Replication Data for: Burn pit smoke condensate-mediated toxicity in human bronchial epithelial cells

Objective: Burn pits are a method of open-air waste management that were common during military operations in Iraq, Afghanistan, and other regions in Southwest Asia. Veterans returning from deployment have reported respiratory symptoms, potentially from exposure to burn pit smoke, yet studies linking burn pit smoke with pulmonary toxicity are lacking. We have previously shown that exposures to condensates from burn pit smoke emissions cause inflammation and cytotoxicity in lung of mice. In this study, we explored the effects of burn pit smoke condensates on human bronchial epithelial cells (HBEC), to understand their impact on cellular targets in human lung. Methods: HBECs were cultured at air-liquid interface (ALI) and exposed to burn pit waste (plywood, cardboard, plastic, mixed, and mixed with diesel) smoke condensates, generated under smoldering and flaming conditions. Cytotoxicity was evaluated by measuring transepithelial electrical resistance (TEER) and lactate dehydrogenase (LDH) release; toxicity scores were quantified for each exposure. Pro-inflammatory cytokine release (Meso Scale Discovery) and modulation of gene expression (Fluidigm) were examined for cardboard and plastic condensate exposures. Results: Burn pit smoke condensates generated under flaming conditions caused severe effects on cell viability, with flaming mixed waste and plywood exhibiting highest toxicity scores. Secretion of tumor necrosis factor (TNF) alpha was reduced by exposure to all burn pit smoke condensates. Expression of detoxifying enzymes (aldehyde dehydrogenase, cytochrome P450) were reduced by several condensates. Conclusions: Exposure to burn pit smoke causes adverse effects on airway epithelial cells, which has the potential to impair pulmonary health. Aberrant cytokine and chemokine secretion and altered gene expression profiles following exposure to condensates suggests that veterans who were exposed to burn pit smoke may be susceptible to airway disease development.