Air Pollution and Markers of Coagulation, Inflammation, and Endothelial Function

Abstract

BACKGROUND Previous studies suggest that air pollution is related to thrombosis, inflammation, and endothelial dysfunction. Mechanisms and sources of susceptibility are still unclear. One possibility is that these associations can be modified by DNA methylation states. METHODS We conducted a cohort study with repeated measurements of fibrinogen, C-reactive protein, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in 704 elderly men participating in the Veterans Administration Normative Aging Study (2000-2009). We investigated short- and intermediate-term air pollution effects on these blood markers, and epigene-environment interactions by DNA methylation of Alu, LINE-1, tissue factor (F3), Toll-Like Receptor 2 (TLR-2), and ICAM-1. RESULTS We found effects of particle number, black carbon, nitrogen dioxide (NO2), and carbon monoxide (CO) on fibrinogen. Ozone was a significant predictor of C-reactive protein and ICAM-1. Particle number, black carbon, NO2, CO, PM2.5, and sulfates were associated with ICAM-1and VCAM-1. An interquartile range increase in 24-hour exposure for NO2; was associated with a 1.7% (95% confidence interval = 0.2% to 3.3%) increase in fibrinogen for ozone a 10.8% (2.2% to 20.0%) increase in C-reactive protein for particle number, a 5.9% (3.6% to 8.3%) increase in ICAM-1; and for PM2.5 a 3.7% (1.7% to 5.8%) increase in VCAM-1. The air pollution effect was stronger among subjects having higher Alu, lower LINE-1, tissue factor, or TLR-2 methylation status. CONCLUSION We observed associations of traffic-related pollutants on fibrinogen, and both traffic and secondary particles on C-reactive protein, ICAM-1, and VCAM-1. There was effect modification by DNA methylation status, indicating that epigenetic states can convey susceptibility to air pollution.

Effects of Temperature and Relative Humidity on DNA Methylation

“…Our findings support previous studies showing an influence of ambient temperature on biomarkers of inflammation 4,5,28 and heart failure, 6 blood viscosity, 7 heart rate variability, 9 blood pressure, 10,11 and cholesterol. 8,12 A correlation between temperature and methylation on repetitive elements has been reported in a previous study focusing on the association of air pollution with LINE-1 and Alu methylation.…”

“…In this cohort, Halonen et al 28 found intermediate-term associations between temperature averaged up to 1 month and C-reactive protein, intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1). Therefore, we focused our analyses on a similar intermediate-term exposure window and considered averages of temperature and relative humidity over 1–3 weeks preceding each participant’s visit.…”

Ambient air pollution and hypertensive disorders of pregnancy: A systematic review and meta-analysis

“…Therefore, many of the hypothesized mechanisms between air pollution and cardiovascular diseases such as inflammation, oxidative stress, and endothelial dysfunction may also apply to HDP (Brook, 2008). In addition, direct links have been reported between air pollution and endothelial dysfunction, which is regarded as a pre-cursor associated with HDP (Bind et al, 2012; Brook and Rajagopalan, 2012; Steegers et al, 2010). Furthermore, the abnormal placentation and failed vascular remodeling caused by endothelial dysfunction may trigger preeclampsia (Powe et al, 2011).…”

Association between Ozone Exposure and Onset of Stroke in Allegheny County, Pennsylvania, USA, 1994-2000

“…In addition, other studies have also found that exposure to air pollutants such as O 3 is associated with increased platelet aggregation and thrombin generation [24], which are known to lie on the pathway of the pathogenesis of cardiovascular events and stroke. Moreover, a recent study found that exposure to ozone and other air pollutants is predictive of the level of C-reactive protein, which suggests systemic inflammatory responses [25]. These mechanisms suggest that systemic inflammatory and vascular changes following exposure are likely to be responsible for the negative effects of air pollutants on risk of stroke.…”