Dataset Information

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.

SUBMITTER: Osborne MT

PROVIDER: S-EPMC7006229 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature

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Publications

A neurobiological mechanism linking transportation noise to cardiovascular disease in humans.

Osborne Michael T MT Radfar Azar A Hassan Malek Z O MZO Abohashem Shady S Oberfeld Blake B Patrich Tomas T Tung Brian B Wang Ying Y Ishai Amorina A Scott James A JA Shin Lisa M LM Fayad Zahi A ZA Koenen Karestan C KC Rajagopalan Sanjay S Pitman Roger K RK Tawakol Ahmed A

European heart journal 20200201 6

<h4>Aims</h4>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 gr ...[more]

PMID: 31769799

Similar Datasets

Project description:BackgroundChronic transportation noise exposure associates with cardiovascular events through a link involving heightened stress-associated neurobiological activity (as amygdalar metabolic activity, AmygA) on 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG-PET/CT). Increased AmygA also associates with greater visceral adipose tissue (VAT) and type 2 diabetes mellitus (DM). While relationships between noise exposure and VAT and DM have been reported, the underlying mechanisms remain incompletely understood. We tested whether: (1) transportation noise exposure associates with greater (a) baseline and gains in VAT and (b) DM risk, and (2) heightened AmygA partially mediates the link between noise exposure and these metabolic diseases.MethodsVAT was measured in a retrospective cohort (N = 403) who underwent clinical 18F-FDG-PET/CT. AmygA was measured in those with brain imaging (N = 238). Follow-up VAT was remeasured on available imaging (N = 67). Among individuals (N = 224) without baseline DM, incident DM was adjudicated over 2 years from clinical records. Noise (24-h average) was modeled at each individual's home address. Linear regression, survival, and mediation analyses were employed.ResultsHigher noise exposure (upper tertile vs. others) associated with greater: baseline VAT (standardized β [95% confidence interval (CI)]= 0.230 [0.021, 0.438], p = 0.031), gains in VAT (0.686 [0.185, 1.187], p = 0.008 adjusted for baseline VAT), and DM (hazard ratio [95% CI]=2.429 [1.031, 5.719], p = 0.042). The paths of: ↑noise exposure→↑AmygA→↑baseline VAT and ↑noise exposure→↑AmygA→↑subsequent DM were significant (p < 0.05).ConclusionsIncreased transportation noise exposure associates with greater VAT and DM. This relationship is partially mediated by stress-associated neurobiological activity. These findings suggest altered neurobiology contributes to noise exposure's link to metabolic diseases.

Project description:BackgroundLower socioeconomic status (SES) associates with a higher risk of major adverse cardiac events (MACE) via mechanisms that are not well understood.ObjectivesBecause psychosocial stress is more prevalent among those with low SES, this study tested the hypothesis that stress-associated neurobiological pathways involving up-regulated inflammation in part mediate the link between lower SES and MACE.MethodsA total of 509 individuals, median age 55 years (interquartile range: 45 to 66 years), underwent clinically indicated whole-body 18F-fluorodeoxyglucose positron emission tomography/computed tomography imaging and met pre-defined inclusion criteria, including absence of known cardiovascular disease or active cancer. Baseline hematopoietic tissue activity, arterial inflammation, and in a subset of 289, resting amygdalar metabolism (a measure of stress-associated neural activity) were quantified using validated 18F-fluorodeoxyglucose positron emission tomography/computed tomography methods. SES was captured by neighborhood SES factors (e.g., median household income and crime). MACE within 5 years of imaging was adjudicated.ResultsOver a median 4.0 years, 40 individuals experienced MACE. Baseline income inversely associated with amygdalar activity (standardized β: -0.157 [95% confidence interval (CI): -0.266 to -0.041]; p = 0.007) and arterial inflammation (β: -0.10 [95% CI: -0.18 to -0.14]; p = 0.022). Further, income associated with subsequent MACE (standardized hazard ratio: 0.67 [95% CI: 0.47 to 0.96]; p = 0.029) after multivariable adjustments. Mediation analysis demonstrated that the path of: ↓ neighborhood income to ↑ amygdalar activity to ↑ bone marrow activity to ↑ arterial inflammation to ↑ MACE was significant (β: -0.01 [95% CI: -0.06 to -0.001]; p < 0.05).ConclusionsLower SES: 1) associates with higher amygdalar activity; and 2) independently predicts MACE via a serial pathway that includes higher amygdalar activity, bone marrow activity, and arterial inflammation. These findings illuminate a stress-associated neurobiological mechanism by which SES disparities may potentiate adverse health outcomes.

Project description:Environmental stressors present in the modern world can have a fundamental effect on the physiology and health of humans. Exposure to stressors like air pollution, heat and traffic noise has been linked to a pronounced increase in non-communicable diseases. Specifically, aircraft noise has been identified as a risk factor for cardiovascular and metabolic diseases, such as arteriosclerosis, heart failure, stroke and diabetes. Noise stress leads to neuronal activation with subsequent stress hormone release that ultimately leads to activation of the renin-angiotensin-aldosterone system, increasing inflammation and oxidative stress, with dramatic effects on the cardiovascular system. However, despite the epidemiological evidence of a link between noise stress and metabolic dysfunction, the consequences of exposure at the molecular, metabolic level of the cardiovascular system are largely unknown. Here we use a murine model system of aircraft noise exposure to show that noise stress profoundly alters heart metabolism. Within days of exposing animals to aircraft noise the heart has a reduced potential for utilising fatty-acid beta-oxidation, the tricarboxylic acid cycle, and the electron transport chain for generating ATP. This is compensated by shifting energy production towards glycolysis. Intriguingly, the metabolic shift is reminiscent of what is observed in failing and ischaemic hearts. Our results demonstrate that within a relatively short exposure time, the cardiovascular system undergoes a fundamental metabolic shift that bears the hallmarks of cardiovascular disease. Overall, aircraft noise induces rapid, detrimental metabolic shifts in the heart, resembling patterns seen in cardiovascular diseases. These findings underscore the urgent need to comprehend molecular consequences of environmental stressors, paving the way for targeted interventions aiming mitigating health risks associated with chronic noise exposure in our modern, noisy environments.

Project description:BackgroundAlthough plausible from a pathophysiological point of view, robust evidence for effects of transportation noise on mental health remains scarce. Meanwhile, psychiatric diseases are among the most prevalent noncommunicable diseases worldwide, and suicide as a mortality outcome highly connected to mental disorders presents a pressing public health issue. The aim of this study was to investigate the association between source-specific transportation noise, particulate matter (PM) air pollution, residential greenness, and suicide by means of a nationwide cohort study.MethodsRoad traffic, railway and aircraft noise exposure as well as exposure to air pollution [PM with aerodynamic diameter ≤2.5μm (PM2.5)] and greenness [normalized difference vegetation index (NDVI)] were linked to 5.1 million adults (age 15 y and older) in the Swiss National Cohort, accounting for their address history. Mean noise exposure in 5-y periods was calculated. Individuals were followed for up to 15 y (2001-2015). Time-varying Cox regression models were applied to deaths by suicide (excluding assisted suicide). Models included all three noise sources, PM2.5, and NDVI plus individual and spatial covariates, including socioeconomic status. Effect modification by sex, age, socioeconomic indicators, and degree of urbanization was explored.ResultsDuring the follow-up, there were 11,265 suicide deaths (10.4% poisoning, 33.3% hanging, 28.7% firearms, 14.7% falls). Road traffic and railway noise were associated with total suicides [hazard ratios: 1.040; 95% confidence interval (CI): 1.015, 1.065; and 1.022 (95% CI: 1.004, 1.041) per 10 dB day-evening-night level (Lden)], whereas for aircraft noise, a risk increase starting from 50 dB was masked by an inverse association in the very low exposure range (30-40 dB). Associations were stronger for females than males. The results were robust to adjustment for residential greenness and air pollution.ConclusionIn this longitudinal, nationwide cohort study, we report a robust association between exposure to road traffic and railway noise and risk of death by suicide after adjusting for exposure to air pollution and greenness. These findings add to the growing body of evidence that mental health disorders may be related to chronic transportation noise exposure. https://doi.org/10.1289/EHP11587.

Dataset Information

A neurobiological mechanism linking transportation noise to cardiovascular disease in humans.

Aims

Methods and results

Conclusion

Publications

A neurobiological mechanism linking transportation noise to cardiovascular disease in humans.

Similar Datasets

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