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Background Diesel exhaust fumes represent one of the most common toxic pollutants. The prolonged effects of acute exposure to this pollutant on inflammatory status and vascular properties are unknown.Methods During a 2-h session, 40 healthy subjects were exposed to diesel exhaust fumes and/or filtered air. Endothelial function was assessed with flow mediated dilation, arterial stiffness with pulse wave velocity and reflected waves with augmentation index. C-reactive protein, fibrinogen, protein C levels and protein S activity were also measured. Standard deviation of normal to normal R–R intervals (SDNN) was used to assess heart rate variability. Measurements were assessed before exposure and 2 and 24?h after diesel exposure.Results Compared with filtered air, exposure to diesel exhaust fumes decreased flow mediated dilation and increased pulse wave velocity and augmentation index up to 24?h after the exposure (p?

Introduction:Diesel exhaust fumes are harmful toxins affecting the population.Short-term impact of diesel fumes has not been studied.Hypothesis:Acute and short-term (24 h) effects of diesel exhaust particles (DEPs) on endothelial function, vascular properties, inflammation.Methods:In this cross over study, 40 healthy subjects (40 years old) were exposed to diesel exhaust particles (DEPs) and filtered air (FA) over a 2hour session. Measurements were assessed before (T0), after 2 hours(T2) and 24 hours after exposure (T24). DEPs were based on mass of microparticles less than 2,5 microns (PM 2,5). Endothelial function, vascular properties were assessed with flow mediated dilation (FMD), pulse wave velocity (PWV) and augmentation index (AIx). Inflammation and fibrinolysis were evaluated with C reactive protein (CRP), fibrinogen and functionalities of protein C and S. Heart rate variability was assessed with standard deviation of normal to normal intervals R-R intervals (SDNN).Results:At T0 of DEP and FA, there was no difference in baseline measurements. Exposure to DEP decreased significantly FMD (T0: 11.97?4.61% ,T2: 7.71?3.36% ,T24: 6.17?3.19%, p<0.001) and SDNN (T0: 63 (48, 82), T2: 70 (50, 92), T24: 57 (41, 72), p<0.001). PWV (T0: 6.09?1.03m/s, T2: 7.22?1.31m/s,T24: 6.90?1.03m/sec, p<0.001), AIx (T0: 6.17?3.19%,T2: 7.71?3.36% ,T24: 11.97?4.61%, p<0.001), CRP (T0: 1.41?.18 mg/L,T2: 1.99?.21mg/L,T24: 2.08?.24mg/L, p=0.04) and fibrinogen (T0: 269?44 mg/dL,T2: 331?75 mg/dL,T24: 307?51 mg/dL, p=0.002) were increased. Functionalities of proteins C and S were significantly reduced (T0: 121?26%,T2: 104?21%,T24: 105?20%, p=0.003), (T0: 77?13, T2: 66?12, T24: 57?13, p<0.001).Conclusions:Short-term exposure to diesel exhaust fumes may have significant prolonged effects with impairment of endothelial function, arterial wall properties, inflammation and fibrinolysis highlighting the harmful impact of particle matter to cardiovascular health.

Introduction:The deleterious action of air pollution on cardiovascular health is undeniable, as it has been linked with increased risk of myocardial infarction and cerebrovascular events. However, its role on carotid atherosclerosis has not been thoroughly investigated especially in patients with coronary artery disease (CAD).Aim:To investigate the impact of air pollution on carotid intima-media thickness (cIMT) in a rural population with or without preexisting CAD.Methods:A cross-sectional study including 1182 volunteers of the Peloponnese region was carried out. The estimation of air pollution exposure was performed via the creation of time series of exposure to microparticles and ozone concentration. According to those measurements, the volunteers were classified to inhabitants of areas of high air pollution (Group I) and low air pollution (Group 2). cIMT was estimated by ultrasonography.Results:From the study population 149 participants had CAD while 1033 subjects did not have CAD, with significant difference on the mean cIMT (CAD: 1.37 ? 0.74, No CAD: 0.96 ? 0.38, p < 0.001). Subsequently, a propensity score analysis was performed adjusting for various confounders (Table 1). Next, a two-way ANOVA was conducted that examined the effect of preexisting CAD and pollution level on mean cIMT, with a statistically significant interaction being noted [F(1, 216) = 4.374, p= 0.038]. Simple main effects analysis showed that people with CAD in Group 1 areas had significantly increased mean cIMT than those in Group 2 areas (Group 1: 1.53 ? 0.79, Group 2: 1.18 ? 0.59, p= 0.002), while people without CAD were found with similar values irrespective of air pollution status (Group 1: 1.45 ? 0.5, Group 2: 1.44 ? 0.52, p= 0.883).Conclusion:Air pollution may significantly contribute to atherosclerosis progression and increase cIMT especially in subjects with CAD, highlighting the additive adverse impact of environmental factors on atherosclerotic cardiovascular disease.