&

Noise Exposure and Cardiovascular

Health
Chayakrit Krittanawong, MDa*,
Yusuf Kamran Qadeer, MDb,
Richard B. Hayes, DDS, MPH, PhDc,
Zhen Wang, PhDd,e, Salim Virani, MD, PhDb,f,g,
Marianne Zeller, PhDh,
Payam Dadvand, MD, PhDi,j,k, and Carl J. Lavie, MDl
From the a Cardiology Division, NYU Langone Health and NYU School of Medicine, New York, NY,
b
Section of Cardiology, Baylor College of Medicine, Houston, TX, c Division of Epidemiology,
Department of Population Health, NYU Grossman School of Medicine, New York, NY, d Robert D.
and Patricia E. Kern Center for the Science of Health Care Delivery, Mayo Clinic,
Rochester, MN, e Division of Health Care Policy and Research, Department of Health Sciences
Research, Mayo Clinic, Rochester, MN, f The Aga Khan University, Karachi, Pakistan, g Baylor
College of Medicine, Houston, TX, USA, h Laboratoire PEC2, EA 7460, Universit
e de Bourgogne-
Franche Comt
e, Dijon, France, i ISGlobal, Barcelona, Spain, j Universitat Pompeu Fabra,
Barcelona, Spain, k CIBERESP (Centro de Investigaci
on Biom
edica en Red Epidemiolog
ıa y Salud
ublica), Madrid, Spain and l John Ochsner Heart and Vascular Institute, Ochsner Clinical School,
P

The University of Queensland School of Medicine, New Orleans, LA, USA.

Abstract: Noise is considered an environmental

stressor adversely affecting well-being and quality of
life, inter-individual communications, and attention
and cognitive function and inducing emotional
responses, corresponding to noise annoyance. In addi-
tion, noise exposure is associated with nonauditory
effects including worsening mental health, cognitive
impairments, and adverse birth outcomes, sleep disor-
ders, and increased annoyance. An accumulating body
of evidence has indicated that traffic noise is also asso-
ciated with CVD, through multiple pathways. It has
been shown that psychological stress and mental
health disorders such as depression and anxiety have a
Funding : None.
*Corresponding Author: Chayakrit Krittanawong, MD, NYU School of Medicine, Cardiology Division, Section
of Cardiology, 50 First Avenue, New York, NY 10016 E-mail: chayakrit.krittanawong@va.gov

Curr Probl Cardiol 2023;48:101938

0146-2806/$ see front matter
https://doi.org/10.1016/j.cpcardiol.2023.101938

Curr Probl Cardiol, December 2023 1

 negative impact on the development of cardiovascular
diseases and outcomes. Likewise, reduced sleep quality
and/or duration has been reported to increase sympa-
thetic nervous system activity, which can predispose to
conditions like hypertension and diabetes mellitus,
known risk factors for CVD. Finally, there seems to be
a disruption in the hypothalamic-pituitary-axis sec-
ondary to noise pollution that also results in an
increased risk of CVD. The World Health Organiza-
tion has estimated that the number of DALYs (disabil-
ity-adjusted life-years) lost resulting from
environmental noise in Western Europe ranges from 1
to 1.6 million, making noise the second major contrib-
utor to the burden of disease in Europe, only after air
pollution. Thus, we sought to explore the relationship
between noise pollution and risk of CVD. (Curr Probl
Cardiol 2023;48:101938.)

Introduction

&
T
raditional cardiovascular (CV) disease (CVD) risk factors, such
as obesity, hypercholesterolemia, smoking, hypertension, diabe-
tes mellitus (DM), and obstructive sleep apnea, have been exten-
sively studied. More research is now being conducted into nontraditional
risk factors, such as noise exposure, and the impact of these environmen-
tal risk factors on CV health. With the growing urbanization worldwide,
noise pollution naturally increased as the development of transportations,
including airports, railways, and road traffic, all contributed to an increase
in environmental noise exposure. Noise is considered as an environmen-
tal stressor reducing well-being and quality of life, disturbing inter-indi-
vidual communications, mental concentration, and induces emotional
responses, corresponding to noise annoyance. It has been documented
that elevated noise exposure is associated with non auditory effects
including worsening mental health, cognitive impairments, adverse
birth outcomes, sleep disorders, and increased annoyance.1 In the last
decades, compelling evidence has indicated that traffic noise was also
associated with CVD, through multiple pathways.2 It has been shown
that mental health disorders such as depression and anxiety have a nega-
tive impact on the development of CVD and CVD outcomes.3 Likewise,
reduced sleep quality and/or duration has been reported to increase sym-
pathetic nervous system activity, which can predispose to conditions

2 Curr Probl Cardiol, December 2023

like hypertension and DM, known risk factors for CVD.4 The signifi-
cance of health impact of noise exposure was quantified by the World
Health Organization, which estimates that the number of DALYs (dis-
ability-adjusted life-years) lost resulting from environmental noise in
western Europe ranges from 1 to 1.6 million.5 Thus, in this review we
sought to explore the relationship between noise pollution and risk of
CVD.

Epidemiological Studies
Noise pollution can take various forms, and the first type of noise pol-
lution we sought to examine was noise pollution related to road traffic.
Road traffic noise is the main source of transportation noise-associated
health effects and a 2020 UE estimation indicate that about 20% of Euro-
peans are exposed to a burden of road traffic noise exceeding the thresh-
old harmful to health (55dB[A]).6 A recent study conducted in the UK by
Huang and colleagues sought to examine the association between road
traffic noise and primary hypertension incidence. They found that long
term exposure to road traffic noise was associated with an increased inci-
dence of primary hypertension, and this effect was heightened in areas
with higher air pollution.7 The additional finding of increased incidence
in higher pollution areas speaks to the role of fine particulate matter in
the development of CVD, a risk factor that we have showed to have a sig-
nificant impact on the development of CVD and CVD mortality.8 Simi-
larly, Bustaffa and colleagues showed, using a retrospective cohort study
in the city of Pisa, that increasing exposure to road traffic was associated
with increased CVD mortality in women, particularly in the highest
exposed areas.9 This relationship was not seen in men, so the authors
argued there may be some biological differences at play. Similarly, Lim
and colleagues, in the Danish Cohort Nursing Study, showed that long-
term exposure to road traffic noise levels greater than 56 dB may result in
increased occurrence of myocardial infarction (MI).10 However, the sex-
specific impact of traffic exposure remains controversial. Recent data
from a retrospective study from a French urban zone indicate that after
adjustment, noise exposure at the home address remained a predictor of
atherothrombotic risk, with LAeq (daily equivalent A-weighted noise
level),24 h (OR [95% CI]: 1.162 [1.011 1.337]) and with Lnight (night
equivalent A-weighted noise level) (OR [95% CI]: 1.159
[1.019 1.317]). The relationship with transportation Lnight was signifi-
cant only for men (OR [95% CI]: 1.260 [1.078 1.472]) but not for
women (OR [95% CI]: 0.959 [0.763 1.205]).11

Curr Probl Cardiol, December 2023 3

 The next type of noise pollution we sought to exam was railway noise.
A robust nationwide study conducted in Switzerland by Vienneau and
colleagues analyzed transportation noise and CVD mortality in the Swiss
population over a 15 year follow-up period. They found that long term
railway noise (as well as road traffic noise) was associated with most
CVD-related causes of death. These associations were independent of air
pollution, led to increased risk of CVD complication with increasing lev-
els, and had a higher incidence in men compared to women. An interest-
ing result from this study was that the risk of CVD mortality often started
in exposure to dB levels below the threshold WHO Environmental Noise
Guideline of 53 dB for road traffic and 54 dB for railway noise.12 Simi-
larly, Sørensen and colleagues evaluated 57,000 individuals over a 5-year
period to determine the effect exposure to railway traffic noise on hyper-
tension. They found that exposure to railway noise above 60 dB was asso-
ciated with 8% higher risk for hypertension.13 Finally, an interesting
study by Eriksson and colleagues, in 2017 in Sweden sought to quantify
the burden of noise pollution related to traffic and railway noise in Swe-
den. Their results indicated that the disability adjusted life-years lost in
Sweden due to traffic noise was 41,033, with 90% being caused by road
traffic noise and 10% being caused by railway traffic noise. They also
found that the most significant contributors to the disability adjusted life
years lost was sleep disturbances, annoyance, and CVD.14 Although these
studies provide important clues about air pollution and CVD, a systematic
review conducted in 2018 by WHO experts concluded that there was
insufficient quality of the evidence to support an association between
exposure to noise and ischemic heart disease (IHD). More studies utiliz-
ing case-control or cohort designs are needed to better assess an associa-
tion between noise exposure and IHD.15
The last type of noise pollution we sought to investigate was noise
related to aircraft and airports. A small-area study conducted in Brazil
sought to evaluate 16 districts near airports that were exposed to a noise
pollution level greater than 50 dB. They found that increasing noise
exposure was associated with CVD, stroke, and IHD mortality.16 Like-
wise, a study conducted by Seidler and colleagues evaluated individuals
in Germany and sought to compare the effects of air traffic noise and
association with hypertension and heart failure (HF). A statistically sig-
nificant linear exposure-risk relationship with HF or hypertensive heart
disease was found for aircraft traffic noise (1.6% risk increase per 10 dB
increase in the 24-h continuous noise level; 95% CI 0.3-3.0%).17
Lastly, the Hypertension and Exposure to Noise study, aimed to assess
the relationship between air traffic noise pollution and risk of

4 Curr Probl Cardiol, December 2023

hypertension. Jarup and colleagues found significant exposur-
e response relationships between night-time aircraft and risk of hyper-
tension, after adjustment for major confounders. For night-time aircraft
noise, a 10-dB increase in exposure was associated with a 14% increase
in hypertension risk.18

Physiological Responses to Acute Noise

The physiological response associated with noise exposure seems to
involve the basic human response to a potential stressor, and thus acti-
vation of the stress response. Selye and then Cannon first described
the so called “Fight or Flight” response that human beings elicit when
confronted with a potentially dangerous stimulus.19,20 Neuronal acti-
vation induced by noise exposure triggers stress signaling pathways
through the hypothalamic-pituitary-adrenal (HPA) axis and sympa-
thetic nervous system (SNS). Corticotrophin-releasing hormone
(CRH) released by the hypothalamus stimulates adrenocorticotropic
hormone (ACTH) liberation from the pituitary gland to the blood, thus
inducing glucocorticoid production by the adrenal cortex. SNS stimu-
lation drives the production of catecholamines, mainly epinephrine,
by the adrenal medulla. These adrenal hormones in turn stimulate
other neurohormonal pathways including the renin-angiotensin-aldo-
sterone system (RAAS), leading to increased vascular inflammation
and oxidative stress, and deteriorating vascular homeostasis.2 These
hormones act to physiologically affect the body in many ways, includ-
ing increasing heart rate, blood pressure, glucose metabolism, and car-
diac output.21

Acute and Chronic Noise and CVD Pathogenesis

A noise reaction model proposed in 2003 by Babisch described 2 path-
ways in which noise could contribute to the development of CVD, one
via a direct pathway (auditory) and one via an indirect (nonauditory)
pathway. The indirect pathways, generally at low sound levels, involves
cognitive and emotional responses through disturbed activities, sleep and
communications potentially leading to annoyance and anxiety/depres-
sion. In this section, we will focus on the direct pathway induced at high
sound levels, as a potential cause of hearing loss22 and leading to acute
changes and risk for CVD development and progression.23 After age-
related hearing loss, noise-related hearing loss is the second most com-
mon type of this condition. Mechanistically, it seems that the pathogene-
sis involving noise-induced hearing loss seems to be due to shearing

Curr Probl Cardiol, December 2023 5

forces impacting the stereocilia of the hair cells of the basilar membrane
of the cochlea, resulting in cell death.24 Wang and colleagues conducted
a case-control study in which they found that exposure to road traffic
noise greater than 70 dB resulted in an increased risk of auditory dam-
age.25 Damage to the auditory system can result in sleep disturbance.26.
Babisch’s model describes stimulation of stress response after sleep dis-
turbance, characterizing the indirect pathway, as a common denominator
with direct pathway and resulting from impaired sleep, in addition to cog-
nitive/emotional disturbances and annoyance.
The importance of sleep on the CV system functioning has recently
gained greater attention. Sleep restriction has neurobehavioral effects
such as deficits in attention, memory, mood, and thought process.27 In
addition, sleep restriction has been shown to be associated with impaired
insulin sensitivity, endothelial function, and sympathetic tone.28-30 A
variety of epidemiological studies have assessed the impact of short sleep
duration and increases in cardiometabolic risk factors such as obesity,
diabetes, hypertension and mortality.31-36
Pathophysiologically, the arousal mechanism in our body is controlled
by the Reticular Activating System, which receives sensory input from
many different modalities, including auditory inputs.37 Information from
the Reticular Activating System is processed in the brain cortex, even
during sleep. Thus, exposure to noise that activates the Reticular Activat-
ing System can lead to arousal and sleep disruption.38
Murine models have shown that aircraft noise exposure for 4 days at
peak sound levels of 85 dBA (mean sound at 72 dBA) induced a rapid
increase in systolic blood pressure, plasma noradrenaline and angiotensin
II levels. These modifications were associated with endothelial dysfunc-
tion, through reduced nitric oxide (NO) bioavailability and endothelial
nitric oxide synthase (eNOS) uncoupling, mediated by stimulation of vas-
cular NADPH oxidase activity.39 In healthy adults or patients with IHD,
nighttime aircraft noise exposure dose-dependently impairs endothelial
function, stimulates adrenaline release, leading to reduced subjective
sleep quality.40
Disruption of circadian rhythm is an emerging risk factor for CVD.
Recent findings support the hypothesis of a role of environmental stres-
sors, traffic noise and air pollution, in the redox regulatory changes of cir-
cadian rhythm.41 The heart-brain axis, through the limbic system and
amygdala activity, may also be involved in the health impact of noise
exposure. In adults who underwent 18FDG PET-CT imaging, higher noise
exposure at residential address was associated with increased amygdala
metabolic activity and vascular inflammation.42

6 Curr Probl Cardiol, December 2023

Noise Mitigation Strategies
Given the negative health consequences of noise pollution, every
effort should be made at the local, state, national, and global levels to
decrease the burden of noise pollution. A recent interesting study in
Zurich found that limiting the vehicle speed limit to 30 km/h reduced
noise annoyance in the study participants.43 Given that increasing
speeds of vehicles contribute to noise, it makes sense to advocate for
decreased speed limits to mitigate this noise. Likewise, working in
urban centers exposes individuals to a great amount of noise. Creating
a ventilation system that could dampen the noise pollution would aid
workers, and this was investigated by Oldham and colleagues. They
proposed a mechanism for combating low frequency sound in tandem
with techniques for reducing high frequency sound to reduce the
ingress of noise from urban sources such as road traffic.44 In addition,
using asphalt for paving roads can decrease the impact of noise from
vehicles.45 Other studies for railway noise have sought to decrease the
impact of noise by utilizing rail/wheel dampers, erecting noise bar-
riers, and incorporating material with better sound absorption at the
base of the railway tracks.46 For aircraft noise, potential strategies to
decrease noise include optimization of aircraft type, regulation of
night flight number, optimization of flight procedure, modification of
operating runways, land use planning and installation of sound insula-
tion windows, as was shown in a study conducted by Xie and col-
leagues in China.47

Limitations
Our review has certain limitations. First, while most studies controlled
for variables like sex, age, and other basic demographic factors, the
response rates were variable and thus some component of selection bias
could have occurred. Second, most of these studies took place in urban-
ized areas, but some areas differ in regard to population, quality of living,
socioeconomic status, health, environmental exposure, and genetic fac-
tors and these could impact the observed results regarding noise pollution
and CVD. Third, more research needs to be conducted to elucidate
whether noise pollution is an independent risk factor for CVD, or if it
operates on the underlying predisposition for individuals with CVD risk
factors or those genetically predisposed to develop CVD. Finally, the
inter-relationship of air pollution and noise pollution needs further inves-
tigation and strategies to target reduction in both these factors need to be
developed.

Curr Probl Cardiol, December 2023 7

Conclusions
Emerging data suggest that there could be additional ways, separate
from the already discussed mechanism of sleep disruption, that noise pol-
lution could impact CVD. One such way is through the gut microbiota.
There is evidence that alterations to the gut microbiota can promote car-
diovascular disease.48,49 Specifically, there exists the gut-brain axis, and
disruptions to this axis can lead to neuropsychiatric and inflammatory dis-
orders, which are risk factors for CVD.50,51 Animal models have shown
that chronic noise exposure results in increased risk of developing neuro-
inflammation, cognitive impairment, increased levels of inflammatory
cytokines, and metabolic disturbances.52,53 Future studies are needed to
investigate these alternative noise-induced mechanisms of CVD, as doing
so could provide novel therapeutic interventions. In conclusion, noise
pollution is associated with increased risk of CVD and CVD mortality.
Legislation is needed to reduce noise pollution at all levels.

Central Illustration

Author’s access
All authors had access to the data and a role in writing the manuscript.

Declaration of Competing Interest

The authors declare that they have no known competing financial inter-
ests or personal relationships that could have appeared to influence the
work reported in this paper.

8 Curr Probl Cardiol, December 2023

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