Abstract
Increasing frequency and intensity of climate-driven wildfires in recent years have resulted in increased human exposures to wildfire smoke and raised serious public health concerns. One potential risk of wildfire smoke exposure is the impairment that it may cause to lung macrophages, which serve as the first line of defense against inhaled pathogens and particles. Size-fractionated wildfire particulate matter (WFPM) collected in the New Jersey/New York metropolitan area during the June 2023 Canadian wildfire event was used to assess the effect on the health and function of THP-1 lung macrophages. Environmentally relevant in vitro WFPM doses were determined using established in vivo and in vitro dosimetry models. Exposure to WFPM(0.1-2.5) (0.1-2.5 μm) for 24 h caused a significant (∼15%) increase in reactive oxygen species, indicating oxidative stress. More importantly, exposure to either WFPM(0.1) (≤0.1 μm) or WFPM(0.1-2.5) significantly reduced THP-1 lung macrophage viability. Additionally, 24 h exposure to either of the WFPM fractions reduced phagocytosis of unopsonized 1 μm polystyrene beads by approximately 50%, which appeared to be due to a defect in binding, which could in turn be a result of scavenger receptor blockade by WFPM or diminished viability and thus ATP depletion, depriving the macrophages of energy required to perform phagocytosis. Together, these findings suggest that WFPM exposure could impair lung macrophage health and function, which could increase susceptibility to respiratory infections. Further mechanistic in vitro and in vivo studies are warranted to better understand the impacts of WFPM on lung innate immunity and the risk of pulmonary infection.