Air pollution is responsible for around 7 million deaths per year, with around half of these attributable to cardiovascular conditions. Pollution modelling in Greater Manchester identified a 1.4% increased incidence of ischaemic heart disease per 1 ug/m3 increase in PM2.5 concentration. Cardiotoxic polyaromatic hydrocarbons like phenanthrene are frequently found adsorbed to the surface of this inhalable fraction of PM. However, the source and impact of phenanthrene-induced inflammation on this cardiovascular dysfunction is unknown. Mice were exposed to environmentally relevant concentrations (3 ug/kg or 30 ug/kg) of phenanthrene by intraperitoneal injection every day for 6 weeks. Single nucleus RNA sequencing was carried out on liver samples of 12 (n=4) male mice to identify changes in expression of pro/anti-inflammatory genes. Thirteen distinct cell populations were identified via UMAP clustering, including a population subset seen only in mice exposed to the high dose of phenanthrene. In this subset, pro-inflammatory genes like LCN, Syt12, TERC, CYP4a31 and APCS were significantly overexpressed by scores of 51.2, 28.8, 17.0, 15.8 and 15.7 respectively. Further RNA velocity analysis in the high dose phenanthrene group suggests rapid differentiation of ‘neutral’ cell types into inflammatory subsets. Initial cytokine panel analysis identified dose-dependent increases in plasma and liver of potent Th2-related cytokines like IL-16 and IL-33, although not significant. Together, these findings demonstrate the range of effects phenanthrene has on the immune system, and subsequently, the cardiovascular system.