A neurobiological mechanismlinking transportation noise to cardiovascular disease in humans

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

Research output: Contribution to journalArticlepeer-review

90 Scopus citations


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 b (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 stressassociated limbic (amygdalar) activity and includes heightened arterial inflammation. This potential neurobiological mechanism linking noise to CVD merits further evaluation in a prospective population.

Original languageEnglish
Pages (from-to)772-782
Number of pages11
JournalEuropean Heart Journal
Issue number6
StatePublished - 1 Feb 2020


  • 18F-FDG-PET/CT
  • Amygdalar activity
  • Arterial inflammation
  • Cardiovascular disease
  • Chronic noise exposure


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