Peat smoke inhalation alters blood pressure, baroreflex sensitivity, and cardiac arrhythmia risk in rats

ABSTRACT

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.

KEYWORDS:

• Wildland fire air pollution
• peat biomass smoke
• cardiovascular
• blood pressure
• baroreceptor sensitivity

Acknowledgments

The authors would like to thank Dr. Colette Miller and Dr. Jason Sacks of the U.S. EPA for their thorough review of this manuscript prior to submission. The authors would also like to thank Judy Richards of the U.S. EPA for her excellent technical assistance.

Availability of data and material

All data (i.e. individual values used to generate means and standard deviations presented in the tables and figures reported in this manuscript) will be made available on the U.S. E.P.A. public data repository located at https://catalog.data.gov/harvest/epa-sciencehub

Disclosure of interest

The authors report no conflict of interest.

Disclaimer

This manuscript has been reviewed by the Center for Public Health and Environmental Assessment, United States Environmental Protection Agency and approved for publication. Approval does not signify that the contents necessarily reflect the views and policies of the Agency nor does mention of trade names or commercial products constitute endorsement or recommendation for use.

Supplementary material

Supplemental data for this article can be accessed on the publisher’s website.

Additional information

Funding

This work was supported by the intramural research program of the Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC.