Acute effect of fine particulate matter on blood pressure, heart rate and related inflammation biomarkers: A panel study in healthy adults

Epidemiological evidence of short-term fine particulate matter (PM(2.5)) exposure on blood pressure (BP), heart rate (HR) and related inflammation biomarkers has been inconsistent. We aimed to explore the acute effect of PM(2.5) on BP, HR and the mediation effect of related inflammation biomarkers. A total of 32 healthy college students were recruited to perform 4 h of exposure at two sites with different PM(2.5) concentrations in Wuhan between May 2019 and June 2019. The individual levels of PM(2.5) concentration, BP and HR were measured hourly for each participant. Blood was drawn from each participant after each visit and we measured the levels of inflammation markers, including serum high-sensitivity C-reactive protein and plasma fibrinogen. Linear mixed-effect models were to explore the acute effect of PM(2.5) exposure on BP, HR, and related inflammation biomarkers. In addition, we evaluated related inflammation biomarkers as the mediator in the association of PM(2.5) and cardiovascular health indicators. The results showed that a 10 μg/m(3) increment in PM(2.5) concentration was associated with an increase of 0.84 (95% CI: 0.54, 1.15) beats/min (bpm) in HR and a 3.52% (95% CI: 1.60%, 5.48%) increase in fibrinogen. The lag effect model showed that the strongest effect on HR was observed at lag 3 h of PM(2.5) exposure [1.96 bpm (95% CI: 1.19, 2.75)], but for fibrinogen, delayed exposure attenuated the association. Increased fibrinogen levels may account for 39.07% (P = 0.44) of the elevated HR by PM(2.5). Null association was observed when it comes to short-term PM(2.5) exposure and BP. Short-term exposure to PM(2.5) was associated with elevated HR and increased fibrinogen levels. But our finding was not enough to suggest that exposure to PM(2.5) might induce adverse cardiovascular effects by the pathway of inflammation.