Acute cardiovascular biomarker responses to ambient PM2.5 and its constituents: A panel study on healthy retirees

Abstract

Ambient fine particulate matter (PM_2.5) remains a environmental risk factor for cardiovascular disease (CVD). However, the specific roles of PM_2.5 and its chemical components in cardiovascular events and the underlying mechanisms have not been fully understood. This study aimed to unravel the associations of short-term exposure to PM_2.5 and its constituents with adverse cardiovascular outcomes. A panel study of healthy retirees was conducted and a linear mixed-effects model used to examine the relationships between PM_2.5, its 18 chemical components, and key cardiovascular biomarkers. Primary outcomes included blood pressure (BP), heart rate (HR), heart rate variability (HRV), interleukin (IL)-6, IL-8, high-sensitivity C-reactive protein (hs-CRP), 8-hydroxy-2’-deoxyguanosine (8-OHdG), tissue-type plasminogen activator (t-PA), platelet monocyte aggregates (PMAs), endothelin-1 (ET-1), creatine kinase (CK), and lactate dehydrogenase (LDH). In addition, stratification by gender and glutathione S-transferase theta 1 (GSTT1) polymorphism was performed. Results showed that short-term PM_2.5 exposure was significantly linked to increased systolic BP (SBP), mean arterial pressure (MAP), HR, IL-6, and ET-1, along with decreases in t-PA and HRV. Metallic components (Mn, Ni, As, Se, Rb, Sr, Mo, Sb, and Cs) and ionic components (F⁻, NO₃⁻, PO₄³⁻, and SO₄²⁻) were particularly associated with elevated BP and reduced HRV. Moreover, gender and GSTT1 polymorphism modified susceptibility to these cardiovascular effects. Overall, these findings suggest that short-term PM_2.5 exposure induces significant cardiovascular and biochemical changes in retirees, including elevated BP, HR, systemic inflammation, endothelial dysfunction, coagulation disturbances, and reduced HRV. PM_2.5 constituents and individual factors, such as gender and GSTT1 polymorphism, contribute to these effects.