Acute exposure to simulated nocturnal traffic noise and cardiovascular complications and sleep disturbance—results from a pooled analysis of human field studies

Emerging evidence highlights the importance of environmental noise exposure as a substantial public health threat [6, 11]. In support of this, the European Environment Agency concludes that at least about 20% of the EU population in average, in many cities this percentage can reach up to 50% of the urban population, are exposed to long-term noise levels considered potentially harmful to health. Specifically, about 95 million people are exposed to harmful road traffic noise levels. Furthermore, it is estimated that at least 18 million people are highly annoyed and 5 million are highly sleep disturbed by long-term transportation noise in the EU, causing about 11,000 premature deaths and 40,000 new cases of ischemic heart disease per year [1].

During the last few years, strong evidence from epidemiological studies has emerged to demonstrate that traffic noise exposure is a risk factor for cardiovascular disease. For instance, in nationwide studies from Switzerland and Denmark, it was shown that transportation noise exposure is associated with all and cause-specific cardiovascular disease mortality [8, 13, 21] as well as significant cardiovascular outcomes including ischemic heart disease and its’ acute manifestations myocardial infarction, angina pectoris, as well as heart failure, atrial fibrillation, and stroke [18‐20]. However, at the same time, it should be noted that evidence from human studies that provide a mechanistic basis for the adverse cardiovascular effects of noise is scarce and scientific knowledge is mainly derived from a series of human field studies [9, 14‐16]. In this context, it is important to identify central pathomechanisms underlying the noise-disease-relationship to establish a central framework that displays how noise initiates and contributes to cardiovascular disease. This may help to intensify efforts to officially acknowledge noise not only as an additional noticed enhancer of cardiovascular disease, but as an established and manifest cardiovascular risk factor in a political and medical setting.

In our field studies, we consistently demonstrated that acute exposure to simulated nocturnal aircraft [14‐16] or train noise [9] was associated with impaired endothelial function and decreased sleep quality. Less consistent or partly insignificant results were observed in the case of stress hormone release, blood pressure, and other hemodynamic and biochemical parameters. Significant heterogeneity in these studies concerning design and sample included the (a) source of noise—aircraft [14‐16] or train noise [9], (b) subjects—younger healthy adults [9, 15] or older subjects with established cardiovascular disease or increased cardiovascular risk [14, 16], (c) number of subjects and sex ratio—N = 75 (61% women) [15], N = 60 (27% women) [14], N = 70 (50% women) [9], or N = 70 (20% women) [16], and (d) the number of noise events and corresponding mean sound pressure levels—30 (43 dB(A)) vs. 60 (46 dB(A)) aircraft noise events [15], 60 aircraft noise events (46 dB(A) [14], 30 (52 dB(A)) vs. 60 (54 dB(A)) train noise events [9], or 60 vs. 120 aircraft noise events (both with a mean value of around 45 dB(A)) [16].

To provide overall and robust estimates acknowledging the heterogeneity between studies, we sought to determine the pooled acute effect of simulated nocturnal traffic noise exposure on cardiovascular and sleep-related outcomes based on the data from our human field studies.

The results of our present pooled analysis demonstrate that acute exposure to simulated nocturnal traffic noise is associated with impaired endothelial function, higher mean arterial pressure, and disturbed sleep quality. We further outlined that feeling in the morning and restfulness of sleep were significantly disturbed after noise exposure during night. These results remained stable when excluding the only study in which train instead of aircraft noise was present. While mostly no effect modification by age and sex was observed in primary and secondary outcome variables, differences in sleep quality and feeling in the morning after study night appeared to be modified by age. We found also evidence for a carry-over effect in the pooled analysis for restfulness and sleep quality by applying appropriate statistical methods as recommended for crossover designs in clinical trials [22].

Babisch has proposed a noise reaction model in which the so-called “indirect pathway” is the crucial route by which noise exposure adversely affects the cardiovascular system [2]. Herein, annoyance and interference with daily routines and, importantly, sleep by chronic low-level noise exposure lead to higher psycho-physiological arousal associated with increased stress hormone levels, blood pressure, and heart rate. This, in turn, generates the development and acceleration of cardiovascular risk factors such as arterial hypertension, arrhythmia, dyslipidemia, increased blood viscosity and blood glucose, and activation of blood clotting factors, finally leading to manifest cardiovascular disease over time. In line, we have recently shown that noise annoyance due to different sources is associated with a higher risk of prevalent and incident atrial fibrillation in the Gutenberg Health Study (GHS), including 15,010 participants [3‐5]. A further study based on data from the GHS also revealed that noise annoyance due to different sources was associated with increased midregional pro-atrial natriuretic peptide levels, a marker that is associated with endothelial function, which in turn was predictive of incident atrial fibrillation and cardiovascular disease as well as all-cause mortality [7].

Our results are in line with recently published epidemiological studies investigating the relationship between long-term exposure to traffic noise and cardiovascular events, as well as mechanistic animal studies (for review, see [11]). For instance, a nationwide study from Denmark demonstrated that road traffic noise at the most exposed façade was associated with a higher risk of incident ischemic heart disease, myocardial infarction, angina pectoris, and heart failure with hazard ratios (HRs) of 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), respectively. Likewise, Vienneau et al. revealed, based on a nationwide cohort from Switzerland, HRs of 1.029 (95% CI 1.024–1.034) and 1.013 (95% CI 1.010–1.017) for the association between road traffic and railway noise and cardiovascular disease mortality, respectively, whereas this association was weaker for aircraft noise (HR 1.003, 95% CI 0.996–1.010) [21]. It is important to note that although these risks increase seem small, the public health impacts are devastating as large parts of the population are routinely exposed to traffic noise and other noise sources [1]. Our results and epidemiological study results suggest that acute reactions in response to traffic noise, such as endothelial dysfunction, increased arterial pressure, and disturbed sleep, will accumulate over time to increase the risk of manifest cardiovascular disease and mortality.

The results of our pooled analysis largely support the noise reaction model, showing important key mechanisms of disease initiation, such as noise-induced endothelial dysfunction, increased arterial pressure, and disturbed sleep. Nevertheless, we did not find evidence of noise-induced changes in heart rate, stress hormones, inflammation, and pulse transit time. Strengths of the present study include the novelty of conducting a pooled analysis of human field studies in the context of acute, controlled exposure to simulated traffic noise, which has several advantages compared to epidemiological designs, where exposure misclassification is more likely and might attenuate/influence or even bias the impact and effect strength of noise on health. A further novel finding includes the positive pooled association between acute nocturnal traffic noise exposure and mean arterial pressure. However, it should be noted that the corresponding confidence intervals are quite wide and that the study from Herzog et al. [9] displays a negative effect estimate, although not significant. Interestingly, this is also the only study in which evidence of a carry-over effect was noticed, which may have interfered with the results. We applied appropriate statistical methods as recommended for crossover designs in clinical trials [22], a substantial advantage compared to the primary studies included in the pooled analysis. Lastly, testing effect modification by sex and age was not done before in this setting. However, the present study also has some limitations that merit consideration. There was evidence for a carry-over effect in the pooled analysis for the secondary outcomes restfulness and sleep quality, which may have interfered with the results. However, care was taken to minimize carry-over effects using counterbalancing (participants were randomly given one of six different sequences of noise and control nights according to the randomization plan) and washout periods (at least three non-study nights between two study nights) where applicable. As stress hormone levels are known to show significant variations over the day, the measurement of associated biomarkers via blood samples hours after awakening may not have been optimal and may explain why stress hormones were not affected by noise in the present analysis. Samples should be collected immediately after awakening by e.g., collecting morning saliva, in future studies. The approach of collecting blood samples directly after awakening may also increase the accuracy of the measurement of other outcomes of interest such as inflammatory markers, that were found not to be affected by noise exposure in the present analysis. However, it may be also the case that an acute scenario of noise exposure is not sufficient to induce a measurable inflammatory response. Measurement of heart rate via standard wearable devices may not be accurate and sensitive enough to detect noise-induced heart rate variations, as it heavily relies on averaging over time periods, as well as it may be susceptible to various disruptive factors during the study night. In addition, measurement of endothelial function in different vascular beds (micro- and macrovascular) would allow a more complete picture of noise-induced vascular damage. Sleep-related variables does not meet the gold standard as it was measured via VAS rather than polysomnography or a wearable device, which could have delivered more objective data on sleep quality. Furthermore, overall sample size is still relatively small, and we cannot rule out the healthy volunteer bias due to the recruitment method. Also, our results only suggest acute noise exposure and not chronic, long-term noise exposure, wherein mechanisms such as adaptation and habituation may come into play. As the present analysis analyzed two distinct samples—young, healthy individuals and older adults with pre-existing cardiovascular conditions, generalizability of the findings to general population is limited, although we did not detect substantial effect modification by age.

In conclusion, our results demonstrate that acute nocturnal traffic noise exposure leads to endothelial dysfunction, higher mean arterial pressure, and disturbed sleep. Our results further highlight key mechanisms regarding the noise-disease-relationship centered on vascular endothelial dysfunction, increased arterial pressure, and impaired sleep quality. Noise is ubiquitous and a major public health challenge, that can only be addressed by appropriate system-level measures.