Scientific background

A report by the World Health Organization (1997) identified excessive noise exposure as the main cause of preventable hearing impairment worldwide, accounting for more than one third of all cases of hearing loss in industrialised nations.

Noise exposure can lead to a temporary or permanent reduction in sensitivity through damage to the outer and inner hair cells in the cochlea [1]. The Control of Noise at Work Regulations Act 2005 set out by the British Health and Safety Executive (HSE) stipulate the maximum legal levels of noise exposure, and require that workers who are exposed to daily equivalent levels of more than 85 dBA be routinely monitored for hearing damage, typically using pure-tone audiometry (PTA). PTA measures the sensitivity of the ear by determining the levels of pure tones that can just be heard at several test frequencies.

Clinically, PTA is used to diagnose hearing loss and to determine the parameters for fitting hearing aids. The principle underlying the determination of the maximum exposure level is that workers should not be exposed to noise that leads to a permanent elevation in audiometric thresholds. However, there is growing evidence that PTA may not be sensitive to some aspects of the damage caused by noise exposure. Individuals with a history of noise exposure, but with normal hearing sensitivity (as measured by PTA), show impaired speech discrimination [2, 3], and impaired performance on temporal processing tasks such as discrimination of noises with different envelope statistics [4], and modulation detection [3].

In a large UK survey, 14% of respondents aged 17-30 reported 'great difficulty' hearing speech in noise, while only 1.8% had impaired sensitivity (thresholds ≥25 dB HL averaged between 0.5 and 4 kHz) [5]. A deficit in hearing ability in the presence of a normal audiogram is sometimes called “sub-clinical” or “hidden” hearing loss.

References

  • [1]. Borg E, et al. (1995). Scand Audiol Suppl 40: 1-147  
  • [2]. Kujala T, et al. (2004). Psychophysiol 41:875-81
  • [3]. Kumar UA, et al. (2012). Noise Health 14: 100-5
  • [4]. Stone MA, et al. (2008). Int. J. Audiol.47: 737-50
  • [5]. Davis AC (1989). Int J Epidemiol 18: 911-7