Pathomechanistic Synergy Between Particulate Matter and Traffic Noise-Induced Cardiovascular Damage and the Classical Risk Factor Hypertension.

Abstract

Significance: In all modern urbanized and industrialized societies, noncommunicable diseases, such as cardiovascular disease (CVD), are becoming a more important cause of morbidity and mortality. Classical risk factors for CVDs, such as hypertension, are reinforced by behavioral risk factors, e.g., smoking and diet, and environmental risk factors, e.g., transportation noise and air pollution. Recent Advances: Both transportation noise and air pollution have individually been shown to increase the risk for CVD in large cohorts. Insights from animal studies have revealed pathophysiologic mechanisms by which these stressors influence the cardiovascular system. Noise primarily causes annoyance and sleep disturbance, promoting the release of stress hormones. Air pollution primarily damages the lung, where it causes local inflammation and an increase in oxidative stress, which can propagate to the circulation and remote organs. Critical Issues: Both noise and air pollution converge at the vascular level, where the inflammatory state and oxidative stress cause dysfunction in vascular signaling and promote atherosclerotic plaque formation and thrombosis. Both inflammation and oxidative stress are key aspects of traditional cardiovascular risk factors, such as arterial hypertension. The similarities among the mechanisms of environmental risk factor-induced CVD and hypertension indicate that a complex interplay between them can drive the onset and progression of CVDs, leading to synergistic health impacts. Future Directions: Our present overview of the negative effects of noise and air pollution on the cardiovascular system provides a mechanistic link to the traditional CVD risk factor, hypertension, which could be used to protect patients with preexisting CVD better. Antioxid. Redox Signal. 42, 827-847.