Health Sciences Review 12 (2024) 100181

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Health Sciences Review

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Educational Review

Human health effects associated with occupational and environmental

acoustic trauma
Noura Gannouni a, c, * , Jing Wang b , Khémais Ben Rhouma c , Abada Mhamdi a
a
Faculty of Medicine of Tunis – UR17ES13, University of Tunis ElManar, Tunisia
b
Institute for Neurosciences of Montpellier (INM), University Montpellier, INSERM U1298, France
c
Laboratory of Integrated Physiology- LR17ES02, Faculty of Sciences of Bizerte- University of Carthage, Tunisia

A R T I C L E I N F O A B S T R A C T

Keywords: Noise is ubiquitous in daily life and can cause both auditory and non-auditory health problems. Noise effects
Noise involve both direct and indirect pathways through which noise affects human health. A direct pathway en­
Hearing loss compasses the interactions between the central auditory system and other regions of the brain. The indirect
Health effects
pathway involves the cognitive and emotional response to a noise-exposure.
Prevention
This review begins by summarizing both auditory and non-auditory health effects of occupational and envi­
Therapeutic strategies
ronmental noise exposures. It then guides the reader to adequate mitigation strategies and preventive measures
to reduce the consequences of noise nuisance.

1. Introduction many years and have been the matter of much research work [14,15].
The effects of noise exposure are divided into two classes: auditory
Anthropogenic noise has increased significantly over the last century (e.g. hearing loss, tinnitus, hyperacusis…) and non-auditory (e.g.
and it is largely recognized as significant stressor for human and animals elevated blood pressure, changes heart rate, stress…).
in both terrestrial [1–3] and marine environments[4–7]. In human so­
ciety, noise has different origins. Occupational noise is hazardous noise
presented in workplace whereas social and environmental noise is 2.1. Auditory effects
defined as noise emitted from all sources except industrial workplaces
[8]. 2.1.1. Noise induced hearing loss
Noise exposure is a major public health problem worldwide. Noise Noise-induced hearing loss (NIHL) is a major health problem, not
produces direct and cumulative adverse effects on human health and only because of the abounding opportunities for over-exposure but also
contribute to develop hearing loss, tinnitus, change heart rate, sleep because potentially damaging exposures are not necessarily painful or
disorders [2], hypertension, ischemic heart diseases, stroke, stress hor­ even annoying [2,16]. NIHL is also one of the most common forms of
mones hyperproduction (including catecholamines and glucocorticoids) sensorineural hearing loss, which is largely preventable and is probably
[9–12]. more widespread than revealed by conventional clinical pure tone
Noise-induced hearing loss remains highly prevalent in occupational threshold testing. Several studies have mostly associated occupational
settings, and is increasingly caused by social noise exposure [2]. Noise noise exposure with direct auditory effects, including hearing loss
pollution significantly impacts public health and could affect the resi­ [17–20]. In addition, NIHL occurs among operators exposed in indus­
dential, social and working environment with corresponding real (eco­ trial settings [21–23]. NIHL can be caused by a one-time exposure to an
nomic) and intangible (well-being) losses [13]. intense impulse sound, or by steady state long-term exposure [24].
The noise exposure may cause reversible damage in the auditory
2. Noise effects sensory organ, the cochlea, causing temporary threshold shift (TTS). In
this case, the cochlea recovers functional capacity in 24 to 48 h after
The harmful effects of noise on human health have been known for traumatic noise exposure [25]. Prolonged or repeated noise exposures
lead to permanent hearing loss (PTS: permanent threshold shift) and

* Corresponding author.
E-mail address: [Link]@[Link] (N. Gannouni).

[Link]
Received 29 April 2024; Received in revised form 6 June 2024; Accepted 9 June 2024
Available online 10 June 2024
2772-6320/© 2024 Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license ([Link]
N. Gannouni et al. Health Sciences Review 12 (2024) 100181

cochlear cell damage [26,27]. ototoxic drugs [47] and ototoxic substances in working environments
Noise exposure may damage several cochlear structural elements [48]. A survey among industrial workers [49] showed that the
including the sensory hair cells [28–30], the spiral ganglion neurons socio-demographic factors (age, seniority, attitudes) contributes to the
[26,30,31], the stria vascularis [32] and the fibrocytes [33], and may genesis of adverse effects on health including hearing loss, and all age
affects intracellular biochemical pathways [34]. Gannouni et al. [30] groups show significant vulnerability to the effect of noise.
explored the neuroepithelial changes that occur in the cochlea of rats
subjected to moderate noise intensities for an extended period of time 2.2. Non-auditory effects
(70 and 85 dB SPL,6 hr/day over 3 months). This type of sound exposure
was comparable to the noise environment at which a substantial per­ The World Health Organization document, Guidelines for Commu­
centage of the current population works is exposed. Using scanning nity Noise, indicates that noise exposure may lead to many detrimental
transmission electron microscopy, the authors showed that the full effects, including auditory and non-auditory effects. In fact, exposure to
quota of sensory hair cells, i.e. the inner (IHCs) and the outer (OHCs) noise can be pathogenic, directly or indirectly, at several levels (phys­
hair cells, was essentially preserved. Nevertheless stereocilia abnor­ ical, psychological, socio-economic) and for various categories of actors
malities were observed on both types of hair cells (Fig. 1A). In addition, (exposed subjects, family environment, company, society) [50].
afferent dendrites contacting the IHCs were swollen (Fig. 1B) and losses
of spiral ganglion neurons were noticed. This suggests that an excito­ 2.2.1. Physiological system
toxic process resulting from excessive glutamate release by the IHCs [35, Noise can have a more global effect on human physiology and act
36] has occurred leading to further neuronal alteration (Fig. 1C) and upon multiple non-auditory systems such as cardiovascular, neuroen­
degeneration. These data strongly suggest that even at moderate levels docrine, and cental nervous systems [51].
noise-exposure with sufficient exposure duration in working environ­ Noise acts as a stressor and one of the most harmful agents for
ments may cause hearing impairments (deficits of understanding speech workers, and may also cause elevated blood pressure [52,53]. Babisch,
in noisy environments, tinnitus and hearing loss) and contribute to reported that noise exposure increases systolic and diastolic blood
premature occurrence of neural presbycusis (Table 1). pressure, changes heart rate, and causes the release of stress hormones
Recent studies showed that, NIHL pathogenesis in human are asso­ [9]. They demonstrated that the persistent chronic noise exposure can
ciated with the production of auto-antibodies [37,38]. To investigate a cause an imbalance in an organism’s homoeostasis with increases in
potential association between the levels of anti-Hsp60 or anti-Hsp70 in established cardiovascular disease risk factors such as blood pressure,
the plasma and NIHL in noise-exposed workers, Yang et al. [38] blood lipid concentrations, blood viscosity, and blood glucose concen­
analyzed the levels of these antibodies in the plasma of 399 workers trations. These dysfunctions increase the risk of cardiometabolic dis­
regularly exposed to noise between 75 and 115 dB and correlated these eases, such as arterial hypertension [52,54], coronary artery disease and
results with the hearing evaluations through audiological assessments. stroke [55–58].
Their results showed that the prevalence of positive anti-Hsp70 was Recent data of Frenis et al. [59] showed distinct changes of the
significantly higher in the workers with slight and moderate cardiovascular/cerebral system in response to a 4 weeks aircraft noise
high-frequency NIHL than in normal-hearing workers. Moreover, the exposure period. The key mechanisms are noise-triggered vascular
prevalence of positive anti-Hsp60 in workers with moderate inflammation and oxidative stress with subsequent endothelial
low-frequency NIHL was also significantly higher than in the dysfunction [59].
normal-hearing workers [38]. Autoantibodies therefore might play a
role in the pathogenesis of NIHL. 2.2.2. Central nervous system
It has been reported that noise exposure may have various direct
2.1.2. Factors associated with noise-induced hearing loss effects on the Central Nervous System (CNS), including oxidative stress,
The exposure to intense noise is the most common cause of hearing imbalance in neurotransmitter levels in brain, alteration of molecular
impairment in employees [39–42]. Several factors are strongly associ­ mechanisms, deterioration of brain morphological structures, and
ated with hearing loss in workers such as age [43,44], smoking [45,46], epigenetic modifications [60–62]. Moreover, mounting research and

Fig. 1. SEM (A) and TEM (B-C) micrographs in the basal region of the cochlea of a rat exposed 6 hr/day over 3 months at an octave band-noise (8–16 kHz) at 85 db
SPL.
A: surface of the organ of Corti showing the bundles of stereocilia in the single row (I) of IHCs and in the 3 rows (O) of OHCs: the bundle of stereocilia are lineraly
arranged in IHCs while they are W shaped in OHCs. Noise exposure-induced damage are visible at the level of both types of hair cells. The IHCs show bending
stereocilia (arrows) and one IHC is missing (asterisk). In the first row of OHCs, some hair cells show fused stereocilia (arrows). Stereocilia are essentially normal in
the OHCs of the two other rows. B: Transverse section of a IHC (I) and its afferent innervation. The presence of several large vacuoles (v) in the cytoplasm of the IHC
suggests a sustain autophagic activity. At the basal pole of the IHC, the dendrites of the spiral ganglion neurons which make synapses with the hair cell are swollen
(asterisks) in a typical feature of excitotoxicity. C: Cell body of a damaged spiral ganglion neuron. The cytoplasm of the ganglion neuron shows signs of metabolic
disorders such as a distorted nucleus (N) and the presence of large dark inclusions (arrows) and vacuoles (v). Scale bars: A = 10 µm; B-C = 5 µm.
The micrographs originated from Gannouni et al., 2015 [30].

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N. Gannouni et al. Health Sciences Review 12 (2024) 100181

Table 1 the decline of cognitive performance, and to social disconnection [2,66,

: Main relevant bibliographic references. 67].
Author Year Focus Type of article References
2.2.3. Immune system
Nirvikalpa 2023 A*, Etiology and risk Review [24]
factors for NIHL. The immune system is composed of multiple immune organs, im­
Screening, prevention, mune cells and immunoactive substances. Many studies have shown that
and treatment of noise can affect innate and specific immune functions and noise of
patients. different duration and intensities can elicit different immune responses
Frenis 2022 NA**, Cardiovascular/ Basic research, [59]
cerebral systems, animal
[68–71]. A recent study has shown that environmental noise pollution
aircraft noise exposure. experiment has a negative impact on both of physiological and the immune system
Hahad 2022 NA, Environmental Review [63] [72].
noise, brain, human and It is widely recognized that noise exposure can indirectly disturb the
animal studies.
immune system by activating the hypothalamic-pituitary-adrenal (HPA)
Saraei 2022 A, Combined effects, Experimental [39]
noise, organic solvent, study axis and the sympathetic-adrenal-medullary (SAM) system [71].
NIHL.
Umayra 2022 NA, Environmental Basic research, [72] 3. Experimental therapeutic strategies against acoustic trauma
noise pollution, animal
physiological and experiment
immune systems,
As a stressor, noise can induce oxidative stress in the body. Physio­
hematological and logically, excess of reactive oxygen species (ROS) in the body can be
spleen parameters. eliminated by endogenous antioxidant enzymes and non-enzymatic
Zhang 2021 NA, Innate immunity Review [37] scavengers, such as vitamins E, C, D and beta-carotene. Under noise-
and specific immunity.
induced oxidative stress conditions, supplementation with exogenous
Arjunan. 2020 NA, Central nervous Basic research [60]
system, oxidative stress, antioxidants can play a role in maintaining the cochlear homeostasis.
neurotransmitters, The use of antioxidants to reduce or prevent noise-induced hearing
cellular loss is of broad interest. The treatment with doses of β-carotene, vitamin
cytoarchitecture, C, Trolox (a synthetic analogue of vitamin E), and magnesium (Mg) have
cognition, genetic.
Paciello 2020 A, NIHL, Polyphenol CA, Basic research, [75]
been shown to effectively reduce hearing loss at multiple post-noise-
therapeutic strategy, animal exposure times [73].
cochlear damage, experiment Ebselen is an organoselenium compound with anti-inflammatory,
inflammatory signaling, anti-oxidant and cytoprotective activity. Ebselen acts as a glutathione
redox balance.
peroxidase mimetic and is thereby able to prevent cellular damage
Sheppard 2020 A, NA, Auditory and Review [40]
non-auditory effects of induced by reactive oxygen species (ROS). Lynch and colleagues [74]
occupational noise. demonstrated that ebselen provided significant therapeutic effects from
Wang 2020 A, NIHL assessment, Review [41] both temporary and permanent threshold shifts following single and
pharmacologic and non- repeated noise exposure.
pharmacologic
treatments, central
Paciello and colleagues [75] investigated the protective capacity of
auditory plasticity. polyphenol caffeic acid in a model of sensorineural hearing loss induced
Abraham 2019 A, Industrial workers, Experimental [22] by noise. Their results demonstrate that the supplementation of poly­
NIHL. study phenol caffeic acid can be considered as a valid therapeutic strategy for
Karafakioglu 2019 NA, Immune deficiency, Basic research, [77]
attenuating noise-induced hearing loss and cochlear damage through
α lipoic acid, animal
antioxidant, protection experiment targeting both inflammatory signaling and cochlear redox balance.
against stress. Srikumar concluded that the supplementation with Triphala pre­
Kroller- 2018 NA, Vascular and Basic research, [61] vented the noise-stress induced changes in the antioxidant status and on
Schon cerebral oxidative stress, animal the cell-mediated immune response in rats [76]. Furthermore, α lipoic
endothelial dysfunction experiment
and inflammation.
acid, another antioxidant has also shown similar therapeutic effects
Aircraft noise. against noise [77]. The identification of novel natural products as po­
Gannouni 2015 A, Cochlear sensory hair Basic research, [30] tential therapeutics targeting oxidative stress and inflammatory path­
cells, Spiral ganglion animal ways is an emerging field.
neurons experiment
It is also relevant to take an interest in alternative therapies to fight
*
A = auditory effects. the effects of sound exposure using medicinal plants and nutritional
**
NA= non-auditory effects. supplements with a great interest in the prevention or even the miti­
gation of damage caused by noise. Indeed, it is considered to use food
conclusive evidence demonstrate that exposure to noise, primarily from supplements rich in essential nutrients which offer a natural solution to
traffic sources, may contribute to increased risk of neuropsychiatric fight both hearing loss and the stress generated by noise.
disorders such as stroke, dementia and cognitive decline, neuro­
developmental disorders, depression, and anxiety disorder [63]. 4. Conclusion
In addition, exposure to continuous noise increased the oxidative
stress and decreased the antioxidant level in various regions of the brain. For a long time, noise was considered as physical phenomenon acting
Also, stress activates the HPA (hypothalamic-pituitary-adrenal) and only on the auditory system. We now know that such a consideration is
secretion of glucocorticoids in adrenal glands, which crosses the blood- false and that the reactions caused by noise involve the whole organism
brain barrier and interacts with the neurons and neuroglia cells that in the form of a general reaction. Noise causes physiological responses
alters the neuroanatomical and neurophysiological functions in brain through direct and indirect pathways that intersect through the arousal
[64,65]. of stress responses that activates the autonomic and endocrine systems,
Finally, hearing loss leads to the inability to understand speech in and affects cardio-vascular function and mental health among other co-
everyday situations may contribute to the decrease of attention to tasks, morbidities.
Interestingly, one common effect of noise on the organism, including

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