Year of Award

2020

Document Type

Professional Paper

Degree Type

Master of Science (MS)

Degree Name

Health and Human Performance (Exercise Science Option)

Department or School/College

School of Integrative Physiology and Athletic Training

Committee Chair

John Quindry

Commitee Members

Brent Ruby, Christopher Migliaccio

Keywords

PM, CVD, Oxidative Stress, Wildland Firefighting

Publisher

University of Montana

Subject Categories

Cardiovascular Diseases

Abstract

The presentation of cardiovascular disease (CVD) and comorbidities in aging and retired wildland firefighters (WLFF) continues to be one of the top health priorities to address by The United States Forest Service. In the past 20 years, experts at multiple meetings and conferences have confronted this growing concern as a formal call to action to investigation the individual components related to working in the wildland fire setting. The inhalation of wood smoke particulate matter (PM) shows evidence of altering homeostasis in WLLF’s in the areas of oxidative stress, inflammation, and arterial stiffness, all of which contribute to the development of (CVD).

To date, comprehensive investigation into the dose response of wood smoke PM and subsequent cardiovascular outcomes remains under studied. Emphasis on a wood smoke PM dose response is based on the inclusion of key variables measuring the size, concentration, sources, and inhalation rate of PM. The literature investigating wood smoke PM induced phycological changes is significantly lack in comparison to the reach studying anthropogenic PM and pollution. Recently, published studies in both field experiments and laboratory simulations provide new insight on how the PM dose of acute exposures alters normative cardiovascular function. There is a growing consensus within the scientific community of wood smoke PM inducing oxidative stress, upregulating inflammatory markers, and elevating pulmonary and systemic inflammation. At this time, fluctuations in autonomic nervous system control of heart rate and vascular tone do not warrant the same strength of confidence as the direct influence of wood smoke PM inhalation. Furthermore, the concentrations, volumes, PM size, and ventilation rates are contextual to each individual dose. What is true in one scenario cannot be extrapolated all wood smoke PM exposures and settings.

Based on the findings of this academic exercise, we recommend that future scientific investigations in this area implement directed dose-response methodology, in combination with clinically relevant outcome measures, in order to determine the effects from multiple PM smoke exposures on the development of CVD aging and pathology.

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© Copyright 2020 Dylan Richmond, John Quindry, Christopher T. Migliaccio, and Brent Ruby