A neurobiological mechanism linking transportation noise to cardiovascular disease in humans

Abstract

Aims Chronic noise exposure associates with increased cardiovascular disease (CVD) risk; however, the role of confounders and the underlying mechanism remain incompletely defined. The amygdala, a limbic centre involved in stress perception, participates in the response to noise. Higher amygdalar metabolic activity (AmygA) associates with increased CVD risk through a mechanism involving heightened arterial inflammation (ArtI). Accordingly, in this retrospective study, we tested whether greater noise exposure associates with higher: (i) AmygA, (ii) ArtI, and (iii) risk for major adverse cardiovascular disease events (MACE). Methods and results Adults (N = 498) without CVD or active cancer underwent clinical 18F-fluorodeoxyglucose positron emission tomography/computed tomography imaging. Amygdalar metabolic activity and ArtI were measured, and MACE within 5 years was adjudicated. Average 24-h transportation noise and potential confounders were estimated at each individual’s home address. Over a median 4.06 years, 40 individuals experienced MACE. Higher noise exposure (per 5 dBA increase) predicted MACE [hazard ratio (95% confidence interval, CI) 1.341 (1.147–1.567), P < 0.001] and remained robust to multivariable adjustments. Higher noise exposure associated with increased AmygA [standardized β (95% CI) 0.112 (0.051–0.174), P < 0.001] and ArtI [0.045 (0.001–0.090), P = 0.047]. Mediation analysis suggested that higher noise exposure associates with MACE via a serial mechanism involving heightened AmygA and ArtI that accounts for 12–26% of this relationship. Conclusion Our findings suggest that noise exposure associates with MACE via a mechanism that begins with increased stress-associated limbic (amygdalar) activity and includes heightened arterial inflammation. This potential neurobiological mechanism linking noise to CVD merits further evaluation in a prospective population.

Reduction of environmental pollutants for prevention of cardiovascular disease: it’s time to act

“…Recent human data provided a molecular proof of the important pathophysiological role of this ‘indirect pathway’ by identifying amygdalar activation (using 18 F-FDGPET/CT imaging) by transportation noise in 498 subjects, and its association with arterial inflammation and major adverse cardiovascular events. 27 These data are indeed consistent with animal experiments demonstrating an increased release of stress hormones (catecholamines and cortisol), higher blood pressure, endothelial dysfunction, 28 neuroinflammation, diminished neuronal nitric oxide synthase (nNOS) expression as well as cerebral oxidative stress in aircraft noise-exposed mice. 29 These changes were substantially more pronounced when noise exposure was applied during the sleep phase (reflecting night-time noise exposure) and was mostly prevented in mice with genetic deletion or pharmacological inhibition of the phagocytic NADPH oxidase (NOX-2).…”

Midregional pro atrial natriuretic peptide: a novel important biomarker for noise annoyance-induced cardiovascular morbidity and mortality?

“…Of note, since noise annoyance also reflects mental stress and has been associated with psychological disorders, it is important to mention that growing evidence suggests that MR-proANP play a role in the neurobiology of affective disorders modulating emotional and endocrine stress responses [ 26 , 36 ]. In addition, recent studies have shown that chronic exposure to transportation noise caused by aircraft and road traffic noise is associated with higher amygdala activity, a limbic structure that is involved in stress perception, leading to vascular inflammation and increased cardiovascular event rates [ 37 , 38 ]. In support of this, MR-proANP was recently shown to predict impaired physical and mental quality of life [ 39 ].…”

Traffic noise and cardiovascular disease mortality: A risk assessment

“…Second, Osborne et al (2020[ 5 ]) speculated the mechanism of the association between transportation noise and subsequent CVD events. The adjusted HR (95 % CI) of noise exposure per 5 dBA increase for major adverse cardiovascular disease events was 1.341 (1.147-1.567), and higher noise exposure was significantly associated with increased metabolic activity of amygdala and arterial inflammation.…”