Noise and Air Pollution and Cardiometabolic Disease: Part 2
- Münzel T, Sørensen M, Gori T, et al.
- Environmental Stressors and Cardio-Metabolic Disease: Part II–Mechanistic Insights. Eur Heart J 2016;Jul 26:[Epub ahead of print].
The following are key points from part 2 of a review on environmental stressors and cardiometabolic disease:
- Air pollution and noise lead to vascular (endothelial) dysfunction, hypertension, atherosclerosis, and complications including myocardial infarction, stroke, and heart failure.
- The following four pathways have been proposed to help explain the systemic effects of air pollution and noise: 1) perturbation of autonomic nervous system; 2) release of pro-inflammatory mediators, modified lipids, or phospholipids; 3) endothelial dysfunction; and 4) activation of pro-thrombotic pathways.
- Acute responses to noise or air pollution are likely mediated via changes in autonomic tone and/or sympathoadrenal activation, alterations in endothelial function, and direct effects of procoagulant pathways and thrombosis.
- The adverse effects of noise are mediated by direct and indirect pathways. The direct pathway is activated by an instantaneous interaction of the acoustic nerve with structures of the central nervous system. As the authors write, "The indirect pathway in turn represents the cognitive perception of sound, and its subsequent cortical activation."
- Oxidative stress pathways are central to the mechanism of vascular damage induced by air pollution.
- There is clear evidence of an association between long-term exposure to particulate matter and the burden of atherosclerosis in humans in cross-sectional studies using such surrogates as carotid intima media thickness, coronary artery and aortic calcium, and ankle brachial indices.
- There are gaps in knowledge of air and noise pollution-mediated disease. In particular, the magnitude, time course, and consequences of co-exposure to noise and air pollution need to be established.
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