Southern, D; Hellier, P; Talibi, M; Leonard, MO; Ladommatos, N; (2021) Re-assessing the toxicity of particles from biodiesel combustion: A quantitative analysis of in vitro studies. Atmospheric Environment , 261 , Article 118570. 10.1016/j.atmosenv.2021.118570.

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Abstract

Biofuels may reduce road transport carbon intensity; however, it is uncertain whether displacing fossil diesel would alter the engine-derived particulate toxicity. The primary objective of this work was to determine whether there is a fuel effect on the comparative in vitro toxicity of biodiesel exhaust particulates relative to those from fossil diesel. A secondary aim was to determine qualitatively whether the observed outcome is related to the organic phase, namely Polycyclic Aromatic Hydrocarbons (PAHs). In vitro and acellular exposure studies were recovered from a literature survey following the PRISMA framework. Biological responses attributable to biodiesel and paired fossil diesel particles, including particle-extracts were selected. To qualify for inclusion, either of the paired responses must differ statistically significantly (p < 0.05) from the control or each other. Paired responses were assigned to one-of-five categories which best represents the pathophysiological role of the biomarker: inflammation, oxidative stress, cytotoxicity, genotoxicity and mutagenicity. Biodiesel reduced particle toxicity in two-thirds of paired responses, however, there were large differences between biodiesels for category-specific biomarkers. Particles derived from Rapeseed oil Methyl Ester (RME) were less inflammatory, whereas Soybean oil Methyl Ester (SME) particles were more inflammatory than fossil diesel on average. Conversely, SME reduced oxidative stress while few trends emerged for mutagenicity and genotoxicity. The largest fuel effect was observed for cytotoxicity: Waste Cooking Oil Methyl Ester (WCOME) increased and Palm oil Methyl Ester (PME) decreased particle cytotoxicity. Particle-phase PAH emissions compiled on a mass-of-soot basis also followed this trend, however, literature focusing on both these aspects is limited; careful consideration of fuel composition and use of normal primary human cell types and omics technologies, could resolve this open question. This assessment systematically compares biological responses from particulate only exposure, with co-exposure necessarily excluded due to an absence of understanding of how gaseous components modify particulate toxicity.

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