Subclinical cardiovascular outcomes of acute exposure to fine particulate matter and its constituents: A glutathione S-transferase polymorphism-based longitudinal study

Abstract

To explore the acute subclinical cardiovascular effects of fine particulate matter (PM2.5) and its constituents, a longitudinal study with 61 healthy young volunteers was conducted in Xinxiang, China. Linear mixed-effect models were used to analyze the association of PM2.5 and its constituents with cardiovascular outcomes, respectively, including blood pressure (BP), heart rate (HR), serum levels of high-sensitivity C-reactive protein (hs-CRP), 8-hydroxy-2′-deoxyguanosine (8-OHdG), tissue-type plasminogen activator (t-PA), and platelet-monocyte aggregation (PMA). Additionally, the modifying effects of glutathione S-transferase mu 1 (GSTM1) and glutathione S-transferase theta 1 (GSTT1) polymorphisms were examined. A 10 μg/m3 increase in PM2.5 was associated with −1.04 (95 % CI: −1.86 to −0.22) mmHg and −0.90 (95 % CI: −1.69 to −0.11) mmHg decreases in diastolic BP (DBP) and mean arterial BP (MABP) along with 1.83 % (95 % CI: 0.59–3.08 %), 5.93 % (95 % CI: 0.70–11.16 %) increases in 8-OHdG and hs-CRP, respectively. Ni content was positively associated with the 8-OHdG levels whereas several other metals presented negative association with 8-OHdG and HR. Intriguingly, GSTT1+/GSTTM1+ subjects showed higher susceptibility to PM2.5-induced alterations of DBP and PMA, and GSTT1-/GSTM1+ subjects showed higher alteration on t-PA. Taken together, our findings indicated that short-term PM2.5 exposure induced oxidative stress, systemic inflammation, autonomic alterations, and fibrinolysis in healthy young subjects. Among multiple examined metal components Ni appeared to positively associated with systematic oxidative stress. In addition, GST-sufficient subjects might be more prone to PM2.5-induced autonomic alterations.