Benzo[a]pyrene (BaP), a major harmful component in PM2.5, is widely present in automobile emissions and atmospheric pollution. BaP exposure directly targets the lungs, often resulting in acute lung injury (ALI). However, comprehensive metabolic and transcriptomic profiles related to BaP-induced ALI remain unexplored. To simulate BaP-induced lung injury, we performed intratracheal instillation of BaP. To investigate how BaP exposure affects lung transcriptome and metabolic profiles, we used RNA sequencing and ultra-performance liquid chromatography-mass spectrometry (UPLC-MS). We aimed to understand the underlying mechanisms of BaP-induced lung damage. Metabolomics analyses indicated that in BaP-exposed animals, most fatty acids, carbohydrates, and steroids were significantly reduced, whereas most amino acids and organic acids remained unchanged. Analysis of transcriptomics data showed that fatty acid synthesis decreased and fatty acid oxidation increased, suggesting that lipid breakdown occurs after BaP exposure. Additionally, there were increases in oxidative stress system activity and decreases in immune system function. Finally, BaP altered mitochondrial, lipid, immune system, and fatty acid pathways, as indicated by pathway enrichment analyses. These results show that BaP substantially affects metabolic and inflammatory responses, enhancing the broader understanding of the underlying mechanisms of ALI after BaP exposure.

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death globally, with smoking as its primary risk factor. The relationship betwee