Air pollution is an environmental health concern throughout the world, and is responsible for an estimated 1 out of 8 deaths. As a common component of air pollution, particulate matter (PM) is one of six criteria air pollutants regulated by the Environmental Protection Agency (EPA), with existing ambient standards for both 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). Previous studies show that PMc can induce health effects such as increased inflammation, and may be more detrimental to susceptible populations when directly compared to PM2.5. These differences in adverse health effects following exposures are not only influenced by the sizes of the particles, but may also be influenced by other factors including PM composition (chemical and biogenic), source and season. Globally, biomass burning is a significant source of air pollution. Wood smoke is generated from residential home heating (wood stoves) during the winter months, from burning biomass fuels for cooking (cook stoves), from forest fires during the summer months, and from prescribed/controlled burns during the fall and spring. Wood smoke emissions lead to exposures in both the indoor and ambient environments. Further, regional forest fires can present significant PM exposures to firefighting personnel during occupational activities. Previous wood smoke exposure studies suggest both acute and chronic detriments, both in the lung, and systemically. However, there is still much to be learned about how wood smoke impacts human health, including investigating relationships between different emission sources, acute and chronic exposures, and resultant health effects. Through three Aims, this project evaluated how different types of PM influenced inflammation and other health measures through both cell studies and a human exposure study. In Aim 1, significant effects were observed in cell studies where PMc was more pro-inflammatory compared to PM2.5. As determined in Aim 2, wood smoke source also played a role in the pro-inflammatory outcome. Results from Aim 2 revealed that wildfire smoke induced significantly more pro-inflammation compared to residential wood stove emissions. Finally, the Aim 3 human exposure study was designed to replicate wood smoke exposures to wildland firefighters during occupational activities. Through a 10-person crossover exposure trial, we evaluated the potential effects of increasing wood smoke exposure on pulmonary and oxidative stress markers in both plasma and exhaled breath condensate. Dose-response relationships in some of the measured markers were observed, including significant changes in pH, 8-isoprostane, and pentraxin-3 (PTX3). The PTX3 findings suggest that it may be a particularly sensitive acute phase protein to be investigated in future controlled and field studies related to smoke exposures. The development of this wood smoke inhalational facility will further research into acute and chronic health impacts of wood smoke exposure, and in the future provide a platform to address unique research questions related to wood smoke exposures and associated adverse health effects.