Ozone exposure and prothrombosis: Mechanistic insights from a randomized controlled exposure trial

Epidemiological studies have associated ozone exposure with cardiovascular diseases, but the molecular mechanisms were not elucidated. We performed an untargeted serum proteomic analysis in a randomized, crossover, controlled exposure trial. We recruited 32 healthy young adults and asked them to receive filtered air and 200-ppb ozone exposures for 2 h in a random order before serum collection. Linear mixed-effect models were used to identify differentially expressed proteins (DEPs) between the two exposures and Gene Ontology enrichment and ingenuity pathway analysis were performed to determine their biological function. A total of 56 DEPs were identified. For example, acute ozone exposure increased coagulation factor X and factor VII-activating protease by 20.96% and 28.35%, respectively. Whereas, protein Z, protein Z-dependent protease inhibitor, and plasminogen decreased by 13.62%, 33.54%, and 10.47%, respectively. We also observed a 42.32% decrease in paraoxonase 3 and evident changes in four apolipoproteins. Additionally, we found 18.21% and 95.82% increases in L-selectin and beta 2-microglobulin, respectively, and significant changes in three complements. DEPs and

Automated summary

This study conducted a proteomic analysis to investigate the impact of ozone exposure on healthy young adults. The results showed that ozone exposure could increase blood coagulation factors and platelet activation, while decreasing some proteins. In addition, ozone exposure was found to be associated with lipid metabolism and immune response.