Details

Autor(en) / Beteiligte

• Osborne, Michael T
• Radfar, Azar
• Hassan, Malek Z O
• Abohashem, Shady
• Oberfeld, Blake
• Patrich, Tomas
• Tung, Brian
• Wang, Ying
• Ishai, Amorina
• Scott, James A
• Shin, Lisa M
• Fayad, Zahi A
• Koenen, Karestan C
• Rajagopalan, Sanjay
• Pitman, Roger K
• Tawakol, Ahmed

Titel

A neurobiological mechanism linking transportation noise to cardiovascular disease in humans

Ist Teil von

• European heart journal, 2020-02, Vol.41 (6), p.772-782

Ort / Verlag

England: Oxford University Press

Erscheinungsjahr

2020

Link zum Volltext

Quelle

Oxford Journals 2020 Medicine

Beschreibungen/Notizen

• 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.