Is Noise Pollution a Cause of Cardiovascular Disease?

There are lots of things that we are told to avoid in order to maintain robust cardiovascular health and prevent disease— smoking, sitting, refined carbohydrates — among others. Each of these is a lifestyle factor that we have more or less complete control over; they’re modifiable risk factors.

Many other “exposures” are also harmful to cardiovascular health, but less controllable than diet or exercise. Take air pollution, for example. Multiple studies have shown that air pollution is a significant cardiovascular risk factor. In fact, a Lancet study published in 2017 estimated that particulate matter (air pollution) contributed to 4.2 million deaths worldwide in 2015. Unfortunately, air pollution isn’t something that most people can willingly “avoid” but are instead just “exposed to.”

What about “noise pollution”? While it might not seem like noise could contribute negatively to health, leading authorities (like the World Health Organization, WHO) are warning of the potential ill-effects of exposure to traffic noise, believe it or not.

Since millions, if not billions of people are exposed to large amounts of noise from traffic and other sources on a daily basis, this could represent a major risk factor to global and public health.

But how exactly does noise lead to the development of cardiovascular disease (CVD), among other ailments? One proposed route is known as the “indirect pathway” by which the perception of noise can lead to “cortical activation” and an emotional, sympathetic response. The subsequent “stress response” increases levels of stress hormones (cortisol, adrenaline) and activates the cardiovascular system.

Interestingly, this effect might not only occur in response to our conscious perception of noise, but also non-consciously during periods when we are asleep. In this way, noise could cause poor health by disrupting certain aspects of our sleep-wake cycle and circadian rhythms, without us even being aware of it.

Some proposed pathways by which noise (and other “pollutants”) may mediate the development of cardiovascular and cardiometabolic diseases. Source: Munzel 2016

Along with disrupted sleep, there are likely other mechanisms involved that link noise exposure with CVD. A recent study sought to examine some of these pathways through which auditory pollution drives CVD development.

The study, titled “ Acute exposure to nocturnal train noise induces endothelial dysfunction and pro‑thromboinflammatory changes of the plasma proteome in healthy subjects” examined the effects of acute nocturnal (nighttime) train noise exposure on vascular function.

The main outcome of this study was a specific marker of blood vessel function called flow-mediated dilation (FMD); which measures the ability of your arteries to dilate (relax) in response to an increase in blood flow. In addition to the FMD measurement, several other outcomes like heart rate, blood pressure, electrical activity of the heart (ECG), and stress hormones were measured.

To gain further mechanistic insight at the molecular level, an analysis of the plasma proteome was undertaken, including 92-cardiovascular-related protein biomarkers. On their own and combined, most of these study outcomes are intricately linked to or known to cause cardiovascular disease. If noise is indeed somehow causing CVD, then it is likely through one of the above pathways.

70 participants (average age 25) without sleep issues or psychiatric disorders completed 3 different study visits in a random order. An interesting and strong aspect of this study was that all visits took place at the participants’ own homes, so they got to sleep in a familiar environment and not a sterile and unfamiliar laboratory setting; a potential confounding factor since most people sleep poorly in a lab environment.

One night was a “control” night — participants just slept normally with no intervention. The two other nights, known as Noise30 and Noise60, involved a recording of train noise playing throughout the night while participants slept. The train noise was designed to simulate what someone living close to a railway might actually experience during sleep. The sound was even recorded from a bedroom of someone living close to one of the local railways. The only difference between these conditions was the number of train noise “events” each night — 30 and 60 events for the Noise30 and Noise60 conditions, respectively.

After each night, participants reported to the laboratory to undergo study measures including FMD and a blood draw. They also completed another FMD after they were given a dose of vitamin C. Vitamin C is an antioxidant, which reduces levels of oxidative stress in the body. Since oxidative stress is potentially one cause of vascular dysfunction, an improvement in vascular function after vitamin C ingestion would show that noise exposure is causing vascular dysfunction through this mechanism.

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The amount of noise that participants were exposed to in the Noise30 and Noise60 experiments was greater than in the control (a good thing), but not different between each of the noise conditions, at least in terms of the peak noise experienced at night. The only difference was thus in the total duration of noise exposure.

Nighttime noise led to a significant reduction in sleep quality, which the participants reported using a subjective scale. This isn’t surprising.

How did the noise (and reduced sleep quality) affect endothelial function? FMD was significantly reduced after both noise conditions compared to the control night — from ~11% down to ~8%. However, more noise didn’t lead to worse endothelial function — the Noise30 and Noise60 conditions had similar (negative) results.

When the participants were given a dose of vitamin C after the noisy nights, FMD improved around 28%, suggesting that part of the vascular dysfunction was attributable to oxidative stress-related mechanisms.

Even though vascular function was impaired, this study didn’t observe any changes in ECG-parameters, heart rate, blood pressure, inflammation, stress hormones, oxidative stress biomarkers, or glucose. Vascular function seemed to be the only thing to take a hit.

Effects of noise on FMD and FMD following vitamin C treatment

The proteomic data shed some light on how noise exposure influences disease risk. There were over 31 proteins (out of the 92) that significantly changed after the noise exposure nights, and many of these are known to be involved in pro-thrombotic, pro-inflammatory, and pro-atherosclerotic pathways, and some metabolic functions as well.

These results indicate that even just a single night of exposure to ambient train noise is sufficient to induce vascular dysfunction and cause alterations in proteins related to cardiovascular disease development.

The significance of this is that, over time, these acute effects can compound, eventually culminating in cardiovascular disease. While one night might not be the straw to break the camel’s back, someone living in an area where they are chronically exposed to even low levels of background traffic and train noise could be silently falling victim to the toxic effects of noise pollution.

Changes to various proteins after noise exposure and some of their functions in relation to cardiometabolic health.

These findings make sense in light of strong data linking sleep disturbances and sleep deprivation to endothelial dysfunction and cardiovascular disease. Short sleep duration is associated with increased CVD risk, and experimental studies have shown that endothelial function (FMD) is reduced after sleep restriction and full sleep deprivation.

It might not be the noise that is causing cardiovascular dysfunction, per se. In this study, at least, many measures involved in sympathetic and neural activation (like ECG, blood pressure, stress hormones) didn’t change in response to the noise exposure, indicating that the “indirect pathway” mentioned earlier may not have been intimately involved in this study’s results. It is clear, however, that oxidative stress is playing a causal role.

As the authors mention, sleep disturbance or fragmentation may be a direct consequence of noise exposure throughout the night and thus, lead to vascular dysfunction as a result.

The biggest strength of this study is the ecological validity. Since it was a “field study” conducted in the participants’ own homes (with the exception of the study measurements in the morning), it makes the findings more generalizable to people living under conditions like those simulated in this study.

Overall, this was a super-interesting and creative study. Before reading this, I hadn’t given any thought to the potential role of noise as a cardiovascular risk factor that could directly cause vascular dysfunction. Sure, I recognized the more obvious factors of air pollution and environmental toxins as potential mediators of poor cardiovascular health, but paid less though to something as seemingly benign as noise.

What this study illustrates is that we are exposed to other types of “stress” that we rarely even think about.

The implications of these findings could be vast — calling for stringent public health measures like sound walls on highways and even recommendations for people living near high-traffic areas and railways. Perhaps people should invest in ear plugs or other accessories to wear at night, which might limit their exposure to ambient noise and improve their sleep quality.

This study also makes me wonder about the effects of having the television, radio, or a podcast playing as you fall asleep. Could even this small background noise be disrupting sleep and influencing health on a molecular level? Just a thought.


Cohen AJ, Brauer M, Burnett R, et al. Estimates and 25-year trends of the global burden of disease attributable to ambient air pollution: an analysis of data from the Global Burden of Diseases Study 2015. Lancet. 2017;389(10082):1907–1918.

Herzog J, Schmidt FP, Hahad O, et al. Acute exposure to nocturnal train noise induces endothelial dysfunction and pro-thromboinflammatory changes of the plasma proteome in healthy subjects. Basic Res Cardiol. 2019;114(6):46.

Münzel T, Sørensen M, Gori T, et al. Environmental stressors and cardio-metabolic disease: part II-mechanistic insights. Eur Heart J. 2017;38(8):557–564.

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