Effects of noise exposure on the cardiovascular system.

Traffic noise is a hot topic. The Corona crisis has taught people to appreciate the peace and quiet that occurred in many places over several weeks as a result of drastically reduced mobility and a decrease in traffic-related noise.

The measurement and description of noise [1]

The objective physical measure for disturbing sound, i.e. noise, is the decibel (dB), a logarithmic measure. An increase of 10 dB corresponds to a doubling of the perceived loudness. A doubling by two equally loud sound sources causes an increase of the dB value by 3 dB. The subjective evaluation of the sound depends on loudness, frequency, tonality, impulsiveness, time of occurrence and duration of the sound. For example, the human ear perceives low and high tones as less loud than medium-high tones at the same sound pressure. Most countries use the so-called A-frequency filter (dB(A)) to describe noise, in order to correct the measured values for the different frequencies of the sound according to human hearing.

For the assessment of the disturbing effect of noise pollution, an average value of the sound levels is used, the so-called energy-equivalent continuous sound level Leq. It measures the total energy of noise events over a certain measurement period, for example the whole day, the whole night, or a whole year. The day-evening-night level Lden, also a mean value, is defined to encompass the entire day. To account for the difference in annoyance during different times of the day, the evening hours are weighted with an addition of 5 dB(A) and the night hours with an addition of 10 dB(A).

To limit noise pollution in Switzerland, the Noise Abatement Ordinance sets planning values, immission limits and alarm values for various types of noise. They are adjusted to the noise sensitivity of the polluted area and are lower during the night. In purely residential areas, for example, the immission limits for day and night are 60 and 50 dB, respectively – these limits define the threshold above which noise significantly disturbs the well-being of the population. The analog alarm values are 70 and 65 dB, respectively, and indicate the urgency of renovations such as the installation of soundproof windows. In order to take into account the different disturbance effects of different types of noise in the limit values, level corrections, so-called K-values, are also applied. For example, for the assessment of limit violations in industrial noise, two to six decibels each are added to the measured values with increasing sound and impulse content.

Traffic noise exposure of the Swiss population and noise abatement measures

Road traffic is the biggest contributor to the noise pollution of the population. According to estimates by the Federal Office for the Environment, one in seven people are exposed to harmful or annoying noise at their place of residence during the day and one in eight at night. Road traffic noise affected, i.e. noise exposure above the immission limit. Road traffic noise is essentially an urban problem, but areas outside the influence of urban core zones are also affected by it to more than 5% (Fig. 1). With 8.3 million inhabitants in Switzerland (as of 2015), this amounts to approx. 1.1 million people during the day and approx. 1.0 million at night. Furthermore, around 16,000 people are affected by harmful or annoying railroad noise at their place of residence during the day and 87,000 at night. Harmful or annoying aircraft noise affects 24,000 people at their homes during the day and 75,000 at night [1].

The first priority in noise abatement measures is to reduce noise emissions at the source (e.g. low-noise road surfaces and tires; speed reduction on roads; lighter vehicles, modern rolling stock on trains; noise-reduced aircraft). The second priority is to combat noise propagation (e.g. construction of noise barriers). If noise emissions from installations cannot be reduced below the limit values due to higher priorities (e.g. national road or railroad construction), noise protection measures on surrounding buildings come into play (e.g. soundproof windows and comfort ventilation).

Traffic noise as a cardiovascular risk factor: suspected mechanisms of action.

Based on existing evidence, airborne particulate matter has been classified as a causal risk factor for cardiovascular morbidity and mortality for several years. Air pollution is considered the most important environmental risk factor from a health perspective, but is immediately followed by traffic noise [2].

It is increasingly scientifically confirmed that noise can ultimately lead to pathophysiological changes in the vascular system via noise pollution, chronic stress, activation of the autonomic nervous and endocrine systems, and disruption of sleep. These changes may eventually result in the recurrence or progression of cardiovascular disease.

The evaluation of noise pollution is influenced by personal factors. These include, for example, individual as well as societal attitudes and value judgments towards the noise source or psychological situation and current activity of the affected person. However, an important finding is that the perception of noise as a stressor is not a prerequisite for its pathophysiological effects.

Noise, whether consciously perceived as a stressor or through its objective stress effects, shifts the balance of stress-associated biological pathways from a repeated acute escape response to a chronicized stress response [3]. Noise, like other chronic stressors, is associated with an increase in blood pressure, blood glucose, blood viscosity and blood lipids, as well as activation of blood coagulation (Fig. 2) . These are all pathophysiologically established biomarkers in the development of cardiovascular disease. It has also been shown that noise can also trigger endothelial dysfunction via oxidative stress and inflammatory processes. Noise exposure was further associated with a decrease in cardiac rhythm variability. In animal models, noise exposure additionally led to inflammatory processes in the intestine, which may also lead to changes in the intestinal flora. Genomic study of noise-induced changes in animal aortic tissue revealed alterations in genes with regulatory function on vascular function, vascular remodeling, and cell death [3].

Epidemiologic evidence on associations between traffic noise and cardiovascular disease.

Based on a meta-analysis of existing evidence, a WHO-commissioned expert group concluded that traffic noise, particularly road traffic noise, increases the risk of ischemic heart disease (stable coronary disease and acute coronary syndromes) based on evidence [4]. WHO estimated that the incidence of ischemic heart disease increases by 8% for every 10 dB increase in noise exposure beginning at 53 dB. At the same time, it may also increase the risk of hypertension, stroke, arrhythmias, heart failure, obesity, and diabetes [5–7]. Recent epidemiological studies further strengthen these suspected associations. In addition, unlike older studies, more recent evidence takes into account concurrent exposure to air pollution and socioeconomic factors. Both also influence the risk of cardiovascular disease. At the same time, they are often strongly correlated with traffic noise. However, when adjusting for these factors in multiple regression models, the association of traffic noise with cardiovascular disease usually persists and often changes only weakly.

Based on an analysis of the dose-response relationship, WHO recommended lowering Lden to protect against cardiovascular disease as follows: below 53 dB for road traffic; below 54 dB for railroad noise; and below 45 dB for aircraft noise. These values are lower than the immission limits of 55 dB currently recommended by the WHO.

Traffic noise at night is particularly critical [8,9]. For self-reported and polysomnographic sleep disorders, noise is particularly relevant in the early morning hours when sleep pressure is less. Also proven are problems falling asleep when exposed to noise in the early hours of the night. However, epidemiologically distinguishing the long-term effects of traffic noise during the day and at different times of the night is challenging. For example, attributing traffic noise to residence is more prone to error during the day, since most people also spend a significant percentage of the daytime at locations other than their homes. Moreover, daytime and nighttime noise at the place of residence are often so highly correlated that their independent effects on health are difficult to elicit. However, there is epidemiological evidence that for acute cardiovascular events, noise during the night is particularly harmful, especially when it occurs in the form of single events that stand out from the general background noise. In contrast, for more chronic cardiovascular endpoints, such as heart failure, traffic noise exposure throughout the day appears to be important.

The research journey – it continues and becomes broader

With regard to an efficient prevention of cardiovascular diseases, it is important on the one hand to characterize the causality of environmental risks even better. On the other hand, against the backdrop of the convergence of different environmental risks (such as air pollution, traffic noise, and lack of green space), especially in urban environments, we want to better understand the health effects of multiple interacting factors.

Exposome research offers a hand in this regard [10]. The exposome has been defined as the totality of all endogenous and exogenous factors to which a human organism is exposed during life. Of course, this cannot be analyzed in this extreme form. Nevertheless, modern technologies offer the possibility of measuring environmental factors and people’s behavior much more precisely by means of sensors, satellite data or wearables than was previously possible using only questionnaire data. In addition, we can use genomic technologies (-omics technologies) to analyze thousands of molecules in various, easily accessible body fluids. In research consortia with large long-term studies and associated biobanks, these technologies are applied to more precisely measure and model, for example, noise exposure and simultaneously other exposures (food environment, built home environment, social environment) of study participants. At the same time, the material stored in the biobanks is used to look for molecular fingerprints that these exposure patterns leave in the body. New insights into biological mechanisms of action of environmental and lifestyle factors can be derived from the associated molecular networks [11]. An understanding of biology is an important pillar of causal understanding.

A public health assessment of the association between traffic noise and cardiovascular disease.

The acute effects of traffic noise on cardiovascular parameters and disease can be clearly demonstrated in laboratory experiments and in humans in natural experiments. Long-term exposure to chronic traffic noise cannot be randomized, analogous to other environmental risks, so evidence is based on observational epidemiologic studies. While the causality of noise associations observed in long-term studies can be approximated using the exposome methods outlined above, it will never be absolute. Therefore, the regulation of noise immis-sions and emissions will always have to take place against a background of some uncertainty. It is the case, however, that the evidence for a causal effect of traffic noise on health is so strong, and that the associated burden of disease is potentially so great, that doing nothing is not an option. It is the task of science, in dialogue with politics, to point out the importance of resting protection measures. These efforts are now receiving support from the Corona epidemic. The new calm brought by the lockdown has made citizens more sensitive to traffic noise. In various regions of Europe, including Switzerland, efforts are now underway to record noise violations by individual vehicles by means of controls, analogous to speed limits and speed checks, and to regulate them better.

An evaluation of the cardiovascular effects of traffic noise from a clinical perspective.

For clinical consideration, it is significant that traffic noise may contribute to both the new onset of cardiovascular disease and the clinical course of existing disease. This means that both primary care physicians and specialists can make recommendations on noise prevention for their patients. In the foreground of the consultation are the recommendations that protect night sleep from too much noise. This includes advice on protecting the bedroom from too much noise by placing it on the quietest side of the house. In the presence of comfort ventilation in the house can also make sense to recommend sleeping with the window closed, especially on not too hot days. If these measures are not possible, sleeping with hearing protection may be recommended. For patients who are particularly sensitive to noise, it may also make sense to recommend a change of residence to a quieter location. From an individual perspective, a change of residence can presumably increase overall health-related quality of life, because noise annoyance and noise sensitivity were associated with considerable limitation in this regard in our own studies [12]. From a public health perspective, of course, it is not a recipe, as it creates the potential for increased traffic and an increase in environmental pollution, including noise. It is therefore all the more important to protect residential areas with measures at the source and adequate long-term spatial planning.

Take-Home Messages

People who are chronically or acutely exposed to high levels of traffic noise have an increased risk of suffering a heart attack and are also likely to develop other cardiovascular diseases and diabetes.
Advise your patients to move their bedroom to the quietest side of the apartment or house to protect against increased cardiovascular risk.
Measures against excessive subjective noise exposure contribute to an improved health-related quality of life.

Literature:

FOEN (ed.): Noise Pollution in Switzerland 2018. Results of the national noise monitoring sonBASE, as of 2015. Federal Office for the Environment. Bern. Environmental State, No. 1820: 30 pp.
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WHO (World Health Organ.). Environmental noise guidelines for the European region 2018. rep, WHO Reg. Off. Eur., Copenhagen. www.euro.who.int/__data/assets/pdf_file/0008/383921/noiseguidelines-eng.pdf?ua=1
Kempen EV, Casas M, Pershagen G, et al: WHO environmental noise guidelines for the European Region: a systematic review on environmental noise and cardiovascular and metabolic effects: a summary. Int J Environ Res Public Health 2018; 15: 379.
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