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.

Decline in Cardiovascular Mortality

“…58 In 2010, an American Heart Association scientific statement indicated that “the overall evidence is consistent with a causal relationship between PM2.5 exposure and CVD morbidity and mortality.” 59 There is also evidence that ambient noise and air pollution have a combined effect on the increased incidence of cardiovascular disease. 60, 61 However, there are no direct data showing that the decreases in these environmental stressors lead to a decline in the incidence of CVD events. These studies suggest an independent improvement in life expectancy and a reduction in cardiovascular events after reduction of the exposure.…”

“…These studies suggest an independent improvement in life expectancy and a reduction in cardiovascular events after reduction of the exposure. 60, 61 …”

“Stressed” About Air Pollution

“…The results confirm and extend the growing body of evidence that PM 2.5 elicits systemic-wide perturbations favoring the development of the metabolic syndrome. 10,11 Sophisticated analyses of the metabolomic footprints further supported heightened activity of both the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis. As posited by the investigators, the concomitant alterations in blood pressure, insulin sensitivity, and serum metabolites (amino acids, fatty acids, lipids) may have arisen as a direct consequence; yet a contribution by other pathways (eg, generation of secondary oxidation products), as has been postulated by others, cannot be ruled out.…”

“…One possible explanation is the triggering of afferent nerves originating from the airways and lungs that mediate reflex efferent pathways that modulate systemic effects. 3,4,10,11 It is also possible that nanoparticles and soluble compounds within PM 2.5 or secondary endogenous biological intermediates, such as oxidized phospholipids, can be transported directly by cranial nerve axons or reach permeable central nervous system sites by the circulation. Our prior animal experiments indeed confirm a pivotal role for hypothalamic inflammation (nuclear factor κB-dependent signaling) in the genesis of peripheral metabolic and hemodynamic abnormalities induced by PM 2.5 exposure.…”

Volcanic smog and cardiometabolic health: Hawaiian hypertension?

“…As such, both the American Heart Association and European Society of Cardiology have deemed PM 2.5 as a causal risk factor for global cardiovascular diseases . In addition, we and others have shown that PM 2.5 air pollution potentiates the development of cardiometabolic conditions—high BP, diabetes mellitus (DM), and atherosclerosis . Short‐term exposures over a few hours to days significantly increase BP by several mechanisms.…”