Cardiologue, directeur de l'Observatoire de la prévention de l'Institut de Cardiologie de Montréal. Professeur titulaire de clinique, Faculté de médecine de l'Université de Montréal. / Cardiologist and Director of Prevention Watch, Montreal Heart Institute. Clinical Professor, Faculty of Medicine, University of Montreal.See all articles
- Chronic exposure to noise from road, rail or air traffic is associated with a small but significant increase in the risk of cardiovascular events.
- This association is largely due to the activation of physiological responses to stress, leading to a series of adaptations (accelerated heart rate, increased viscosity and coagulability of the blood, increased blood pressure), which generate an inflammatory and pro-oxidant climate that can contribute to the development of these diseases.
It is now well established that many cardiovascular diseases are the result of certain unfavourable lifestyle habits, in particular smoking, a sedentary lifestyle, stress, being overweight, and a poor diet. The potential for preventing cardiovascular disease is therefore enormous: studies indicate that eliminating these risk factors by adopting an overall healthy lifestyle could prevent up to 85% of these diseases and significantly increase life expectancy.
In recent years, it has also been possible to demonstrate that other environmental factors, which are much more difficult to control by individuals, also contribute to the development of cardiovascular disease and the premature mortality associated with it. This is particularly striking with regard to air pollution, which alone is responsible for around 4.5 million deaths globally, mostly on the Asian continent (Figure 1). However, we should not forget the contribution of other environmental stressors to excess cardiovascular mortality, in particular those associated with climate change (extreme heat, forest fires) or the increasing urbanization of societies (light pollution, noise).
Figure 1. Excess mortality linked to cardiovascular disease attributable to air pollution each year worldwide. From Hahad et al. (2023).
Among these factors, noise linked to transport activities (road, rail and air traffic) is increasingly recognized as an environmental stressor that is associated with a wide range of health problems, particularly at the cardiovascular level. A large number of studies carried out in Europe, where more than 100 million people are exposed daily to road, rail and air traffic noise above the standards considered safe, suggest that these noise sources could contribute to almost 50,000 cases of cardiovascular disease and 12,000 premature deaths each year in this region. It is also estimated that 22 million Europeans are irritated by noise every day, and 6.5 million of them suffer from chronic sleep problems.
Noise can be very simply defined as unwanted and irritating sound. The intensity of noise emissions is the main factor that determines the degree of irritation felt in response to noise, and it is for this reason that all studies investigating the impact of noise on health measure noise in terms of sound pressure.
From a physical perspective, sounds are vibrations that are detected by the ear as small changes in air pressure. Since the human ear can detect a wide range of these pressure variations, the logarithmic decibel (dB) scale is used to represent this wide range of values more simply (see Figure 2).
Figure 2. Decibel scale and representative examples of noise sources. Adapted from the ministère de la Santé et des services sociaux du Québec (2016).
It is important to note that the logarithmic nature of the decibel scale means that every 10 dB multiplies the sound energy by 10 (Table 1). For example, if the volume inside a house is 60 dB and it reaches 90 dB following sudden exposure to a loud noise (siren, plane, construction), the difference of 30 dB corresponds to 1,000 times greater sound intensity (10 × 10 × 10). However, this does not mean that the noise is perceived 1,000 times louder, because the auditory sensation does not vary linearly with the variation in sound levels (see Table 1). A simple rule of thumb is that each 10 dB increase corresponds approximately to noise perceived twice as loud. In reality, the sound that went from 60 to 90 dB in the previous example is therefore heard 8 times louder (2 × 2 × 2).
Table 1. Variation of auditory sensation according to increase in sound levels.
|Increased noise level
|Multiple of sound energy
|Variation in auditory sensation
|2 times louder noise
|4 times louder noise
|8 times louder noise
|32 times louder noise
It should also be noted that noise is also a perception, i.e., a subjective interpretation of a sound by the brain. There are therefore variations in the reaction to a given noise depending on the person or the context in which it occurs. For example, a noise that occurs at night is generally perceived as more annoying than the same noise occurring during the day.
It has also been observed that the source of the noise can greatly influence the degree of negative response of people exposed to it: for example, it is well documented that at equal intensity, noise from airplanes causes greater irritation than noise from road or rail traffic (Figure 3).
Figure 3. Relationship between exposure to noise and the percentage of people who are very irritated by noise. Note that the day-evening-night noise levels (LDEN) indicator is used to estimate cumulative noise exposure over a 24-hour period, taking into account increased sensitivity during the evening and night. Increased corrective terms (penalties) are therefore applied, with an addition of 10 dB for noise that occurs at night and 5 dB for noise that occurs in the evening. From Münzel et al. (2020).
The effects of noise on cardiovascular health
As mentioned earlier, a very large number of epidemiological studies have noted a significant association between repeated exposure to road, rail and air traffic noise and an increased risk of cardiovascular disease. This effect is particularly well documented for road traffic (Figure 4): according to calculations carried out by a group of experts commissioned by the WHO, from 53 dB, each increase of 10 dB increases the risk of ischemic heart disease by 8% (RR=1.08), and this increase is considered conclusive, i.e., it has a high level of scientific certainty. A slightly lower increase (6% per 10 dB) has also been reported for air traffic, but its degree of certainty is lower given that these results come from ecological studies, i.e., carried out at the scale of entire populations and that do not collect information specific to individuals in these populations (see here and here, for example).
Figure 4. Increase in the risk of coronary heart disease according to the level of exposure to road traffic (red) and air traffic (blue). From Münzel et al. (2017).
More recent reviews come to similar conclusions, i.e., there is a slight (around 2-5% for each increase of 10 dB) but significant increase in the risk of cardiovascular events as a function of prolonged exposure to traffic noise, whether from road, air or rail traffic (see here, here and here, for example).
It is well documented that repeated exposure to noise causes sleep disruption as well as an emotional and cognitive response that can take the form of annoyance, irritation or anger when the noise interferes with thoughts, feelings or daily activities.
One thing these negative responses have in common is causing a stress reaction. In a broad sense, stress can be thought of as a programmed biological response, which is set in motion in reaction to a situation that is perceived as dangerous or destabilizing, either physically or psychologically. Noise, which is by definition a sound aggression, is therefore a stressor, in the same way as any situation or event that is interpreted negatively.
This is important because stress is known to significantly increase the risk of cardiovascular events, with an effect similar to those associated with well-documented risk factors such as excess abdominal weight and hypertension (Figure 5). It is therefore likely that the stress response caused by traffic noise represents the main mechanism responsible for the negative effects of noise on cardiovascular health.
Figure 5. Association between different lifestyle factors and the risk of myocardial infarction. Note that psychosocial factors (a combination of home, work and financial stress, incidence of tragic events and depression) are associated with an increased risk similar to that associated with excess abdominal weight and hypertension. Conversely, daily consumption of fruits and vegetables, regular exercise (4 or more hours per week), and alcohol consumption (3 or more drinks per week) are associated with a reduction of approximately 20-25% of the risk. From Yusuf et al. (2004).
The proposed model is as follows (Figure 6): the physiological response to noise involves two distinct pathways, a direct pathway, which represents the activation of the neural circuits of hearing, and an indirect response, which rather calls upon an emotional and cognitive response to noise. In the direct pathway, high intensity sounds can damage the hair cells of the inner ear, leading to reversible hearing fatigue (temporary elevation of the hearing threshold) or, for higher intensity sounds (> 85 dB(A)), to irreversible hearing loss.
Figure 6. Proposed pathophysiological mechanisms of the effect of noise on cardiovascular health. Noise elicits physiological responses through two distinct pathways (direct and indirect), which converge towards the activation of the physiological response to stress. Chronic activation of this response favours the onset or exacerbation of cardiovascular risk factors and can promote the development and progression of cardiovascular disease. From Münzel et al. (2021).
As for the indirect pathway, it is activated by sounds of lesser intensity, but which are perceived chronically. This repeated exposure generates extra-auditory effects, in particular a disruption of usual activities (sleep, conversation, leisure activities), which can trigger negative emotional and cognitive reactions (embarrassment, irritation, anger).
In both cases (direct and indirect pathways), exposure to noise triggers the activation of physiological responses to stress, namely the sympathetic nervous system and the corticotropic axis (hypothalamus-pituitary-adrenal) and leads to the release of stress hormones such as catecholamines (adrenaline, norepinephrine) and cortisol.
Activation of these stress pathways leads to a cascade of effects, including increased heart rate, increased blood viscosity and coagulability, and increased blood pressure. Stress hormones are also responsible for activating the renin-angiotensin-aldosterone system (RAAS), which contributes to increased blood pressure, and also cause inflammation and oxidative stress that can damage blood vessels and contribute to developmental cardiovascular disease.
Chronic stress is the central link between noise and cardiovascular health because it increases blood pressure, cardiac output, blood viscosity and clotting factors, while simultaneously influencing glucose and lipid levels, all of which represent important risk factors for the development of cardiovascular disease.
Cardiovascular risk factors
Three main risk factors for cardiovascular disease influenced by prolonged exposure to traffic noise were studied:
Hypertension. High blood pressure (hypertension) represents the leading risk factor for cardiovascular disease, being responsible for 10.8 million premature deaths worldwide in 2021. An association between hypertension and traffic noise has been repeatedly reported; for example, a meta-analysis of 26 studies carried out by a WHO-led expert group reported an increase in the relative risk of hypertension of 5% (RR=1.05) for every 10 dB of LDEN from road traffic. Increases in blood pressure have also been reported for people exposed to rail and air traffic.
Endothelial dysfunction. Several studies have shown that the main cardiovascular risk factors (hypertension, hypercholesterolemia, diabetes, smoking) have the common characteristic of disrupting the integrity of the endothelium, generating a pro-inflammatory, pro-oxidant and procoagulant microenvironment that promotes the development of atherosclerosis. This endothelial dysfunction also appears to occur in response to chronic exposure to traffic noise: for example, a study using 18F‐fluorodeoxyglucose (18F‐FDG) positron emission tomography showed that noise exposure caused activation of the limbic system (the amygdala, in particular), the region involved in the response to stressors. This activation was correlated with an increased degree of inflammation of the coronary arteries and an increased risk of several cardiovascular events, including myocardial infarction, stroke, and sudden death. These observations therefore suggest that traffic noise, and the subsequent sleep disruption and stress, create a pro-inflammatory and pro-oxidant climate that impairs endothelial function and may therefore contribute to the negative effects of traffic noise on cardiovascular health.
Metabolic factors. Longitudinal studies (monitoring populations over a given period of time) have reported that chronic exposure to traffic noise is associated with an increased risk of developing type 2 diabetes, an important risk factor for cardiovascular disease. This increase in risk seems to vary depending on the source of the noise, being for each 10 dB increase of approximately 10% for road traffic, 3% for rail traffic, and 1-4% for air traffic.
This increase in the risk of diabetes due to chronic exposure to noise could be explained by its well-documented negative effect on sleep quality and duration. It is indeed well established that sleep exerts a strong influence on the immune system and that sleep disturbances can unbalance immunity and generate pro-inflammatory conditions. The resulting chronic inflammation disrupts insulin secretion from the pancreas, reduces insulin sensitivity, and disrupts hormones involved in appetite control, all factors implicated in the development of type 2 diabetes.
The contribution of traffic noise to the development of cardiovascular disease is also suggested by the positive effects associated with a reduction in this noise. One of the best examples is certainly that of COVID-19: the confinement of the population, the closure of borders, and the travel restrictions caused by the pandemic led to a reduction of around 60% in global air traffic between 2019 and 2020 and, as a result, a drastic reduction in noise related to airport activities. For example, there was a reduction of up to 30 dB(A) in LDEN in the surroundings of the three Île-de-France airports (Paris–Charles-de-Gaulle, Paris-Orly, and Paris-Le Bourget) and, in Montréal, a reduction of almost 80% in the number of people exposed to noise levels of LDEN = 55–60 dB(A).
A major study suggests that this drastic reduction in aircraft noise had beneficial effects on the blood pressure of people who are normally regularly exposed to air traffic (LDEN = 61 dB). During a previous study, this team of researchers noted that these people exposed to aircraft noise had higher blood pressure than a control population not exposed to air traffic. During the COVID-19 pandemic, this cohort’s level of noise exposure fell from 61 dB to 47 dB, a major reduction that translated into less irritation from air traffic and a concomitant drop in systolic (121.2 vs. 117.9 mm Hg) and diastolic (75.1 vs. 72.0 mm Hg) pressure as well as arterial stiffness, as measured by the pulse-wave velocity technique. It therefore appears that reductions in air traffic noise levels could reverse the adverse effects of noise on cardiovascular health.
Given the socio-economic importance of road, rail and air traffic, reducing traffic noise is obviously not easy. For road traffic, since it is mainly the noise generated by the contact between tires and the road that is the cause, the replacement of combustion engine cars with battery electric cars will only lead to a minor reduction in road traffic noise. More effective noise reduction strategies include building noise barriers along busy roads and reducing speed limits. As for aircraft noise, planning flight routes to minimize overlap with densely populated areas and banning night flights, during which takeoff and landing are not permitted, are the strategies most likely to reduce the exposure of populations living nearby. Meanwhile, railway noise can be reduced by grinding railway tracks, replacing cast-iron brakes with composite materials, and implementing nighttime bans. Finally, people living in houses or apartments exposed to noise pollution can reduce indoor noise levels through the installation of sound-absorbing windows.