Road traffic noise exposure and its impact on health: evidence from animal and human studies—chronic stress, inflammation, and oxidative stress as key components of the complex downstream pathway underlying noise‑induced non‑auditory health effects

Vol:.(1234567890)
En i onmen al Science and Pollu ion Resea ch (2024) 31:46820–46839
h ps://doi.o g/10.1007/s11356-024-33973-9
REVIEW ARTICLE
Road a ic noise exposu e andi s impac onheal h: e idence
omanimal andhuman s udies—ch onic s ess, in lamma ion,
andoxida i e s ess askey componen s o  hecomplex downs eam
pa hway unde lying noise‑induced non‑audi o y heal h e ec s
AneA egi1,2· Osca Vegas1,2· Ai anaLe xundi2,3,4· AnaSil a5,6· IsabelFe ei a5,6· AinhoaBe ezia ua2·
Ma iaTe esaC uz5,6,7· Ne eaLe xundi1,2,3
Recei ed: 26 Oc obe 2023 / Accep ed: 8 June 2024 / Published online: 8 July 2024
© The Au ho (s) 2024
Abs ac
In hea ily u banized wo ld sa u a ed wi h en i onmen al pollu an s, oad a ic noise s ands ou as a signi ican ac o
con ibu ing o widesp ead public heal h issues. I con ibu es in he de elopmen o a di e se ange o non-communicable
diseases, such as ca dio ascula diseases, me abolic dys egula ion, cogni i e impai men , and neu odegene a i e diso de s.
Al hough he exac mechanisms behind hese non-audi o y heal h e ec s emain unclea , he noise eac ion model cen es
on he s ess esponse o noise. When exposed o noise, he body ac i a es he hypo halamic–pi ui a y–ad enal axis and he
sympa he ic ne ous sys em, leading o he sec e ion o s ess ho mones like ca echolamines and co isol. P olonged exposu e
o noise-induced s ess esul s in ch onic in lamma ion and oxida i e s ess. This e iew unde sco es he ole o in lamma ion
and oxida i e s ess in he p og ession o noise-induced ascula dys unc ion, dis up ion o he ci cadian hy hm, accele -
a ed aging, neu oin lamma ion, and changes in mic obiome. Addi ionally, ou ocus is on unde s anding he in e connec ed
na u e o hese heal h ou comes: These in e connec ed ac o s c ea e a cascade e ec , con ibu ing o he accumula ion o
mul iple isk ac o s ha ul ima ely lead o se e e ad e se heal h e ec s.
Keywo ds Road a ic noise· En i onmen al s esso · In lamma ion· Oxida i e s ess· Non-audi o y heal h e ec s
Abb e ia ions
ACTH Ad enoco ico opic ho mone
AD Alzheime ’s disease
AMPK AMP-ac i a ed kinase
ADHD A en ion-de ici /hype ac i i y
diso de
BMAL1 and BMAL2 B ain and muscle a n -like
p o ein-1 and p o ein-2
CVD Ca dio ascula disease
CLOCK Ci cadian locomo o ou pu
cycles p o ein kapu
CRH Co ico ophin- eleasing
ho mone
CRY1 and CRY2 C yp och omes 1 and 2
Responsible Edi o : Philippe Ga igues
* Ma ia Te esa C uz
[email p o ec ed]
1 Facul y o Psychology, Uni e si y o  heBasque Coun y
(UPV/EHU), 20008SanSebas ian, Spain
2 En i onmen al Epidemiology andChild De elopmen
G oup, Biogipuzkoa Heal h Resea ch Ins i u e, Paseo Doc o
Begi is ain S/N, 20014SanSebas ian, Spain
3 Spanish Conso ium o Resea ch On Epidemiology
andPublic Heal h (CIBERESP), Ins i u o de Salud Ca los III,
C/Mon o e de Lemos 3-5, 28029Mad id, Spain
4 Depa men o P e en i e Medicine andPublic Heal h,
Facul y o Medicine, Uni e si y o  heBasque Coun y
(UPV/EHU), 48940Leioa, Spain
5 Cen e o Neu oscience andCell Biology andIns i u e
o Biomedical Imaging andLi e Sciences, Uni e si y
o Coimb a, 3000-548Coimb a, Po ugal
6 Cen e o Inno a i e Biomedicine andBio echnology
(CIBB), Uni e si y o Coimb a, Coimb a, Po ugal
7 Facul y o Pha macy, Uni e si y o Coimb a,
3000-548Coimb a, Po ugal
46821En i onmen al Science and Pollu ion Resea ch (2024) 31:46820–46839
eNOS Endo helial ni ic oxide
syn hase
HO-1 Heme oxygenase-1
HPA Hypo halamic-pi ui a y-ad enal
IHD Ischemic hea disease
MACE Majo ad e se ca dio ascula
e en s
MAPK Mi ogen-ac i a ed p o ein
kinases
NIH Na ional Ins i u es Heal h
nNOS Neu onal ni ic oxide syn hase
NO Ni ic oxide
NF-κB Nuclea ac o -κB
NRF2 Nuclea ac o e y h oid
2- ela ed ac o 2
OR Odds a io
PER1, PER2, and PER3 Pe iods 1, 2, and 3
ROS Reac i e oxygen species
REDD1 Regula ed in de elopmen and
DNA damage esponses 1
RR Rela i e isk
SCI Sys emic ch onic in lamma ion
NOX-2 NADPH oxidase
WHO Wo ld Heal h O ganiza ion
In oduc ion
Cu en ly, 55% o he global popula ion li es in ci ies and
his numbe p ojec ed o ise o 68% by 2050. Eu ope, in
pa icula , has a highe u ban popula ion, wi h 74% o Eu o-
peans cu en ly li ing in u ban a eas (Uni ed Na ions 2018).
In his scena io, he es ablishmen o sus ainable and heal hy
u ban en i onmen s is c ucial. Wi hin he exposome, which
includes he sum o all en i onmen al con ibu ions du -
ing he li e cou se, in ol ing ex e nal ac o s, beha iou al
ac o s, li es yle ac o s, and biological esponses (Daibe
e al. 2019), en i onmen al noise s ands as he second mos
se ious en i onmen al isk ac o in Eu ope, wi h ai pollu-
ion being he p ima y con ibu o (Eu opean En i onmen
Agency 2020).
The Wo ld Heal h O ganiza ion (WHO) de ines i as noise
c ea ed om all sou ces, excep wo kplace noise (WHO
2018). Howe e , acco ding o he En i onmen al Noise
Di ec i e, en i onmen al noise is desc ibed as unwan ed
o ha m ul sound de i ed om human ac i i ies, includ-
ing noise emi ed by means o anspo — oad a ic,
ail a ic, ai a ic, and om si es o indus ial ac i i y
(Di ec i e 2002/49/EC 2002). This di ec i e de ines day-
e ening-nigh noise le els abo e 55dB(A) as ha m ul, wi h
oad a ic noise as he p edominan sou ce. Mo e han 113
million people a e a ec ed by oad a ic noise exposu e
abo e he ecommended alues, meaning ha a leas 20% o
Eu opeans a e exposed o a ic noise le els ha can cause
ad e se heal h e ec s. The o e all numbe o people exposed
o noise le els abo e 55dB o igina ed by o he means is 22
million o ailway noise, 4 million o ai c a noise, and
less han 1 million o noise c ea ed by indus ial ac i i ies
(WHO 2018).
Acco ding o se e al e iews conduc ed by some WHO
expe chai s, exposu e o oad a ic noise could cause non-
audi o y heal h e ec s, including ad e se bi h ou comes
(Nieuwenhuijsen e al. 2017), ca dio ascula disease (CVD)
and me abolic e ec s ( an Kempen e al. 2018), sleep dis-
u bances (Basne and McGui e 2018), o cogni i e impai -
men (Cla k and Pauno ic 2018a). Howe e , he e idence
ega ding he ela ionship be ween en i onmen al noise
and some o he men ioned ou comes is e y sca ce. This
does no mean ha he e is no ela ionship, bu mo e quali y
esea ch is needed. Mo eo e , in Eu ope, long- e m exposu e
o noise causes 12,000 p ema u e dea hs and 48,000 cases
o ischemic hea disease pe yea . Fu he mo e, 6.5 million
people expe ience ch onic sleep dis u bances, and 12,500
schoolchild en s uggle wi h lea ning di icul ies (Eu opean
En i onmen Agency 2020).
In his e iew, we summa ize he cu en unde s and-
ing o he molecula pa hways and mechanisms unde lying
he non-audi o y heal h e ec s o noise. Ou objec i e is o
unde s and how noise co ibu es in he mos common heal h
ou comes, including in lamma ion and oxida i e s ess, as-
cula dys unc ion, dys egula ion o he ci cadian hy hm,
me abolic dis u bances, age- ela ed diseases, changes in
he mic obiome, and men al heal h ou comes. Mos e iews
add essing he mechanisms unde lying noise-induced non-
audi o y e ec s ha e ocused on only one heal h ou come,
he mos common being ascula dys unc ion. Howe e ,
gi en he in e ela ion be ween hese ou comes, his e iew
ein o ces he impo ance o a holis ic app oach, conside ing
all ou comes and hei in e ac ions.
Noise eac ion model
Acco ding o he noise eac ion model p oposed by Babisch
(Babisch 2003), noise can induce ha m ul e ec s h ough
wo pa hways. The model sugges s ha high noise le els
(> 85 dBA), can di ec ly cause heal h p oblems such as
hea ing loss o di ec physiological changes due o sleep
dis u bances. In con as , indi ec pa hway is ela ed o lowe
noise le els impai ing daily ac i i ies, communica ion o
sleep. This pa hway in ol es cogni i e pe cep ion, leading o
co ical ac i a ion and emo ional esponses like annoyance
(Münzel e al. 2021). I is belie ed ha when annoyance is
high and ch onic, a mechanism o psychological habi ua ion
occu s: isola ion o noise om consciousness and educ ion
46822 En i onmen al Science and Pollu ion Resea ch (2024) 31:46820–46839
o emo ional o e load in he p e on al co ex, esul ing in
less annoyance (Recio e al. 2016).
Howe e , he physiological esponse o noise pe sis s:
I causes a p ima y s ess eac ion. Speci ically, i igge s
he ac i a ion o he hypo halamic–pi ui a y–ad enal (HPA)
axis and he sympa he ic ne ous sys em. Hence, a cascade
o eac ions occu s, including he elease o s ess ho mones
such as co isol, ad enaline, and no ad enaline(Daibe e al.
2019). HPA axis ac i i y is go e ned by h ee ho mones:
co ico opin- eleasing ho mone (CRH), ad enoco ico-
opic ho mone (ACTH), and co isol, he main gluco-
co icoid in humans. Ac i a ion o he HPA axis igge s
he elease o CRH, which s imula es ACTH p oduc ion
and modula es co isol syn hesis. Ele a ed co isol le els
se e as a nega i e eedback mechanism, supp essing he
elease o CRH and ACTH and hus es o ing basal le -
els o s ess ho mones (He man e al. 2016). Howe e , in
cases o ch onic s ess, dys unc ion in he HPA axis occu s,
and bu e ing mechanisms may p o e insu icien o e u n
o baseline condi ions. This physiological phenomenon is
known as allos a ic load and has been associa ed wi h se -
e al de imen al heal h ou comes (Mc Ewen 1998; Guidi
e al. 2021). Noise has been iden i ied as a ch onic s esso
ha igge s a chain eac ion o oxida i e, in lamma o y,
and me abolic e ec s, esul ing in non-audi o y heal h ou -
comes (Hahad e al. 2021). A s udy ha associa es nigh -
ime ai c a noise exposu e wi h an inc eased isk o Tako -
subo synd ome, a ca diomyopa hy linked o excessi e s ess
ho mone elease, suppo s his idea o he impo ance o he
indi ec pa hway (Münzel e al. 2016).
Co isol measu emen p o ides an es ima ion o HPA axis
ac i i y. Acu e co isol le els can be measu ed in biological
samples, namely blood, sali a, and u ine samples (Hellham-
me e al. 2009; W igh e al. 2015; Mlili e al. 2021). Mos
o he esea ch has ocused on he e ec o ai c a noise in
sali a y co isol, epo ing ele a ed sali a y co isol le els
in pa icipan s li ing nea ai po s (Selande e al. 2009;
Le è e e al. 2017; Baudin e al. 2019). In con as , s udies
in ega d o oad a ic noise a e inconclusi e. A sys ema ic
e iew concluded ha oad a ic noise was ela ed o highe
u ina y o sali a y co isol le els (Hohmann e al. 2013);
howe e , ecen s udies ha e shown no associa ion be ween
oad a ic noise and sali a y co isol (Wallas e al. 2018;
Bloemsma e al. 2021). Conce ning ch onic co isol le els,
hai co isol was epo ed as a iable ool o assessing he
link be ween en i onmen al noise exposu e and ch onic
s ess (Michaud e al. 2022). To he bes o ou knowledge,
only one s udy measu ed hai co isol and ound no associa-
ion be ween esiden ial exposu e o oad a ic noise and
hai co isol concen a ion in 14–15-yea -old adolescen s
(Ve heyen e al. 2021).
The e o e, i is hough ha ch onic elease o s ess
ho mones due o noise-induced ac i a ion o he HPA axis
and sympa he ic ne ous sys em p oduces a s a e o ch onic
in lamma ion and oxida i e s ess, as de ailed in Fig.1
In lamma ion andoxida i e s ess
In lamma ion is he body’s eac ion h ough which immune
and non-immune cells a e ac i a ed, o e adica e ha m ul
s imuli and p omo e issue epai and eco e y. An impo -
an aspec o he in lamma o y esponse is empo al egula-
ion: I is ac i a ed when a h ea is p esen and ends once
he h ea is o e (Fu man e al. 2019). Fac o s ha induce
in lamma ion (e.g., pa hogens, damaged cells, oxic chemi-
cals, and physical and psychological s esses) igge he
p oduc ion o in lamma o y media o s. These media o s
ac i a e he downs eam componen s o he in lamma o y
pa hway (Medzhi o 2008; Hahad e al. 2019). This p ocess
is egula ed and usually las s o a ew days, allowing elimi-
na ion o he he h ea wi hou causing undue issue damage
(Leiba e al. 2023). Any ailu e in his con ol could p o oke
ch onic in lamma ion, cha ac e ized by he in il a ion o
mononuclea immune cells (monocy es, mac ophages, lym-
phocy es, and plasma cells), issue des uc ion, and ib osis
(Khansa i e al. 2009). While acu e in lamma ion is i al
o immune esponse, sys emic ch onic in lamma ion (SCI)
has been linked o a ious diseases such as CVD, cance ,
me abolic dys egula ion, and neu odegene a i e diseases
(Fu man e al. 2019).
The ha m ul e ec s o ch onic in lamma ion a e mainly
caused by o e p oduc ion o eac i e oxygen species (ROS)
and deple ion o an ioxidan s (Halliwell 2006). ROS, uns a-
ble molecula species wi h one o mo e unpai ed elec ons,
a e c ucial o he egula ion o se e al signalling pa h-
ways (e.g. cell di e en ia ion, p oli e a ion and an ioxidan
egula ion) (Halliwell and Gu e idge 1985). None heless,
an imbalance be ween he p oduc ion o ROS and an i-
oxidan de enses, known as oxida i e s ess, can lead o a
oxic inc ease in ROS le els, which can induce cell dam-
age. Ele a ed ROS le els can gene a e o he ROS, such as
hyd ogen pe oxide (H2O2), supe oxide anions (O2•−), and
hyd oxyl adicals (OH•). This, in u n, esul s in oxida i e
damage o cellula lipids and p o eins and mu a ions in he
genome, ul ima ely leading o cell dea h (Halliwell and
Gu e idge 1985; Hajam e al. 2022). ROS-induced oxida-
i e s ess dis up s a ious o gan sys ems, including he
ne ous sys em, kidneys, li e , and ca dio ascula sys em
(Khansa i e al. 2009).
Se e al molecula pa hways a e ac i a ed in esponse
o s ess, leading o he excessi e gene a ion o ROS and
in lamma o y signalling. Myeloid cells igge he ini ial
esponse in he in lamma o y p ocess. Once ec ui ed
o he inju y si e, hese cells gene a e ROS, as well as
in lamma o y cy okines, chemokines, and p os aglandins.
46823En i onmen al Science and Pollu ion Resea ch (2024) 31:46820–46839
Nuclea ac o -κB (NF-κB), mi ogen-ac i a ed p o ein
kinases (MAPK) and JAK-STAT signalling pa hways
(Chen e al. 2018), and he ansc ip ion ac o nuclea
ac o e y h oid 2- ela ed ac o 2 (NRF2) inhibi cell
dea h by p omo ing an i-in lamma o y and an ioxidan
p ocesses. NRF2 appea s o se e as a i al p o ec i e
mechanism agains a ious en i onmen al s esso s (Bayo
Jimenez e al. 2022). Noise-induced oxida i e s ess
appea s o ac i a e NRF2 and igge he p oduc ion o
i s a ge genes. Con e sely, NRF2 de iciency exace ba es
noise-induced damage, while i s ac i a ion has p o ec i e
e ec s (Bayo-Jimenez e al. 2021).
Fig. 1 Summa y o he cu en knowledge o he mechanism by
which oad a ic noise induces ch onic s ess ho mones, sys emic
in lamma ion, and oxida i e s ess impac on se e al heal h ou comes.
As p oposed by he noise eac ion model, in he indi ec pa hway,
noise causes sleep dis u bances and annoyance ( ep esen ed in he
uppe side in blue), which cause HPA axis and SNS ac i a ion: highe
le els o co isol, sys emic in lamma ion, and oxida i e s ess (in
g ay) cause he main de imen al heal h ou comes induced by eac-
i e oxygen species (ROS) (summa ized in yellow). Changes in he
mic obiome, noise-induced ascula dys unc ion, neu oin lamma ion,
dys egula ion o he ci cadian hy hm, accele a ed aging, and Alzhei-
me ’s disease (AD) like b ain, as well as he in e ela ionships among
all o hese heal h ou comes, esul in he accumula ion o mul iple
isk ac o s leading o se ious ad e se heal h e ec s (below in g een).
Figu e made by au ho , based on he p e ious esea ch
46824 En i onmen al Science and Pollu ion Resea ch (2024) 31:46820–46839
In lamma ion andoxida i e s ess by oad
a ic noise exposu e
P e ious s udies sugges ha in lamma ion and oxida i e
s ess play key oles in he de elopmen o by oad a ic
noise-induced damage (Daibe e al. 2020). The mecha-
nisms h ough which i con ibu es o he o e all disease
bu den emain unclea , p ima ily due o he absence o
well-es ablished esea ch models in bo h humans and ani-
mals. P e ious e iews ha e ocused on he ole o ROS
and in lamma ion in noise-induced ca dio ascula dys-
unc ion (Daibe e al. 2019, 2020; Münzel e al. 2022),
dys egula ion o he ci cadian clock (Daibe e al. 2022),
neu odegene a i e diso de s (Manukyan 2022), accele -
a ed aging (Hahad e al. 2021), and psychia ic diso de s
(Hahad e al. 2022). Howe e , we aim o p o ide a gen-
e al o e iew o his issue and explo e he in e connec ion
be ween he di e se non-audi o y heal h ou comes.
Animal s udies Expe imen al esea ch conduc ed on animal
models has shown ha noise exposu e can lead o ex a-
audi o y e ec s, mos ly in he b ain and immune sys em,
by igge ing oxida i e s ess (Cheng e al. 2011; Cui and
Li 2013; Molina e al. 2016; Pascuan e al. 2014). Manikan-
dan e al. (2006) epo ed heigh ened ac i i y o an ioxidan
enzymes in he hippocampus o a s exposed o acu e noise,
whe eas he ac i i y dec eased in hose ch onically exposed.
In ano he s udy, mice exhibi ed inc eased immune unc-
ion a e 3-day noise exposu e, bu dec eased immune unc-
ion and oxida i e s ess we e obse ed in mice exposed o
28days (Zheng and A iizumi 2007).
Münzel e al. es ablished a p o ocol o ai c a noise
exposu e o s udy i s e ec s on mice. They exposed mice
o high le els o noise (maximum 85dB, mean 72dB) o
43s, and epea ed his exposu e 69 imes, ying o mimic
ai c a noise exposu e. This has been ully explained else-
whe e (Münzel and Daibe 2018). Following his p o ocol
o ou consecu i e days, hey obse ed ele a ed sys olic
blood p essu e, as well as inc eased le els o ca echola-
mines, angio ensin-II, and endo helin-1. Noise-exposed ani-
mals exhibi ed signs o oxida i e s ess and in lamma ion,
including eNOS uncoupling as well as inc eased le els o
IL-6, exp ession o he NADPH oxidase 2 (NOX-2) p o-
ein, and ni o y osine-posi i e p o eins. Addi ionally, hey
obse ed an inc ease in he in il a ion o na u al kille cells
and neu ophils in o he ascula u e (Münzel e al. 2017).
Neu oin lamma ion, ce eb al oxida i e s ess, o ci cadian
dys egula ion due o ai c a noise exposu e we e a oided
in Nox2 knockou mice (K ölle -Schön e al. 2018), as well
as he p o-in lamma o y pheno ype and ac i a ion o ci cu-
la ing leukocy es (Eck ich e al. 2021). No ably, same noise
exposu e p o ocol was used in he a o emen ioned s udies.
F enis e al. ound ha elimina ion o monocy es and mac-
ophages ( he main lysozyme M-posi i e in lamma o y cells)
blocked noise-induced in lamma ion, oxida i e s ess, and
ascula dys unc ion, sugges ing he ele ance o NOX-2 o
noise e ec s (F enis e al. 2021a). Gi en he c oss-ac i a ion
o endo helin-1 and NOX-2, and he ac ha bo h inc ease
unde noise exposu e, he s imula ion o one o hem may
lead o a icious cycle ha esul s in oxida i e s ess ( he
pa hway is ully explained in F enis e al. (2021b)). I should
be no ed ha he majo i y o s udies in es iga ing noise-
induced edox imbalance in animals used ex emely high
sound p essu e le els, which y o mimic ai c a noise
exposu e a he han oad a ic noise (Molina e al. 2016),
and bo h loudness and o he cha ac e is ics ( equency and
pa e n) may de e mine de imen al noise e ec s (Münzel
e al. 2017). Mo eo e , animal s udies a e no always eliable
p edic o s o human ou comes (B acken 2009)."
Human s udies E idence om human ield s udies also sug-
ges s ha oxida i e s ess plays an impo an ole in noise-
de i ed heal h e ec s. The adminis a ion o he an ioxidan
Vi amin C diminished endo helial dys unc ion associa ed
wi h ain and ai c a noise exposu e (Schmid e al. 2013;
He zog e al. 2019). In a s udy published in 2020, he au ho s
epo ed heigh ened ac i i y in he amygdala among indi-
iduals esiding in a eas wi h high oad a ic noise (Osbo ne
e al. 2020). The amygdala, a pa o he limbic sys em, is
esponsible o emo ional esponses, including ea , anxie y,
and agg ession. I also p ocesses physiological and beha -
iou al eac ions o s ess and plays a c ucial ole in he b ain’s
esponse o en i onmen al s esso s including noise (Sp eng
2000; Powell-Wiley e al. 2021). Inc eased amygdala ac i -
i y is linked o a highe isk o CVD due o inc eased a he o-
scle o ic in lamma ion (Osbo ne e al. 2022). In ac , highe
noise exposu e p edic s majo ad e se ca dio ascula e en s
(MACE) and is associa ed wi h inc eased a e ial in lamma-
ion (Osbo ne e al. 2020). Recen ly, he same esea che s
demons a ed ha he combina ion o ai pollu ion and oad
a ic noise also con ibu es o an inc eased isk o MACE
and a e ial in lamma ion (Osbo ne e al. 2022).
Acco ding o obse a ional coho s udies, long- e m expo-
su e o oad a ic noise induces al e a ions in blood biochem-
is y and immune esponse in adul s, including ele a ed le els
o IL-12 and high-sensi i i y C- eac i e p o ein (hsCRP) o
a educed NKT cell popula ion (Cai e al. 2017; Kim e al.
2017; Kupciko a e al. 2021). Howe e , i is wo h no ing ha
hese indings we e no uni o m ac oss all s udies (Michaud
e al. 2022). In e es ingly, he Swiss SAPALDIA coho con-
cluded ha DNA me hyla ion was associa ed wi h long- e m
exposu e o oad a ic noise and ai pollu ion. This associa-
ion was linked o pa hways ela ed o in lamma ion, cellula
de elopmen , and immune esponses (Eze e al. 2020).

46825En i onmen al Science and Pollu ion Resea ch (2024) 31:46820–46839
As p e iously no ed, ROS a e i al o he egula ion
o se e al signalling pa hways ha a e linked o nume -
ous heal h e ec s. Hence, he upcoming sec ion p o ides a
comp ehensi e o e iew o how in lamma ion and oxida-
i e s ess ac as media o s o non-audi o y heal h ou comes
induced by oad a ic noise.
Noise‑induced heal h e ec s
The s a e o ch onic s ess esul ing om oad a ic noise
exposu e, cha ac e ized by al e a ions in he HPA axis and
s ess ho mones, sys emic in lamma ion, and oxida i e
s ess, can a ec a ious sys ems and con ibu e o a wide
ange on non-audi o y diseases (Fig.1). In his e iew, we
ocus on i s e ec s on he ci cadian dys egula ion, me abolic
al e a ions, aging and age- ela ed diseases, changes in he
gu mic obiome, ascula dys unc ion, and men al heal h
ou comes. Summa y o he main indings explained in his
sec ion is a ailable in Table1, whe e bo h animal and human
s udies a e p esen ed.
Noise andme abolic al e a ions
Road a ic noise has been sugges ed o al e me abolic
homeos asis and is mainly associa ed wi h diabe es melli us.
As p e iously s a ed, noise induces changes in he HPA axis,
p omp ing he elease o co isol and o he s ess ho mones,
po en ially esul ing in me abolic dis u bances (Babisch
2003). Me abolic al e a ions a e also posi i ely co ela ed
wi h sleep diso de s and ci cadian dis up ions (Depne e al.
2014; Smiley e al. 2019), and hese al e a ions ha e been
associa ed wi h noise (Basne and McGui e 2018).
Human s udies A WHO expe e iew ound ha he e is
s ill a limi ed numbe o publica ions explo ing he connec-
ion be ween oad a ic noise and me abolic changes, and
he exis ing esul s a e inconsis en . The e o e, e idence
o he isk o ge ing ype-2 diabe es melli us in esponse
o a ic noise is o low quali y ( an Kempen e al. 2018).
Howe e , mo e ecen s udies ha e obse ed a posi i e asso-
cia ion be ween he isk o ype-2 diabe es melli us de elop-
men and oad a ic noise (Ohlwein e al. 2019; Liu e al.
2023), and e en long- e m exposu e o combined noise
sou ces (Sø ensen e al. 2023).
Animal s udies Animal s udies also suppo he idea ha
noise induces me abolic al e a ions, wi h se e al s udies
showing ha noise exposu e p o okes al e a ions in blood
biochemis y, diabe es, and insulin esis ance in mice
(Liu e al. 2016; Mo akinyo e al. 2019). No ably, in hese
expe imen s, high-noise exposu es we e used, which may
be a om eal oad a ic noise exposu e cha ac e is ics.
Table1 esumes noise exposu e cha ac e is ics used in
animal s udies: high in ensi y (a ound 85–100dB) noises,
exposed du ing a ce ain ime, epea ed se e al imes. Road
a ic noise, howe e , is usually mo e cons an and wi h
lowe in ensi y. I has o be no ed ha oad a ic noise le -
els could each e en highe le els in some ci ies, mos o
hem Asian ci ies (Uni ed Na ions 2022). Thus, noise expo-
su es used du ing animal expe imen s a e simila o ai c a
noise: high in ensi y, in e mi ed noises, usually sepa a ed
by a noise- ee pe iod (Basne e al. 2017). Al hough e i-
dence ega ding he link be ween oad a ic noise exposu e,
me abolic al e a ions, and ype-2 diabe es melli us emains
unclea , exis ing s udies imply a po en ial mechanis ic con-
nec ion in ol ing annoyance, sleep dis u bances, al e a ions
in he HPA axis, and he elease o s ess ho mones. Noise
could impac glucose me abolism by p omo ing li e glucose
p oduc ion, dec easing glucose abso p ion, encou aging a
b eakdown in adipocy es, and inhibi ing insulin sec e ion.
These e ec s can esul in insulin esis ance and in lam-
ma ion, bo h linked o diabe es de elopmen (Sha ma and
Singh 2020). In addi ion, me abolic al e a ions, abno mal
lipid p o iles, and insulin esis ance a e isk ac o s o CVD
(O mazabal e al. 2018).
Noise andmic obiome
In ecen yea s, he e has been a signi ican su ge in esea ch
in es iga ing he link be ween gu mic obio a and a ious
diseases. Fu he mo e, he ela ionship be ween in lamma-
ion, edox signaling, and he gas oin es inal mic obiome
has been elucida ed (F enis e al. 2021b). S ess has he abil-
i y o in luence hese gas o-in es inal mic oo ganisms, as
ci cula ing concen a ions o glucoco icoids and ca echo-
lamines can modula e mic obial g ow h (Ka l e al. 2018). I
has o be no ed ha changes in gu mic obio a a e associa ed
wi h se e al diseases, such as ca diome abolic diseases, neu-
oin lamma ion, and neu odegene a i e diso de s (Collins
e al. 2012; Jones and Neish 2017; Campbell and Colgan
2019; Mou e al. 2022), which a e also associa ed wi h oad
a ic noise (Münzel e al. 2021; Hahad e al. 2022).
Animal s udies Al hough ew s udies ha e ocused on noise
exposu e and he mic obiome, dec eased gu mic obio a
di e si y and composi ional al e a ions we e obse ed in
mice exposed o high-noise o 4h pe day o 30 consecu-
i e days (Cui e al. 2016, 2018). Ano he s udy disco e ed
ha dis up ions in he gu mic obio a we e associa ed wi h
an imbalance be ween oxida i e and an i-oxidan pa hways,
educed igh junc ion p o ein le els in he in es ine and hip-
pocampus, and sys emic in lamma ion igge ed by noise
46826 En i onmen al Science and Pollu ion Resea ch (2024) 31:46820–46839
Table 1 Summa y o he main indings ega ding he noise-induced non-audi o y heal h ou comes
Heal h ou come Main inding Human/animal model Noise exposu e Re e ence
S ess ho mones
Inc eased sali a y o u ina y
co isol le els in pa ici-
pan s unde highe oad a -
ic noise exposu e
Human Road a ic noise Hohmann e al. (2013)
No associa ion be ween oad
a ic noise and sali a y
co isol
Human Road a ic noise Wallas e al. (2018)
Bloemsma e al. (2021)
No associa ion be ween
esiden ial exposu e o oad
a ic noise and hai co isol
concen a ion
Human Road a ic noise Ve heyen e al. (2021)
In lamma ion
Inc eased immune unc-
ion was obse ed a e
3-day noise exposu e and
dec eased immune unc ion
a e 28days o exposu e
Mice 90dB, 5h/day, 3 o 28days Zheng and A iizumi (2007)
Inc eased le els o IL-6 Mice 85dB du ing 43s, 69 epe i-
ions
Münzel e al. (2017)
P o-in lamma o y pheno-
ype and he ac i a ion o
ci cula ing leukocy es we e
a oided in Nox2 knockou
mice
Mice 85dB du ing 43s, 69 epe i-
ions
Eck ich e al. (2021)
Exposu e o oad a ic noise
causes inc eased le els o
IL-12 and high-sensi i i y
C- eac i e p o ein (hsCRP)
le els, and dec eased NKT
cell popula ion
Human Road a ic noise Cai e al. (2017); Kim e al.
(2017); Kupciko a e al.
(2021)
Long- e m exposu e o oad
a ic noise and ai pollu-
ion was associa ed wi h
he en ichmen o pa hways
ela ed o in lamma ion,
cellula de elopmen , and
immune esponses
Human Road a ic noise Eze e al. (2020)
46827En i onmen al Science and Pollu ion Resea ch (2024) 31:46820–46839
Table 1 (con inued)
Heal h ou come Main inding Human/animal model Noise exposu e Re e ence
Oxida i e s ess
Inc eased hippocampal ac i -
i y o an ioxidan enzymes
in animals exposed o acu e
noise, while ac i i y was
dec eased in ch onically
exposed ones
Ra s 100dB, 4h/day, 30days Manikandan e al. (2006)
Inc eased exp ession o
NOX-2
Mice 85dB du ing 43s, 69 epe i-
ions
Münzel e al. (2017)
Neu oin lamma ion, ce eb al
oxida i e s ess, o ci cadian
dys egula ion due o ai c a
noise exposu e we e a oided
in Nox2 knockou mice
Mice 85dB du ing 43s, 69 epe i-
ions
K ölle -Schön e al. (2018)
An ioxidan Vi amin C
diminished noise-exposu e
induced endo helial dys-
unc ion
Human T ain noise
Ai c a noise
He zog e al. (2019); Schmid
e al. (2013)
Me abolic al e a ion
Noise causes me abolic al e a ions, induces al e a ions in blood biochemis y, diabe es, and
insulin esis ance
Mice 95dB, 4h/day, 20days
400–3600Hz (dB no de ined)
Liu e al. (2016, 2018);
Mo akinyo e al. (2019)
Changes in gu mic obiome
P obio ic ea men alle i-
a ed anxie y-like beha iou
in noise exposed a s, by
es o ing unc ioning o
HPA axis and gu -b ain-
mic obio a axes
Ra s 95dB, 4h/day, 30days Hadizadeh e al. (2019)
P omo ing gu mic obio a
homeos asis wi h Lac o-
bacillus hamnosus GG
imp o ed gu bac e ial
balance
Ra s 20–20,000Hz ( dB no
de ined)
Li e al. (2023a, b)
Dec eased gu mic obio a
di e si y and composi ional
al e a ions we e obse ed
a e noise exposu e o
4h/d du ing 30 consecu-
i e days
Mice 400–3600Hz (dB no de ined) Cui e al. (2016, 2018)
46828 En i onmen al Science and Pollu ion Resea ch (2024) 31:46820–46839
Table 1 (con inued)
Heal h ou come Main inding Human/animal model Noise exposu e Re e ence
Imbalance be ween oxida i e
and an i-oxidan pa hways
and sys emic in lamma ion
in esponse o noise we e
ela ed wi h al e a ions in
gu mic obio a
Mice 20–20kHz (98 dB, 4 h/
day,30 days)
Chi e al. (2021)
Vascula dys unc ion
Ca dio ascula dys unc ion
Exposu e o ai c a noise
caused endo helial dys-
unc ion, inc eased blood
p essu e, inc eased le els o
neu oho mones, and highe
sensi i i y o asocons ic-
o s, including endo helin-1
and no ad enalin. Reduc-
ion in NO bioa ailabili y
was obse ed, due o eNOS
uncoupling/dys unc ion and
NO eac ion wi h supe ox-
ide in an oxida i e s a e
Mice 85dB du ing 43s, 69 epe i-
ions
K ölle -Schön e al. (2018);
Münzel e al. (2017)
O se ing up egula ion eNOS
mRNA le els and main
enzymes esponsible o
eNOS co ac o
Mice 85dB du ing 43s, 69 epe i-
ions
Münzel e al. (2017)
Road a ic noise exposu e
caused endo helial dys unc-
ion ma ke s o in lamma-
ion and oxida i e s ess
Human T ain noise
Ai c a noise
Ai c a noise
He zog e al. (2019); Schmid
e al. (2015); Schmid e al.
(2013)
Ce eb o ascula dys unc ion
Reduced dend i ic coun
in he hippocampus and
inc eased oxida i e s ess
in he on al co ex a e
exposu e o noise
Ra s 100dB, 4h/day, 30days Manikandan e al. (2006)
Exposu e o noise caused
hippocampal al e a ions ha
could unde lie beha iou al
e ec s
Ra s 95–97dB, 2h/day,
Single day/ i e consecu i e
days
U an e al. (2012)
Noise-induced hippocampal
oxida i e s ess and changes
in aminoacide gic neu o-
ansmi e s
Ra s 95–97dB, 2h/day,
Single day/15 consecu i e
days
Molina e al. (2020)
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