Short-term exposure to diesel fumes affects vascular properties and inflammation markers

Introduction and methods

Diesel exhaust fumes are thought to contribute to over 50% of atmospheric particles with a mass of <10 µM average aerodynamic diameter and thereby represent one of the most common pollutants [1,2]. Epidemiological studies have demonstrated that occupational exposure to diesel exhaust fumes can lead to high rates of CV morbidity, and acute and chronic respiratory disease [3,4]. Animal studies have shown that exposure to diluted diesel fumes accelerates atherosclerosis and impairs left ventricle systolic performance, sympathetic drive and fibrosis/fibrinolysis [5,6].

However, it remains unclear whether only long-term exposure or also short-term exposure to diesel fumes can affect inflammatory responses, endothelial function and vessel wall properties. This study investigated the impact of short-term exposure to diesel exhaust fumes on arterial elasticity, vascular function and inflammatory biomarkers.

This proof-of-principle, randomized, crossover study included 40 healthy volunteers. Average age was 41±13 years, 25 participants were male and 15 were active smokers. Participants were randomized in a 1:1 ratio to be exposed to controlled amounts of filtered air and diesel exhaust fumes in two 2-hour sessions with an interval of 4 weeks (one session with filtered air and one session with diesel exhaust fumes). Endothelial function was estimated by flow mediated dilation (FMD). Carotid-femoral pulse wave velocity (PWV) as an index of aortic stiffness, and augmentation index (Aix) of the central aortic pressure waveform were also measured. Protein C plasma levels, protein S activity, serum C-reactive protein (CRP) and fibrinogen were measured from fasting venous blood samples. All measurements were performed before exposure (T0), at the end of the 2h exposure period (T2) and 24h after the end of exposure (T24).

Main results

• Linear mixed model analysis showed that exposure to diesel exhaust fumes resulted in a in short-term (T2 vs T0) mean decrease of FMD (4.5%, P<0.001) and mean increase of PWV (1.19 m/s, P<0.001) and AIx (5.88%, P<0.001), compared to filtered air, after correction for intrasubject variability and multiple variables.
• After 24h, the mid-term (T24 vs T0) mean relative decrease was 5.75% for FMD (P<0.001), and the mean increase of PWV was 0.98 m/s (P<0.001) and 6.03% (P<0.001) for AIx, compared to filtered air.
• Heart rate variability (HRV), as quantified as mean standard deviation of normal to normal intervals (SDNN) based on Holter measurements, was increased in both exposure groups at T2 (70 and 80 ms for diesel vs air) vs T0 (63 and 62 ms),and declined at T24 (57 and 76 ms).
• Linear mixed model analysis showed that short-term (T2 vs T0) exposure to diesel fumes led to a mean relative decrease of 17.4% (P<0.001) in protein C levels and of 11.4% (P<0.001) in protein S activity and a mean increase of 0.42 mg/L (P<0.001) for CRP and 60.1 mg/dl (P<0.001) for fibrinogen, compared to filtered air.
• 24h After exposure, the mean relative decrease was 12.3% (P<0.001) for protein C levels and 18.5% (P<0.001) for protein S activity, and mean increase of CRP was 0.47 mg/L (P<0.05) and 46.0 mg/dL (P<0.001) for fibrinogen, compared to filtered air.
• No different patterns of changes were found in vascular (FMD, PWV, AIx) and HRV parameters between smokers and non-smokers after exposure to diesel exhaust fumes. CRP levels significantly increased after exposure to diesel fumes in smokers compared to non-smokers at both T2 and T24 (P-interaction <0.001).

Conclusion

References

Find this article online at European Journal of Preventive Cardiology