|
 
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| REVIEW ARTICLE |
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| Year : 2022 | Volume
: 6
| Issue : 4 | Page : 226-231 |
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Is noise exposure a risk factor for cardiovascular diseases? A literature review
Andre Faria1, Ana Clara Caldas1, Ismail Laher2
1 Faculty of Medicine, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil
2 Department of Anesthesiology, Pharmacology and Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada
| Date of Submission | 12-Oct-2022 |
| Date of Acceptance | 22-Nov-2022 |
| Date of Web Publication | 16-Dec-2022 |
Correspondence Address:
Prof. Ismail Laher
Department of Anesthesiology, Pharmacology and Therapeutics, Faculty of Medicine, University of British Columbia, 2176 Health Sciences Mall, Vancouver, British Columbia, V6T 1Z3
Canada
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/hm.hm_48_22
We are exposed to noise on a daily basis, and noise pollution is increasingly becoming more intense, especially with more people living in the urban areas. Cardiovascular diseases (CVDs) are the leading cause of mortality worldwide and of global public health concern. Preventing and treating CVDs requires a better understanding of the associated risk factors. There is emerging evidence that noise pollution, especially related to the various forms of transport, is likely a contributor to the pathogenesis and aggravation of CVDs. We review key epidemiological data that address the link between excessive noise exposure and CVDs in humans and present proposed pathophysiological mechanisms underlying this association.
Keywords: Annoyance, cardiovascular disease, noise, oxidative stress, transport
How to cite this article:
Faria A, Caldas AC, Laher I. Is noise exposure a risk factor for cardiovascular diseases? A literature review. Heart Mind 2022;6:226-31 |
| Introduction | |  |
Cardiovascular diseases (CVDs) are the leading cause of mortality worldwide, causing 17.9 million deaths per year.[1] The most relevant risk factors related to the pathophysiology of these conditions involve environmental factors, lifestyle habits, and genetic traits in a complex and multidimensional dynamic. Studies of nonmodifiable risk factors (e.g., sex, age, and ethnicity) and modifiable lifestyle factors (e.g., smoking, physical inactivity, unhealthy diet, and excess alcohol consumption) have consistently shown to increase the risk of CVDs, both individually and in combination.[2] However, despite this well-established relationship, recent results suggest that environmental factors such as mental stress and noise pollution may also have a significant influence on CVDs.[3],[4],[5],[6],[7],[8],[9],[10],[11],[12],[13]
The disability-adjusted life years (DALYs) measure is commonly used to evaluate the health burden produced by an intervention on morbidity and mortality rates. It estimates the number of healthy years lost by a population, either by an illness, disability, or early death, related to a specific exposure. According to the World Health Organization, the estimated annual DALYs loss due to noise exposure in Western Europe is approximately 1 million years.[6] It is estimated that ischemic heart disease (IHD) causes an annual loss of 61,000 years, and that noise pollution increases the risk of incident IHDs by 8% for every 10 decibels (dB) at levels exceeding 53 dB (95% confidence interval [CI], 1.01–1.15).[14] Epidemiological data indicate that those chronically exposed to high levels of environmental noise are at increased risk of CVDs such as myocardial infarction.[15] Moreover, one in three individuals is affected by daytime noise while one in five have disturbed sleep at night due to excessive environmental noise, especially related to traffic. Therefore, excessive environmental noise is a cause of nuisance but raises public concern in terms of cardiovascular health.
The mechanisms underlying noise-induced CVDs were poorly understood until recently, mainly because of the lack of efficient models for translational research relevant to humans. The current literature indicates that noise annoyance, chronic stress and sleep disturbance, as well as the consequent activation of the autonomic and endocrine systems, are largely responsible for the pathophysiologic alterations that directly or indirectly contribute to the initiation and progression of CVDs.
| Methodology | | |
A thorough literature search was carried out using Google Scholar and PubMed databases and we selected only articles published in peer-reviewed academic journals using the following terms: CVDs, cardiovascular risk, noise, transport noise, oxidative stress and environmental factors. Additional resources were identified by using PubMed's “related citations” feature. Only studies published in the last 10 years, whose main finding dealt with the relationship between noise exposure and the development of CVDs, were chosen. The abstract was used to select the 31 primary research papers chosen for inclusion in this review. The remaining references were gathered from the bibliographies associated with these cited papers.
| Impact Of Noise On Hearing | | |
Noise is defined as an unpleasant, disagreeable, and unwanted sound that leads to discomfort of a living being.[16] However, this explanation is subjective and hampers the establishment of an unambiguous definition, since sound perception varies greatly with the setting and over time in the same individual. In addition, hearing sensitivity can vary depending on the time of exposure and circumstances. For instance, night time disturbance can be achieved at lower volumes compared to the same exposure during the daytime.
Measuring sound intensity in decibels is a strategy to standardize sonorous perception. For illustrative purposes, the normal breathing pattern is ~10 dB, normal conversations ~60 dB and a thunder-clap close to 120 dB.[16] Continued exposure to noise above 70 dB over time causes hearing loss.[14],[15],[16],[17] It is important to appreciate that dB units are measured on a logarithmic scale, meaning that if the smallest audible sound is considered to be 0 dB, a 10 dB sound is 10 times stronger and a 20 dB sound is 100 times louder, and so on. The volume and the duration of exposure to the sound defines how harmful the noise is. In general, the louder the noise is, the less time will be required before hearing loss occurs [Figure 1].[14],[16],[18],[19] | Figure 1: Increased sound levels from various source, have distinct effects on hearing health. The threshold for hearing harm is 70 dB, however the sound intensity and the time of exposure determine the rate and degree of harm[14],[16],[18],[19]
Click here to view |
| Cardiovascular Effects of Noise Exposure – Epidemiological Evidence | | |
Besides a direct effect on hearing loss, noise disturbance is also intimately associated with negative systemic health outcomes. The harmful effects on cardiovascular and autonomic homeostasis are especially important, even for noise levels that commonly occur in urban areas [Figure 2].[19],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30] Although the starting point for detrimental effects of noise pollution is quite similar (~50 dB) for different cardiovascular outcomes, there are noticeable differences in the intensity of the afflicted risks, for example, aircraft noise exposure increases the risk of myocardial infarction nearly four times more than the increased risk for heart failure. | Figure 2: Cardiovascular risk due to different sources of transportation noises. Cardiovascular harms to health start before effects on hearing (50 dB vs. 70 dB). Some risks are more pronounced than others even for the same source (e.g., the risk for myocardial infarction is greater than the risk of stroke related to exposure to aircraft noise). It is important to note that the data serve mainly illustrative purposes since they were retrieved from different studies using a different methodology in distinct populations, hampering scientifically significant comparative conclusions[19],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30]
Click here to view |
A recent meta-analysis reported that an average exposure to road traffic noise higher than 50 dB can have detrimental effects on cardiovascular health by increasing the risk of IHD, which imposes a 6% increase in risk for every 10 dB increase in sound levels (95% CI, 1.03–1.09).[21] Noteworthy, this association remained relatively unchanged even when confounding factors such as smoking and sedentary life styles were considered, suggesting road traffic noise may be an independent factor for CVDs. This association was further strengthened by a cohort study published in 2022, in which the enhanced risk of IHD, myocardial infarction, angina pectoris, and heart failure, in hazard ratios (HRs) were 1.052 (95% CI, 1.044–1.059), 1.041 (95% CI, 1.032–1.051), 1.095 (95% CI, 1.071–1.119), and 1.039 (95% CI, 1.033–1.045) per 10 dB higher for 10-year mean exposures, respectively.[31]
The effects of noise from other transportation modalities (such as aircraft and railway noise) on IHD yielded inconclusive findings, likely due to the low quality of evidence and the lack of large prospective cohort studies.[21],[22] However, two recent cohort studies in Western Europe report that rail and aircraft sonorous pollution increased myocardial infarction risk by 18% (95% CI, 0.93–1.46) and 26% (95% CI, 1.004–1.048), respectively.[23],[24]
The most in-depth results currently available on the effects of noise on CVDs comes from the analysis of the relationship between hypertension and noise exposure. A meta-analysis of 24 studies conducted in 2012 revealed a significant odds ratio of 1.034 for prevalent hypertension for every 5 dB (A) increase in road traffic noise (95% CI, 1.011–1.056).[32] Because the meta-analysis was based on cross-sectional research, the interpretation of causality is constrained. On-going studies on incident hypertension complement the cross-sectional findings by demonstrating that exposure to traffic noise is directly related to hypertension.[32],[34],[35],[36]
A large cohort study reported in 2011 that for every 10 dB increase in traffic noise, the risk of incident stroke and coronary heart disease increased by 14% (95% CI, 1.03–1.25).[25] This finding was further validated by two separate studies from London, the United Kingdom, on aircraft and traffic noise.[26],[27] In a community of 3.6 million people who live near Heathrow Airport, daytime and nighttime aircraft noise levels above 55 dB significantly increased the risk for stroke hospitalization by 24% (95% CI, 1.08–1.43) and 29% (95% CI, 1.14–1.46), respectively, when compared to levels below 50 dB.[30] This finding not only indicates that noise pollution negatively affects the risk of stroke but that nocturnal noise may be particularly dangerous. In a more recent analysis, road traffic noise was also associated with a higher risk of incident stroke (HR = 1.06/95% CI, 1.03–1.08). In contrast, railway noise was not associated with stroke, and for the few persons exposed to aircraft noise, stroke was associated with low exposure, but there was no association for those in the high-exposure group.[37]
There is recent evidence that atrial fibrillation and heart failure can be initiated by noise pollution.[23],[28],[29],[30],[36],[38] Road traffic, railway, and aircraft noise can increase the risk of heart failure. The increases in risk ranged from 2% to 8% for every 10 dB increase, depending on the study and the kind of exposure.[23],[28],[29],[30] Only a few studies have examined the impact of noise on the risk of atrial fibrillation; some of these studies found a positive connection, while others found no association, emphasizing the need for additional research on noise and this prevalent condition.[30],[36],[37] The most recent results from a cohort study in Denmark report that road traffic, railway, and aircraft noise increased incident risk for atrial fibrillation, ranging from 2%–6%.[38] The association remained positive even after adjustment for air pollution. This emerging evidence suggests an association between noise exposure and CVDs and hopefully serves as a springboard for futures researches.
It is also important to note that the enhanced risk for CVDs begins at intensities lower than those associated with hearing harms (50 dB vs. 70 dB) and even lower than volumes of regular conversations normally considered harmless (50 dB vs. 60 dB). These findings are likely due to stress and personal perception of annoyance in the pathophysiology of cardiovascular outcomes.
Additionally, there is emerging evidence that noise exposure also harms brain and associated neuropsychiatric functions.[39] The Chicago Health and Aging Project (5,227 participants) showed that residential noise exposure increased the risks of mild cognitive impairment and Alzheimer's disease by 36% (95% CI, 1.15–1.62) and 29% (95% CI, 1.08–1.55), respectively, for every 10 dB increase.[40] Poorer global cognitive scores and mild cognitive impairments were also linked to exposure to traffic-related noise, according to data from a German study.[41] Interestingly, a significant interaction between noise and past and current smokers indicates that lifestyle risk factors may amplify the detrimental effects of noise exposure on cognition.[39],[40],[41] Road traffic noise exposure was also linked to 4% (95% CI, 1.03–1.11) higher odds of depression and 12% (95% CI, 1.04–1.30) higher odds of anxiety with every 10 dB increase in noise according to a recent meta-analysis.[42] It is important to remember that the majority of studies were cross-sectional and generally of poorer quality. More substantial evidence was provided in a meta-analysis reporting that aircraft noise exposure increased depression risk by 12% (95% CI, 1.02–1.23), compared to lower levels attributed to road traffic and railroad noise (where there were 2%–3% increases in depression risk [not scientifically significant]).[43]
| Pathophysiology | | |
The mechanisms linking noise and the development of CVDs were mostly unknown until recently, largely due to the lack of models for translational (animal) research applicable to humans. It is hypothesized that noise annoyance and consequent chronic stress, activation of the autonomic and endocrine system, and disruption of sleep may play a role in the etiopathogenesis of noise-induced CVDs. Current data suggest that noise annoyance and chronic stress can eventually result in the pathophysiologic changes that will either directly or indirectly contribute to the onset and progression of CVDs.[44],[45]
The noise-reaction model developed by Babisch proposes that CVD can result from a dual pathway from which noise affects human physiology.[44] This initial concept has been improved, and a noise reaction scheme with both a direct and indirect approach has been created [Figure 3]. The first, or direct pathway, includes consequences that result from loud noise; loud noise will harm hair cells and auditory system sensory receptors and interfere with sleep. In the second, the “indirect pathway”, increased noise levels disrupt sleep, communication, and activities, causing subsequent emotional and cognitive disturbances and, ultimately, discomfort. The resulting chronic stress response, with an important role for cortisol, leads to pathophysiologic changes either acutely or over a longer time period, causing negative health outcomes. This model can explain the enhanced cardiovascular risk due to relatively prolonged exposure to transportation noise of only 50 dB when regular conversations can reach 60 dB (usually of shorter durations) without the same repercussions.[21],[22],[23],[24],[25],[26],[27],[28],[29],[30],[36],[38] Besides the intensity and duration of the stimuli, personal perception also plays a crucial role in the risk of noise pollution on CVDs, since the resulting annoyance and consequently increased secretion of stress hormones are key triggers to the pathophysiology of the outcomes. | Figure 3: The hypothalamic-pituitary-adrenal axis is activated in the stress response to noise, which is characterized by inflammation, thrombosis, and altered gene expression. Created with BioRender.com
Click here to view |
Uncertainty exists regarding the molecular mechanisms linking noise, vascular injury, and CVDs. Chronic stress reactions can cause vascular (endothelial) dysfunction by augmenting oxidative stress, and subsequent activation of prothrombotic pathways and vascular inflammation.[46],[47] These reactions involve the activation of the autonomic nervous system as well as higher circulating levels of cortisol. This hormone, commonly referred to as “the stress hormone,” participates in a complex system of positive and negative feedback mechanisms that secretes catecholamines and alters blood pressure, blood lipid levels, blood sugar, blood viscosity, and heart rate.[19] It is important to note that these pathophysiologic pathways may not be mutually exclusive, and can be activated at different times after noise exposure, and range in significance depending on the duration and intensity of noise exposure.
The stress response, which is characterized by sympathetic system activation and elevated levels of catecholamines, cortisol, and angiotensin-II, initiates a chain of events that eventually results in vascular damage.[19] Angiotensin II is a powerful stimulator of the vascular and phagocytic nicotinamide adenine dinucleotide phosphate oxidase to increase oxidative stress in the blood and vasculature. Reactive oxygen species scavenge nitric oxide (NO) and cause endothelial NO synthase uncoupling, so limiting the bioavailability of NO.
Oxidative stress and excessive inflammation have synergistic effects. When immune cells (monocytes/macrophages, natural killer cells, and neutrophils) invade the vasculature, they produce more superoxide, which leads to oxidative protein modifications, as well as harmful redox-regulatory effects on cellular signaling pathways. Increased blood pressure, pronounced impairment of vasodilation, and lower endothelial NO generation are all caused by higher amounts of circulating and tissue glucocorticoids.[46] Increases in catecholamine levels, as well as cross-activation by glucocorticoids, activate vasoconstriction pathways. Heart failure, coronary artery disease, arterial hypertension, and metabolic disturbances can all result from these vascular changes.[19],[46],[48]
Studies show that if subjects were previously exposed to noise, then the association between noise and endothelial function is more apparent (“priming effect”).[47] This suggests that the vasculature is likely to be sensitized to vascular injury in response to repeated exposures to noise, and that the vasculature is unlikely to be desensitized to the harms of chronic exposure to noise. Furthermore, patients with preexisting coronary artery disease have a more significant negative correlation between noise and endothelial function.[46],[47] Interestingly, there was no link between noise sensitivity/annoyance to endothelial dysfunction after nighttime exposure, suggesting that endothelial function declines in response to nighttime noise regardless of whether or not there is an annoyance reaction to noise. This finding is supported by recent findings showing that nighttime noise can interfere with the nocturnal physiological decline in blood pressure decrease and so increase cardiovascular risk.[48]
| Conclusion | | |
This brief literature review summarizes the evidence indicating that noise is associated not only with auditory harms but also to cardiovascular health impairments. Several observational and experimental studies report that noise exposure leads to annoyance, disruption of sleep, and daily activities, in addition to increasing the occurrence of hypertension and CVDs.
Our current understanding of the pathophysiological mechanisms suggests that noise is linked to oxidative stress, vascular dysfunction, autonomic imbalance, and metabolic abnormalities, all of which can amplify the negative effects on cardiovascular risk factors such as arterial hypertension. Noise pollution can accelerate atherosclerosis, raise the risk of cardiovascular events and worsen prognosis when there are preexisting cardiovascular risks.
The need for additional studies on the interaction between noise as a novel risk factor for CVDs and its collective impact on cardiometabolic health is becoming increasingly urgent. Future studies should focus on establishing efficient translational models to better elucidate the mechanistic pathways underlying noise-induced CVDs in humans and identify possible therapeutic targets. Studies to identify new specific biomarkers are still in their infancy.
Ethical statement
The ethical statement is not applicable for this article.
Financial support and sponsorship
Nil.
Conflicts of interest
Dr. Ismail Laher is an Editorial Board Member of Heart and Mind. The article was subject to the journal's standard procedures, with peer review handled independently of Dr. Ismail Laher and the research groups. There are no conflicts of interest.
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