In vitro effects induced by diesel exhaust at an air–liquid interface in a human lung alveolar carcinoma cell line A549

Particulate Matter Toxicity Is Nrf2 and Mitochondria Dependent: The Roles of Metals and Polycyclic Aromatic Hydrocarbons

“…54 Exposure of mice to different concentrations of PM from biodiesel burning have been found to activate the Nrf2/heme oxygenase (HO)-1 and inflammation via the nuclear factor kappa-B (NF-κB)/tumor necrosis factor (TNF)-α pathways. 49,77 In addition, exposure of endothelial cells residing at the air−liquid interface (ALI) to standard diesel exhaust PM (SRM2975) induced significant activation and nuclear translocation of Nrf2. 78 In the atmosphere, PAHs can further react and form oxygenated or nitrated derivatives by atmospheric aging processes.…”

“…It is yet to be determined whether AhR is activated in correlation with Nrf2 in lung tissue and whether this induction enhances or aggravates protection through Nrf2 signaling PAHs can also generate strong proinflammatory responses, for example, the release of the proinflammatory cytokines IL-1β, IL-6, and TNF-α from macrophages increases after exposure to PM 2.5 organic extracts 40,81,107 In addition, exposure to a PM mixture of diesel exhaust together with an urban-like pollutant mixture has been found to produce a significant IL-8 inflammatory response in A549 lung cells. 77,108 Acrolein and p-tolualdehyde (representative VOCs) elicit an inflammatory response and cellular damage in A549 cells. 109 Furthermore, mouse macrophages exposed to PAHs show induction of IL-1β, Toll-like receptor, and NF-κB, indicating an increased inflammatory response.…”

“…Furthermore, positive associations have been observed between traffic-related pollutants (PM 2.5 PAHs, black carbon, and NOx) and Nrf2-gene expression in a Los Angeles cohort (elderly subjects with coronary artery disease) . Exposure of mice to different concentrations of PM from biodiesel burning have been found to activate the Nrf2/heme oxygenase (HO)-1 and inflammation via the nuclear factor kappa-B (NF-κB)/tumor necrosis factor (TNF)-α pathways. , In addition, exposure of endothelial cells residing at the air–liquid interface (ALI) to standard diesel exhaust PM (SRM2975) induced significant activation and nuclear translocation of Nrf2 …”

Biodiesel Exhaust Toxicity with and without Diethylene Glycol Dimethyl Ether Fuel Additive in Primary Airway Epithelial Cells Grown at the Air–Liquid Interface

“…In terms of the exposure impact on epithelial cells, our results typically agree with our and others’ previous work ,,, where exposure to tallow and soy biodiesel and blends of 10–20% biodiesel in diesel also resulted in increases in the release of protein as an epithelial damage marker and/or increased expression of immune mediators IL-6 and IL-8. The mediators measured can be classified as innate immune cytokines with IL-6 being grouped as an acute-phase immune marker released in response to injury and IL-8 as a chemoattractant of various immune cells such as neutrophils, , and both cytokines are commonly found to be increased after exposure to mineral diesel exhaust in the cell, animal, and human exposures. − The observed further increase in release with the DGDME additive fuels suggests a greater immunogenic response is needed in response to a more toxic exhaust, a finding contrary to the previous DGDME toxicity study which did not measure any changes in cell viability caused by DGDME blended fuel when compared to diesel controls …”