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Abstract Road traffic is an important source of urban air pollutants. Due to increasingly strict controls of exhaust emissions from road traffic, their contribution to the total emissions has strongly decreased over time in high-income countries. In contrast, non-exhaust emissions from road vehicles are not yet legislated and now make up the major proportion of road traffic emissions in many countries. Brake wear, which occurs due to friction between brake linings and their rotating counterpart, is one of the main non-exhaust sources contributing to particle emissions. Since the focus of brake wear emission has largely been on particulate pollutants, little is currently known about gaseous emissions such as volatile organic compounds from braking and their fate in the atmosphere. This study investigates the oxidative ageing of gaseous brake wear emissions generated with a pin-on-disc tribometer, using an oxidation flow reactor. The results demonstrate, for the first time, that the photooxidation of gaseous brake wear emissions can lead to formation of secondary particulate matter, which could amplify the environmental impact of brake wear emissions.

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.

A new HPLC method for the simultaneous quantitative analysis of adenosine triphosphate (ATP), adenosine diphosphate (ADP), and adenosine monophosphate (AMP) was developed and validated. ATP, ADP, and AMP were extracted from human bronchial epithelial cells with a rapid extraction procedure and separated with a C18 column (3 × 150 mm, 2.7 µm) using isocratic elution with a mobile phase consisting of 50 mM of potassium hydrogen phosphate (pH 6.80). The absorbance was monitored at 254 nm. The calibration curves were linear in 0.2 to 10 µM, selective, precise, and accurate. This method allowed us to quantify the nucleotides from two cell models: differentiated NHBE primary cells grown at the air–liquid interface (ALI) and BEAS-2B cell line. Our study highlighted the development of a sensitive, simple, and green analytical method that is faster and less expensive than other existing methods to measure ATP, ADP, and AMP and can be carried out on 2D and 3D cell models.