanding of the biological mechanisms and physicochemical determinants that drive toxicity of a key air pollution source may increase confidence in epidemiological findings and in turn help reduce uncertainty in standard setting.

Description:

Wildland fires (WF) are linked to adverse health impacts related to poor air quality. The cardiovascular impacts of emissions from specific biomass sources are however unknown. The purpose of this study was to assess the cardiovascular impacts of a single exposure to peat smoke, a key regional WF air pollution source, and relate these to baroreceptor sensitivity and inflammation. Three-month-old male Wistar-Kyoto rats, implanted with radiotelemeters for continuous monitoring of heart rate (HR), blood pressure (BP), and spontaneous baroreflex sensitivity (BRS), were exposed once, for 1-hr, to filtered air or low (0.38 mg/m3 PM) or high (4.04 mg/m3) concentrations of peat smoke. Systemic markers of inflammation and sensitivity to aconitine-induced cardiac arrhythmias, a measure of latent myocardial vulnerability, were assessed in separate cohorts of rats 24 hr after exposure. PM size (low peat = 0.4–0.5 microns vs. high peat = 0.8–1.2 microns) and proportion of organic carbon (low peat = 77% vs. high peat = 65%) varied with exposure level. Exposure to high peat and to a lesser extent low peat increased systolic and diastolic BP relative to filtered air. In contrast, only exposure to low peat elevated BRS and aconitine-induced arrhythmogenesis relative to filtered air and increased circulating levels of low-density lipoprotein cholesterol, complement components C3 and C4, angiotensin-converting enzyme (ACE), and white blood cells. Taken together, exposure to peat smoke produced overt and latent cardiovascular consequences that were likely influenced by physicochemical characteristics of the smoke and associated adaptive homeostatic mechanisms.

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