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Vol. 86. Issue 6.
Pages 665-666 (November - December 2020)
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Vol. 86. Issue 6.
Pages 665-666 (November - December 2020)
Editorial
DOI: 10.1016/j.bjorl.2020.04.001
Open Access
Is noise-induced hearing loss still a public health problem after decades of legislation?
A perda auditiva induzida pelo ruído ainda é um problema de saúde pública após décadas de legislação?
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Vagner Antonio Rodrigues da Silvaa,
Corresponding author
vagrodrigues@hotmail.com

Corresponding author.
, Edson Ibrahim Mitreb, Agrício Nubiato Crespoa
a Universidade Estadual de Campinas (UNICAMP), Faculdade de Ciências Médicas, Departamento de Oftalmo e Otorrinolaringologia, Campinas, SP, Brazil
b Faculdade de Ciências Médicas da Santa Casa de São Paulo, Departamento de Otorrinolaringologia, São Paulo, SP, Brazil
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Exposure to noise is a common and the most preventable cause of hearing loss. Occupational noise is responsible for approximately 16% of disabling hearing loss in adults. Noise-Induced Hearing Loss (NIHL) is the second most common occupational illness or injury, even after decades of study, regulation and interventions in the workplace to try to prevent it.1

NIHL is irreversible, manifesting first and predominantly at the frequencies of 3kHz, 4kHz and 6kHz. It takes longer for the frequencies of 0.25kHz, 0.5kHz, 1kHz, 2kHz and 8kHz to be compromised.1 It rarely leads to profound hearing loss. It generally does not exceed 40dB HL at low frequencies and 75dB HL at high frequencies. After exposure to noise has ceased, NIHL does not progress.1,2

NIHL etiopathogenesis is a multifactorial one. Several genes are involved in different mechanisms that increase susceptibility to noise.3 The noise can induce an excessive production of free radicals that remain active for up to seven days inside the cochlea. There is a reduction in intracellular Adenosine Triphosphate (ATP) caused by sustained activation of AMP-Activated Protein Kinase (AMPK), leading to cell apoptosis. Proteins such as caspase 3 and c-Jun N-terminal kinase (JNK) can be activated by noise and cause apoptosis. An excessive accumulation of intracellular calcium can also initiate the oxidative stress chain. Another known phenomenon is synaptopathy, which is the loss of connections between the inner hair cells and their afferent neurons, resulting from glutamate excitotoxicity at postsynaptic terminals.1

Risk awareness must be associated with patient motivation to take the necessary measures to reduce exposure to potentially harmful noise, both in the workplace and during leisure activities.4 Headphones can produce a sound pressure of up to 126dB HL. Ambient noise at nightclubs and concerts is another common source of leisure noise that range from 104.3–112.4dB HL, with an average level of 97.9dB HL.5

Listening to music during sports activities increases attention, reduces fatigue and increases alertness. The effects obtained on performance depend on the characteristics of the stimulus, the individual and the intensity and type of activity. The more pleasant a song is, the louder you want to hear it.

The appropriate frequency of occupational audiometric tests is poorly studied, and it is not based on population studies. There is general medical agreement that it audiometry should be performed annually. Brazilian legislation is the only one that establishes that the first periodic audiometric examination must be performed after six months of work, becoming annual as of the second periodic examination.

Although the improvement in the standards and control of exposure to noise have advanced since the end of World War II, NIHL remains a significant public health problem. The problems caused by NIHL go beyond the auditory symptoms and may affect the vestibule, which increases the risks of accidents in the workplace, in addition to insomnia, irritability and arterial hypertension, decreasing productivity and resulting in risks to the workers’ health. There is much to be done to prevent the condition in populations that are genetically at greater risk for NIHL. The popularization of headphones to listen to music has resulted in early sensorineural hearing loss in young individuals and adolescents. It makes it difficult to identify workers whose audiometric thresholds have worsened exclusively due to their professional activity.

Conflicts of interest

The authors declare no conflicts of interest.

References
[1]
A. Lie, M. Skogstad, H.A. Johannessen, T. Tynes, I.S. Mehlum, K.C. Nordby, et al.
Occupational noise exposure and hearing: a systematic review.
Int Arch Occup Environ Health, 89 (2016), pp. 351-372
[2]
A.S. Nordmann, B.A. Bohne, G.W. Harding.
Histopathological differences between temporary and permanent threshold shift.
Hear Res, 139 (2000), pp. 13-30
[3]
A. Konings, L. Van Laer, G. Van Camp.
Genetic studies on noise-induced hearing loss: a review.
Ear Hear, 30 (2009), pp. 151-159
[4]
G.W. John, A. Grynevych, D. Welch, D. McBride, P.R. Thorne.
Noise exposure of workers and the use of hearing protection equipment in New Zealand.
Arch Environ Occup Health, 69 (2014), pp. 69-80
[5]
E. Van Dyck.
Corrigendum: Musical intensity applied in the sports and exercise domain: an effective strategy to boost performance?.
Front Psychol, 10 (2019), pp. 1434

Please cite this article as: Silva VA, Mitre EI, Crespo AN. Is noise-induced hearing loss still a public health problem after decades of legislation? Braz J Otorhinolaryngol. 2020;86:665–6.

Copyright © 2020. Associação Brasileira de Otorrinolaringologia e Cirurgia Cérvico-Facial
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Brazilian Journal of Otorhinolaryngology (English Edition)

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