Environmental stressors and cardio-metabolic disease: part II-mechanistic insights

Abstract

Environmental factors can act as facilitators of chronic non-communicable diseases. Ambient noise and air pollution collectively outrank all other environmental risk factors in importance, contributing to over 75% of the disease and disability burden associated with known environmental risk factors. In the first part of this review, we discussed the global burden and epidemiologic evidence supporting the importance of these novel risk factors as facilitators of cardiometabolic disease. In this part, we will discuss pathophysiological mechanisms responsible for noise and air pollution-mediated effects. Akin to traditional cardiovascular risk factors, a considerable body of evidence suggests that these environmental agents induce low-grade inflammation, oxidative stress, vascular dysfunction, and autonomic nervous system imbalance, thereby facilitating the development of diseases such as hypertension and diabetes. Through their impact on traditional risk factors and via additional novel mechanisms, environmental risk factors may have much larger impact on cardiovascular events than currently appreciated. In the second part of this review, we discuss deficiencies and gaps in knowledge and opportunities for new research.

Keywords: Air pollution; Atherosclerosis; Cardiometabolic disease; Cardiovascular risk factor; Environment; Inflammation; Noise; Oxidative stress.

Figure 1

Proposed pathophysiological mechanisms of cardiovascular disease induced by environmental air pollution and noise. ox-PAPC, oxidatively modified 1-palmitoyl-2-arachidonoyl-sn-phosphatidylcholine; 7-KC, 7-ketocholesterol.

Figure 2

Hypothetical framework of investigations that combine technological innovation in biometric data with personalized exposure information in real time to study interactive effects of environmental risk factors on cardiovascular end-points. ABP, ambulant blood pressure monitoring; BC, black carbon; PM, particulate matter.