Air pollution is the most important environmental risk factor for disease and premature death, and exposure to combustion particles from vehicles is a major contributor. Human epidemiological studies combined with experimental studies strongly suggest that exposure to combustion particles may enhance the risk of cardiovascular disease (CVD), including atherosclerosis, hypertension, thrombosis and myocardial infarction. In this review we hypothesize that adhered organic chemicals like polycyclic aromatic hydrocarbons (PAHs), contribute to development or exacerbation of CVD from combustion particles exposure. We summarize present knowledge from existing human epidemiological and clinical studies as well as experimental studies in animals and relevant in vitro studies. The available evidence suggests that organic compounds attached to these particles are significant triggers of CVD. Furthermore, their effects seem to be mediated at least in part by the aryl hydrocarbon receptor (AhR). The mechanisms include AhR-induced changes in gene expression as well as formation of reactive oxygen species (ROS) and/or reactive electrophilic metabolites. This is in accordance with a role of PAHs, as they seem to be the major chemical group on combustion particles, which bind AhR and/or is metabolically activated by CYP-enzymes. In some experimental models however, it seems as PAHs may induce an inflammatory atherosclerotic plaque phenotype irrespective of DNA- and/or AhR-ligand binding properties. Thus, various components and several signalling mechanisms/pathways are likely involved in CVD induced by combustion particles. We still need to expand our knowledge about the role of PAHs in CVD and in particular the relative importance of the different PAH species. This warrants further studies as enhanced knowledge on this issue may amend risk assessment of CVD caused by combustion particles and selection of efficient measures to reduce the health effects of particular matters (PM).

中文翻译：

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多环芳烃作为燃烧颗粒心血管效应介质的潜在作用

空气污染是导致疾病和过早死亡的最重要的环境风险因素，而接触车辆燃烧颗粒是一个主要原因。人类流行病学研究与实验研究相结合强烈表明，接触燃烧颗粒可能会增加心血管疾病（CVD）的风险，包括动脉粥样硬化、高血压、血栓形成和心肌梗塞。在这篇综述中，我们假设附着的有机化学物质，如多环芳烃 (PAH)，会导致燃烧颗粒暴露引起的 CVD 的发展或加剧。我们总结了现有人类流行病学和临床研究以及动物实验研究和相关体外研究的现有知识。现有证据表明，附着在这些颗粒上的有机化合物是 CVD 的重要触发因素。此外，它们的作用似乎至少部分是由芳烃受体（AhR）介导的。其机制包括 AhR 诱导的基因表达变化以及活性氧 (ROS) 和/或反应性亲电子代谢物的形成。这与 PAH 的作用一致，因为它们似乎是燃烧颗粒上的主要化学基团，与 AhR 结合和/或被 CYP 酶代谢激活。然而，在一些实验模型中，无论 DNA 和/或 AhR 配体结合特性如何，PAH 似乎都可能诱导炎症性动脉粥样硬化斑块表型。因此，燃烧颗粒引起的 CVD 可能涉及多种成分和多种信号机制/途径。我们仍然需要扩大对多环芳烃在 CVD 中的作用的了解，特别是不同多环芳烃种类的相对重要性。这值得进一步研究，因为加强对这一问题的了解可能会修正对燃烧颗粒引起的 CVD 的风险评估，并选择有效的措施来减少特定物质 (PM) 对健康的影响。