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Inhalation Toxicology
International Forum for Respiratory Research
Volume 31, 2019 - Issue 6
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Research Articles

Smoldering and flaming biomass wood smoke inhibit respiratory responses in mice

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Pages 236-247 | Received 21 Jun 2019, Accepted 06 Aug 2019, Published online: 20 Aug 2019
 

Abstract

Background: Acute and chronic exposures to biomass wildfire smoke pose significant health risks to firefighters and impacted communities. Susceptible populations such as asthmatics may be particularly sensitive to wildfire effects. We examined pulmonary responses to biomass smoke generated from combustion of peat, oak, or eucalyptus in control and house dust mite (HDM)-allergic mice.

Methods: Mice were exposed 1 h/d for 2 consecutive days to emissions from each fuel type under smoldering or flaming conditions (∼40 or ∼3.3 mg PM/m3, respectively) while maintaining comparable CO levels (∼60–120 ppm).

Results: Control and allergic mice reduced breathing frequency during exposure to all biomass emissions compared with pre-exposure to clean air. Smoldering eucalyptus and oak, but not peat, further reduced frequency compared to flaming conditions in control and allergic groups, while also reducing minute volume and peak inspiratory flow in control mice. Several biochemical and cellular markers of lung injury and inflammation were suppressed by all biomass emission types in both HDM-allergic and control mice. Control mice exposed to flaming eucalyptus at different PM concentrations (C) and times (T) with the same C × T product had a greater decrease in breathing frequency with high concentration acute exposure compared with lower concentration episodic exposure. This decrease was ameliorated by PM HEPA filtration, indicating that the respiratory changes were partially mediated by biomass smoke particles.

Conclusion: These data show that exposure to smoldering eucalyptus or oak smoke inhibits respiratory responses to a greater degree than peat smoke. Anti-inflammatory effects of CO may possibly contribute to smoke-induced suppression of allergic inflammatory responses.

Acknowledgements

The authors thank Lisa Copeland, Rachel Grindstaff, Richard Jaskot, Todd Krantz, Allen Ledbetter, Molly Windsor, Judy Richards, and Erica Stewart for their technical assistance, and Drs Barbara Buckley and Mehdi Hazari for manuscript review. M. M. Hargrove was an Oak Ridge Institute for Science and Education (ORISE) participant with the U.S. EPA.

Disclosure statement

No potential conflict of interest was reported by the authors.

Data availability

Data supporting the results and analyses from the published paper will be available on the Environmental Dataset Gateway of the U.S. EPA: https://edg.epa.gov/metadata/catalog/main/home.page. The DOI 10.23719/1503946 has been reserved for the data and will be active when the publication process is complete and a public page for the dataset has been generated.

Disclaimer

The research described in this article has been reviewed by the National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency and approved for publication. Approval does not signify that the contents necessarily reflect the views or the policies of the Agency nor does mention of trade names or commercial products constitute endorsement or recommendation for use.

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