57 Noise-Induced Hearing Loss

57.1 Aetiology and Background

The ear is a sound-sensitive organ but can be damaged by excessive noise levels. Excessive noise can arise from a variety of sources: occupational, such as factory machinery, building sites, and high-impact tools and military firearms; recreational, such as shooting, home power tools, standing too close to speakers at concerts or nightclubs and personal stereos. Motorcycling and car air bags are also recognised causes of noise damage.

Changes in manufacturing industries, machinery designs and regulations have led to a change in the pattern of noise exposure and consequent complaints, with more frequent presentation, in a medicolegal setting, of tinnitus and hyperacusis. New industries, such as call centres, have brought novel forms of noise exposure with damaging consequences, such as ‘acoustic shock’.

Worldwide though, noise-induced hearing loss (NIHL) is still one of the leading causes of sensory disability. Occupational deafness is a compensable disease and legislation exists to protect the employee (Health and Safety at Work Act). European legislation stipulates a first action level at 80 dB (A) for an 8-hour working day, at which point an employer is obliged to monitor the hearing levels of his or her workforce and to monitor noise levels at the workplace. At the second action level of 85 dB (A), he or she is statutorily obliged to provide a hearing protection programme to include hearing protection, monitoring and efforts to reduce sound levels at source.

57.2 Pathology

Biological variability (inherited or genetic susceptibility) means that individuals are not affected equally by the same noise exposure. However, with increasing noise levels above 90 dB (A), a greater proportion of the exposed population will exhibit pathological changes. The susceptibility of individuals to NIHL seems to be the same as the susceptibility to presbycusis indicating the inherited susceptibility to both conditions is linked.

Initially, noise exposure may lead to temporary threshold shift (TTS), which is a recoverable phenomenon. There are no obvious pathological changes in TTS and the condition may be due to metabolic ‘exhaustion’ of the hair cells of the cochlea. It is thought that repeated episodes of TTS may predispose patients to presbycusis at an earlier age compared to those who have not had such episodes.

There is substantial experimental evidence from animal studies that shows a change in cochlear blood flow associated with acoustic stimulation. With increasing and repeated noise exposure, there is permanent mechanical and metabolic damage, initially to the outer hair cells (OHCs) of row 1, and subsequently to the OHCs in rows 2 and 3 and the inner hair cells. Damage also occurs to the supporting pillar cells and the stria vascularis. The audiometric hearing loss tends to parallel the loss of hair cells.

57.3 Clinical Features

TTS may be perceived as tinnitus and pressure in the ears following excessive noise exposure. Permanent threshold shift (PTS) is frequently asymptomatic initially and is often found on routine screening audiometry carried out in the workplace. Such screening is a requirement of any hearing protection programme. When PTS becomes symptomatic, the first complaint is usually reduced understanding for speech, especially when there is background noise. As hearing loss becomes more profound, the patient complains more of being hard of hearing. Unfortunately, tinnitus is a frequent accompanying symptom in NIHL occurring in 40% of such patients. Examination will usually be normal (unless the patient has had previous middle ear disease).

57.4 Acoustic Shock

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