Lung function measures following simulated wildland firefighter exposures.

Across the world, biomass smoke is a major source of air pollution and is linked with a variety of adverse health effects. This is particularly true in the western U.S. where wood smoke from wildland forest fires are a significant source of PM2.5. Wildland firefighters are impacted as they experience elevated PM2.5 concentrations over extended periods of time, often occurring during physical exertion. Various epidemiological studies have investigated wood smoke impacts on human health, including occupational field exposures experienced by wildland firefighters. As there are numerous challenges in carrying out these field studies, having the ability to research the potential health impacts to this occupational cohort in a controlled setting would provide important information that could be translated to the field setting. To this end, we have carried out a simulated wildland firefighter exposure study in a wood smoke inhalation facility. Utilizing a randomized crossover trial design, we exposed 10 participants once to clean filtered-air, 250 µg/m3, and 500 µg/m3 wood stove-generated wood smoke PM2.5. Participants exercised on a treadmill at an absolute intensity designed to simulate wildland firefighting for 1.5 hr. In addition to measured PM2.5 smoke concentrations, mean levels of CO2, CO, and % relative humidity were continuously monitored and recorded and were representative of occupational "real-world" exposures. Pulmonary function was measured at three time points: before, immediately after, and 1-hr post-exposure. Although there were some reductions in FVC, FEV1, and FVC:FEV1 measures, results of the spirometry testing did not show significant changes in lung function. The development of this wood smoke inhalational facility provides a platform to further address unique research questions related to wood smoke exposures and associated adverse health effects.

Measured Pulmonary and Systemic Markers of Inflammation and Oxidative Stress Following Wildland Firefighter Simulations.

OBJECTIVE: A controlled human exposure study was conducted to investigate the impact of inhalational exposures to wood smoke PM2.5 on measured concentrations of airway and systemic inflammatory biomarkers. METHODS: Mimicking wildland firefighter activities, 10 participants were exposed to three doses of wood smoke PM2.5 (filtered-air, 250 µg/m, and 500 µg/m) while exercising on a treadmill. Exhaled breath condensate (EBC) and blood plasma samples were obtained pre-, immediately post-, and 1-hour postexposure. 8-isoprostane, pH, and myeloperoxidase were measured in EBC, while H2O2, surfactant protein D, and pentraxin-3 (PTX3) were measured in both EBC and plasma. RESULTS: Only pH, 8-isoprostane, and PTX3 displayed significant changes when comparing pre- and postexposures. CONCLUSIONS: Markers of inflammation and oxidative stress, including PTX3, pH, and 8-isoprostane in EBC and/or plasma, are sensitive to wood smoke inhalation, with further investigations warranted.

Comparison of how ambient PMc and PM2.5 influence the inflammatory potential.

Airborne particulate matter (PM) is one of the six criteria air pollutants currently regulated by the U.S. Environmental Protection Agency (EPA), with existing ambient standards for PM2.5 and PM10. Currently there are no health-based regulations for the size fraction between 2.5 and 10 µm, commonly known as the coarse fraction (PMc). The present study investigates current gaps in knowledge for PMc including exposure toxicity and PM ratios (PMc:PM2.5) in PM10. Throughout the world, all the three PM size fractions have been shown to be associated with adverse impacts. Recent studies have shown that PMc can be more detrimental to susceptible populations when directly compared to PM2.5, and that the PMc fraction in PM10 can account for the majority of the inflammatory response from PM10 exposure. In our studies we utilized a bone marrow-derived mouse macrophage in vitro system to compare the inflammatory potential of PMc, PM2.5 and mixtures of the two. The result was a linear increase in interleukin(IL) -1ß with increasing levels of exposure to winter and summer PMc, as compared to PM2.5, which exhibited logarithmic growth. Also, exposure to PM10 as a function of PM2.5 and PMc mass ratios showed that IL-1ß and TNF-α levels increased synergistically with a greater burden of PMc. Endotoxin content in the PM did not correlate with these results, suggesting that other activators in PMc are likely responsible for activating the NF-κB pathway and the inflammasome.