Neurobiological Mechanism Linking Transportation Noise to Cardiovascular Disease in Humans; European Heart Journal, Nov. 26, 2019
Mass General Hospital press release, Nov. 26, 2019, about the study
A Dec. 13, 2019 Boston. com article about the study
Selected Excerpts
Discussion: Chronic exposure to heightened transportation noise associates with an increased incidence of CVD [cardiovascular disease]. Until now, basic gaps remained in our understanding of the underlying mechanisms, including how noise initially triggers a physiologic response and results in physical disease. The current study implemented 18F-FDG-PET/CT imaging of the brain and arteries to provide new insights. We observed that higher noise exposure associates with heightened amygdalar metabolic activity and increased atherosclerotic inflammation. Further, we observed that higher noise exposure associates with an increased risk of MACE after adjustments for important confounders including CVD risk factors, baseline subclinical atherosclerosis, socioeconomic status, air pollution, and healthcare access. Moreover, we observed that the link between noise and MACE may be mediated in part by a multi-organ pathway that begins with up-regulated amygdalar activity and involves heightened arterial inflammation.
The independent relationship between noise exposure and cardiovascular disease: According to the WHO, 45 000 life-years are lost annually to noise-related CVD in Western Europe, and the Global Burden of Disease Study acknowledges that occupational noise exposure increases the risk for developing disease.24 , 25 Several studies have shown that the risk of MACE is dose-dependent above 50–60 dB.5 , 25 Other studies have shown that the association between noise and CVD is independent of CVD risk factors, socioeconomic factors, behavioural factors, and air pollution.7–9 The current study demonstrates a greater risk for CVD consequent to noise than previously reported and adds to prior observations by accounting for important confounders to confirm an independent relationship between noise exposure and MACE. Moreover, subgroup analyses showed that increased noise exposure was a significant risk factor for MACE even in individuals with seemingly lower clinical CVD risk (e.g. those without baseline CAC). In other words, chronic noise exposure is an independent and clinically under-recognized CVD risk factor and may have an important effect even in individuals otherwise presumed to have low CVD risk.
Mechanistic insights: Although much of the underlying biology linking noise to CVD is well described, our findings may shed further light on a multiorgan mechanism linking noise exposure to CVD. This mechanism likely begins in the limbic system of the brain and involves the amygdala. The amygdala is intimately linked to the response to bothersome auditory stimuli,16 , 17 and noise exposure increases amygdalar blood flow.16 Noise disrupts the circadian rhythm and leads to oxidative stress and inflammation within neural tissues with subsequent activation of the hypothalamic–pituitary–adrenal (HPA) axis and sympathetic nervous system (SNS).12–14 , 17 These changes activate haematopoietic tissues and trigger altered gene expression and increased oxidative stress, endothelial dysfunction, and inflammation that lead to increased ArtI, non-calcified coronary plaque burden, and CRP.14 , 19 , 21 Hence, prior studies provide a framework that supports the amygdala as a potential conduit linking noise exposure to CVD.
Conclusion: Transportation noise exposure associates with increased risk for CVD events after comprehensively accounting for confounders, including CVD risk factors, baseline subclinical atherosclerosis, socioeconomic factors, healthcare access, and air pollution. Moreover, the link between noise exposure and CVD may be partially mediated by a mechanism that begins with up-regulated stress-associated neurobiological activity and involves heightened arterial inflammation. Although a prospective study is needed to confirm the generalizability of these results, the findings point to a potentially important biologic pathway that could be targeted to reduce CVD associated with noise exposure.