Gasoline emissions contain high levels of pollutants, including particulate matter (PM), which are associated with several health outcomes. Moreover, due to the depletion of fossil fuels, biofuels represent an attractive alternative, particularly second-generation biofuels (B2G) derived from lignocellulosic biomass. Unfortunately, compared to the abundant literature on diesel and gasoline emissions, relatively few studies are devoted to alternative fuels and their health effects. This study aimed to compare the adverse effects of gasoline and B2G emissions on human bronchial epithelial cells. We characterized the emissions generated by propane combustion (CAST1), gasoline Surrogate, and B2G consisting of Surrogate blended with anisole (10%) (S+10A) or ethanol (10%) (S+10E). To study the cellular effects, BEAS-2B cells were cultured at air-liquid interface for seven days and exposed to different emissions. Cell viability, oxidative stress, inflammation, and xenobiotic metabolism were measured. mRNA expression analysis was significantly modified by the Surrogate S+10A and S+10E emissions, especially CYP1A1 and CYP1B1. Inflammation markers, IL-6 and IL-8, were mainly downregulated doubtless due to the PAHs content on PM. Overall, these results demonstrated that ultrafine particles generated from biofuels Surrogates had a toxic effect at least similar to that observed with a gasoline substitute (Surrogate), involving probably different toxicity pathways.

In this study, we investigated the impact of iron-rich nanoparticles derived from different locations in the subway on the innate immune system in blood. Nanoparticles were generated from Third Rail, Rail, and Wheel materials and characterized using several techniques. The response in a human whole-blood model was analyzed using ELISA and capillary immunoelectrophoresis. All nanoparticles were iron oxides, but Third Rail nanoparticles also contained Silicon and were highly thrombo-inflammatory, activating Factor XI-induced coagulation and pro-inflammatory kallikrein/kinin pathways. Wheel and Rail nanoparticles were less reactive, mainly activating the kallikrein/kinin pathway, leading to milder inflammatory reactions. The strong thrombo-inflammatory properties of Third Rail nanoparticles are attributed to their high Silicon content. None of the nanoparticles significantly activated the complement system. In conclusion, we found that the elemental composition of nanoparticles is crucial in determining whether activation leads to kallikrein/kinin system activation and bradykinin release or Factor XI activation and thrombosis.