Combustion of biodiesels in place of fossil diesel (FD) has been proposed as a method of reducing transport-related toxic emissions in Europe. While biodiesel exhaust (BDE) contains fewer hydrocarbons, total particulates and carbon monoxide than FD exhaust (FDE), its high nitrogen oxide and ultrafine particle content may still promote pulmonary pathophysiologies. Using a complement of in vitro and in vivo studies, this review documents progress in our understanding of pulmonary responses to BDE exposure. Focusing initially on hypothesis-driven, targeted analyses, the merits and limitations of comparing BDE-induced responses to those caused by FDE exposure are discussed within the contexts of policy making and exploration of toxicity mechanisms. The introduction and progression of omics-led workflows are also discussed, summarising the novel insights into mechanisms of BDE-induced toxicity that they have uncovered. Finally, options for the expansion of BDE-related omics screens are explored, focusing on the mechanistic relevance of metabolomic profiling and offering rationale for expansion beyond classical models of pulmonary exposure. Together, these discussions suggest that molecular profiling methods have identified mechanistically informative, novel and fuel-specific signatures of pulmonary responses to biodiesel exhaust exposure that would have been difficult to detect using traditional, hypothesis driven approaches alone.

中文翻译：

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组学方法阐明生物柴油引起的肺毒性机制的潜力

在欧洲，有人提出用燃烧生物柴油代替化石柴油（FD）作为减少运输相关有毒物质排放的方法。虽然生物柴油废气 (BDE) 比 FD 废气 (FDE) 含有更少的碳氢化合物、总颗粒物和一氧化碳，但其高氮氧化物和超细颗粒含量仍可能促进肺部病理生理学。本综述利用体外和体内研究的补充，记录了我们对接触 BDE 的肺部反应的理解进展。首先侧重于假设驱动的有针对性的分析，在政策制定和毒性机制探索的背景下讨论了比较 BDE 引起的反应与 FDE 暴露引起的反应的优点和局限性。还讨论了组学主导的工作流程的引入和进展，总结了他们发现的对 BDE 诱导毒性机制的新见解。最后，探讨了扩展 BDE 相关组学筛选的选项，重点关注代谢组学分析的机制相关性，并为超越经典肺部暴露模型的扩展提供了基本原理。总之，这些讨论表明，分子分析方法已经确定了生物柴油废气暴露的肺部反应的机械信息丰富的、新颖的和燃料特异性的特征，而仅使用传统的、假设驱动的方法很难检测到这些特征。