New review of cerebral consequences of environmental noise exposure – including plane noise

A group of scientists, mainly in Germany, have done further studies on the impact of noise on health. This includes aircraft noise, as well as noise from roads, railways, wind turbines and general background noise. They say there has been more research on cardiovascular impacts, but little on brain and “associated neuropsychiatric outcomes.”  These impacts include depression, anxiety, cognitive decline and risk of strokes. As with the impacts on the cardiovascular system, the mechanism of damage may be the involvement of reactive oxygen species/oxidative stress and inflammatory pathways. The authors looked at a number of studies, some on mice. The results are unclear, but indicative of the negative impact of noise – perhaps especially the intermittent but loud noise from aircraft – is potentially damaging. The impact may be worse when aircraft noise exposure is in addition to other noise sources. Anecdotally, the mental health impacts of depression and anxiety, for vulnerable people, from inescapable plane noise, at home, are well known.


Cerebral consequences of environmental noise exposure

by numerous authors.

May 2022

In  Environment International
Volume 165, July 2022


The importance of noise exposure as a major environmental determinant of public health is being increasingly recognized. While in recent years a large body evidence has emerged linking environmental noise exposure mainly to cardiovascular disease, much less is known concerning the adverse health effects of noise on the brain and associated neuropsychiatric outcomes. Despite being a relatively new area of investigation, indeed, mounting research and conclusive evidence demonstrate that exposure to noise, primarily from traffic sources, may affect the central nervous system and brain, thereby contributing to an increased risk of neuropsychiatric disorders such as stroke, dementia and cognitive decline, neurodevelopmental disorders, depression, and anxiety disorder.

On a mechanistic level, a significant number of studies suggest the involvement of reactive oxygen species/oxidative stress and inflammatory pathways, among others, to fundamentally drive the adverse brain health effects of noise exposure. This in-depth review on the cerebral consequences of environmental noise exposure aims to contribute to the associated research needs by evaluating current findings from human and animal studies. From a public health perspective, these findings may also help to reinforce efforts promoting adequate mitigation strategies and preventive measures to lower the societal consequences of unhealthy environments.

Conclusions and future considerations

Recently the hypothesis was put forward that genetic (familial) predisposition for non-communicable diseases may be outcompeted by environmental risk factors and leading environmental health experts are calling for an environment-wide association study (EWAS) (Sainani, 2016). This change of dogma is also reflected by statements such as “Genetics loads the gun but the environment pulls the trigger” (Bray et al., 2004Olden and Wilson, 2000), also put forward by F. Collins, the director of the NIH. This shift was triggered by the exposome concept based on the study of life-long environmental exposure and its association with biochemical changes in the organism and adverse health effects (Wild, 2005Vrijheid, 2014). Whereas it is well accepted that environmental chemical pollution contributes dramatically to the global burden of disease and mortality (up to 9 to 12.6 million annual deaths, reflecting 16–20% of total mortality worldwide), as reported by the Lancet Commission on Pollution and Health (Landrigan et al., 2018), the (WHO, 2016), and the Global Burden of Disease Study (Cohen et al., 2017Collaborators GBDRF, 2017), the impact of mental stress and physical environmental factors causing mental stress, especially traffic noise, are far less well studied. Most societal prevention action plans and global estimations of environmental adverse health effects neglect the non-chemical environmental health risk factors mental stress, noise, nocturnal artificial light exposure, and climate changes (Daiber and Munzel, 2020). In order to address this research gap and to respond to the associated research need, we have summarized the current knowledge on the adverse effects of noise on the brain and the relation to neuropsychiatric outcomes. The cardiovascular health impact by noise was summarized in full detail by a systematic review of the WHO Environmental Noise Guidelines for the European Region (Kempen et al., 2018). Also the impact of noise on mental health was summarized by a systematic review of the WHO Environmental Noise Guidelines for the European Region (Clark and Paunovic, 2018), supported by specific assessment of adverse effects of noise on annoyance (Guski et al., 2017), cognition (Clark and Paunovic, 2018), and sleep (Basner and McGuire, 2018). With our present review we aimed to provide a mechanistic link for the observed clinical outcomes.

In order to further increase the quality of existing clinical/epidemiological data, future large-scale exposome studies addressing the health side effects of noise exposure on the brain and mental health are urgently warranted. Considering the accumulation of environmental risk factors in urbanized areas (e.g. noise, light pollution, air pollution, and psychosocial stress), the health problems, disease burden, and number of deaths associated with the totality of these environmental stressors may even be higher than all estimations in the past (Daiber and Munzel, 2020Munzel and Daiber, 2018). Mitigation strategies and preventive measures at this level may result in substantial lowering of societal consequences by unhealthy environments, e.g. lowering of the global burden of disease and public health costs. Future animal and human studies on adverse health effects of noise should focus on markers of oxidative stress (e.g. 3-nitrotyrosine and markers of lipid peroxidation) and inflammation (e.g. IL-6, sVCAM-1) in order to obtain a quantitative image of the inflicted damage (Munzel et al., 2021Bagheri Hosseinabadi et al., 2019). Also, mechanistic studies would be helpful addressing changes of circadian rhythm (e.g. Per1, Cry1, BMAL1 and CLOCK) as well as regulators of circadian rhythm (e.g. FOXO-3, NRF2) (Kroller-Schon et al., 2018Bayo Jimenez et al., 2021). In addition, measurement of stress hormones such as catecholamines, cortisol, or down-stream activated endocrinal systems such as the renin-angiotensin-aldosterone axis could provide important insights into the degree of noise-mediated stress responses and activation of detrimental hormonal pathways (Munzel et al., 2021Daiber et al., 2020). Human studies associated noise annoyance, anxiety disorders, and depression with the clinical manifestation of atrial fibrillation (Beutel et al., 2016Hahad et al., 2018Hahad et al., 2021), underlining the strong stress-dependent component in the adverse health effects of noise. Animal research should clearly define the applied noise on a qualitative and quantitative basis, which includes besides the duration of exposure also mean sound pressure levels, frequencies, pattern (continuous versus interrupted) as we have reported previously that continuous white noise at similar exposure duration and mean sound pressure levels was not harmful in contrast to aircraft noise with irregular breaks (Munzel et al., 2017). Human studies should clearly state the mean sound pressure level (e.g. Leq or Lden) and at least try to report separate health effects by noise at day versus at night as nighttime noise is more detrimental for cardiovascular health and probably also other systems’ dysregulation (Munzel et al., 2020). Preferably, human studies should measure the real noise exposure in the sleeping room during night and not the mean sound pressure values at the address level as many factors may influence the indoor noise exposure such as the presence of sound insulation windows or sleeping with open windows. This research complications may also require to conduct more mechanistic field studies with clearly defined nocturnal noise exposures and assessment of an advanced set of functional as well as biochemical parameters as done by us in the past (Schmidt et al., 2013Herzog et al., 2019Schmidt et al., 2021). Human studies should not only concentrate on noise exposure-clinical outcome associations (e.g. calculate the increased risk of ischemic heart disease, hypertension, or diabetes with increasing mean sound pressure levels) – whereas these association studies are highly important, e.g. for defining safe legal limits for noise exposure, mechanistic insights from large population studies with clearly defined sophisticated endpoints such as changes in epigenetic markers or arterial stiffness are also highly warranted (Foraster et al., 2017Eze et al., 2020). As we also know that environmental noise co-localizes with other environmental risk factors such as air pollution, light pollution or heat islands in highly urbanized areas, especially big cities (Munzel et al., 2021Munzel et al., 2021), future human studies should carefully adjust for these other environmental risk factors besides the common confounders such as sex, age, social status, work strain, and others. Research gaps may comprise the knowledge on the reversibility of noise-induced damage as not much is known on the persistence of the adverse health effects of noise. Also, resilience should be addressed in more detail to understand why some individuals are more resistant to noise-mediated stress responses. This could also help to identify new targets for pharmacological or life style interventions against the adverse health effects of noise.

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