10.2.5 Noise 1671

10.2.5 Noise 1671

10.2.5  Noise 1671 inference, lungs that are too small for their bodies, are more liable to lung rupture on rapid ascents. Possible pre-​existing blebs, bullae, or air-​trapping on postincident CT of chest in a small case series of pulmonary barotrauma after free ascents in candidates with unusually large lungs (volumes greater than 120% of predicted) has raised concerns for some diving clin- icians. Until more is known, it would be prudent to consider care- fully all candidates with ‘outlier’ spirometry values, whether too large or small. The FEV1/​FVC ratio has not been found to be especially helpful. What matters most in diving is the time constant of emptying of the full lungs. The peak expiratory flow (PEF)/​FVC ratio is a reasonable measure of this, and PEF should be at least 1.5 times predicted FVC per second. Past or current asthma used to be an absolute contraindication to diving on theoretical grounds of increased risk of lung rupture on fast ascents. Childhood asthma often disappears, however, and very many people with current mild asthma are known to dive fre- quently without ill effect. The British Thoracic Society’s guidelines permit diving in asymptomatic asthma with normal spirometry, negative exercise test, PEF no more than 10% below best values, and requiring no more than regular inhaled anti-​inflammatory agents. Alternative causes of osteonecrotic lesions must be excluded be- fore a dysbaric aetiology is accepted. If lesions are asymptomatic, the medical examiner might consider restriction from experimental or provocative deep diving. Symptomatic lesions will be more re- strictive and, if the articular surface collapses, a joint replacement might be required. MRI has been shown to be more sensitive than traditional plain X-​ray screening. MRI can detect potential lesions within days of a dsybaric insult, whereas X-​ray evidence may take several months to appear. Some lesions visible on MRI, including those in juxta-​articular locations, have remained asymptomatic and have resolved spontaneously. As a result, such lesions require careful serial monitoring before any decision is made that will limit a diver’s employability in the long-​term. Conclusion More effective therapies for DCI are sought, either instead of, or to supplement recompression. Surface oxygen is used as a first aid measure but might have a role as a definitive treatment in selected groups. Intravenous perfluorocarbons and lidocaine have both attracted interest, but more evidence is required. An intervention as simple as an oral non​steroidal anti-​inflammatory drug showed promise in reducing compression requirements in a recent randomized controlled study. Further meticulous data collection will help to identify subgroups who need minimal or more aggressive treatment from the outset. It will also help to clarify issues of safety of drugs, and of medical conditions, while diving. A local hyperbaric facility can advise on management of diving disorders. In Britain, if the nearest suitable facility is not known, the British Hyperbaric Association provides a 24-​h advice line (07831 151523)  for England, Wales, and Northern Ireland and Aberdeen Royal Infirmary (0345 408 6008) provides the service for Scotland. There are many helpful organizations around the world. The Divers’ Alert Network, for instance, has international coverage, and contact details can be obtained from http://​www. diversalertnetwork.org/​contact/​international.asp FURTHER READING Bennett M, Mitchell S, Dominguez A (2003). Adjunctive treatment of decompression illness with a non-​steroidal anti-​inflammatory drug (tenoxicam) reduces compression requirements. Undersea Hyperb Med, 30, 195–​204. Bove AA (2004). Bove and Davis’ diving medicine, 4th edition. W.B. Saunders, Philadelphia, PA. British Thoracic Society Fitness to Dive Group (2003). British Thoracic Society guidelines on respiratory aspects of fitness for diving. Thorax, 58, 3–​13. Brubakk A, Neuman T (eds) (2003). Bennett and Elliott’s physiology and medicine of diving, 5th edition. W.B. Saunders, London. Edmonds C, et al. (eds) (2015). Diving and subaquatic medicine, 5th edition. CRC Press, Boca Raton, FL. Lundgren CEG, Miller JN (eds) (1999). The lung at depth. Dekker, New York, NY. Macdiarmid JI, et  al. (2004). Co-​ordinated investigation into the possible long-​term health effects of diving at work. In: Examination of the long-​term health impact of diving: the ELTHI diving study. HSE Books, HMSO, Norwich. Naval Sea Systems Command, U.S. Department of the Navy (2018). U.S. Navy Diving Manual (Revision 7, Change A, April 2018). https://www.navsea.navy.mil/Portals/103/Documents/SUPSALV/ Diving/US%20DIVING%20MANUAL_REV7_ChangeA-6.6.18. pdf?ver=2018-06-15-102549-030 Slade JB, et  al. (2001). Pulmonary edema associated with scuba diving: case reports and review. Chest, 120, 1686–​94. Smart D, et  al. (2015). Joint position statement on persistent for- amen ovale (PFO) and diving. South Pacific Underwater Medicine Society (SPUMS) and the United Kingdom Sports Diving Medical Committee (UKSDMC). Diving Hyperb Med, 45, 129–​31. UK Health and Safety Executive (2009). Research report RR761—​ Differential pressure hazards in diving. http://​www.hse.gov.uk/​re- search/​rrpdf/​rr761.pdf Wilmshurst P, Bryson P (2000). Relationship between the clinical fea- tures of neurological decompression illness and its causes. Clin Sci, 99, 65–​75. Wilmshurst PT, et  al. (1989). Cold-​induced pulmonary oedema in scuba divers and swimmers and subsequent development of hyper- tension. Lancet, i, 62–​5. 10.2.5  Noise David Koh and Tar-​Ching Aw† ESSENTIALS Noise can affect hearing in the occupational setting but can have other effects where exposures are non​occupational. For clinical † It is with great regret that we report that Tar-Ching Aw died on 18 July, 2017.

SECTION 10  Environmental medicine, occupational medicine, and poisoning 1672 purposes, noise is measured in decibels weighted according to the sensitivity of the human ear (dB(A)). Regardless of source, the effects of overexposure to noise are similar. Initially there is a temporary threshold shift, where reversibility of hearing loss is possible with re- moval away from further noise. Noise-​induced hearing loss occurs following prolonged or intense exposure, with poor prospects for improvement of hearing. The classical audiogram for noise-​induced hearing loss shows a 4 kHz dip. Non​auditory effects of prolonged noise exposure include annoyance, sleep disturbance, hypertension, and cardiovascular disease, stress, and impaired cognitive perform- ance. Prevention of noise-​induced hearing loss is by reducing ex- posure to noise at source, minimizing exposure time, using hearing protection, and participating in surveillance. Introduction Noise is any unwanted sound. Excessive noise damages the coch- lear hair cells, breaking and disrupting the cilia, which act as local electromechanical amplifiers. This can result in physical and psychological harm. Exposure The two important characteristics of sound are its intensity and fre- quency. The human audible sound intensity range is 0–​120 decibels. The decibel (dB) scale is logarithmic rather than linear, therefore every increase in sound intensity of 3 dB is equivalent to a doubling of sound intensity. In young adults, the ear sound frequency ranges from 20 Hz to 20 kHz, but its sensitivity is not equal across this range. To mimic the response of the human ear and to allow for the variation in ear sensitivity to different frequencies, sound level meters apply a weighting to the sound intensities, and express the readings as dB(A), that is, decibels weighted by the A scale (as de- fined by international standards). Typical sound levels are 65 dB(A) for normal conversation at a distance of 1 m; 140 dB(A) for a jet aircraft taking off 25 m away; and 160 dB(A) for a rivet gun near the ear. Noisy industries include manufacturing, construction, engineer­ ing, metalworking, motor sports, the military, and entertainment industries. Instantaneous noise levels can be assessed using a noise meter. For cumulative noise exposure, a personal noise dosimeter provides an ‘equivalent noise dose’ by averaging the frequencies and intensities over an 8-​h shift. In the United Kingdom, the Control of Noise at Work Regulations 2005 stipulate an exposure limit of 87 dB(A) averaged over 8 h/​day or 140 dB(A) for any instantaneous impulse noise. Besides occupational exposure, lower intensity community noise (e.g. from airports or urban traffic) is recognized to be associated with adverse health effects. Several studies have shown increased mortality from cardiovascular diseases among people living near noisy airports. The use of personal music players at excessive vol- umes for prolonged periods can also result in significant and haz- ardous noise exposure. There is also evidence that background noise can impair learning in schools. Clinical effects Exposure to loud noise can cause auditory and non​auditory effects. There is wide variation in individual susceptibility. Massive impulse pressures (e.g. from bomb blasts), can cause acute acoustic trauma. There can be a perforation of the tympanic membrane or disruption of the ossicular chain with associated pain and hearing loss, or occa- sionally hyperacusis. An early response to loud noise exposure (e.g. among those who work in noisy environments or those attending loud mu- sical events) is temporarily increased hearing threshold. This temporary threshold shift might be accompanied by tinnitus. The transient dullness of hearing typically lasts up to 24 h, after which hearing thresholds return to normal. With continuing exposure, the magnitude of this temporary sensorineural hearing loss and the recovery time increase until, after months or years, there is a permanent shift in threshold, which might be accompanied by tin- nitus. Hearing damage due to chronic or variable noise exposure might not become apparent until early or middle age, depending on when exposure commenced, and on duration and intensity of the noise. On audiograms, noise-​induced hearing loss is detected as a dip at 4 kHz (Fig. 10.2.5.1). Affected people find it difficult to distin- guish between similar sounds, particularly consonants, in the pres- ence of moderate background noise. With severe hearing loss, the listener may experience ‘loudness recruitment’, a rapid, uncomfort- able increase in sound perceived when intensity increases beyond the already abnormal hearing thresholds. With continued noise exposure, the 4-​kHz dip on audiograms extends to lower frequen- cies and hearing thresholds worsen. This might be combined with presbyacusis (age-​related hearing loss) in later years. Worldwide, about 16% of hearing loss is estimated to be associ- ated with occupational noise exposure. In addition to hearing loss, noise exposure can lead to non-​ auditory effects such as sleep disturbance, hypertension, and car- diovascular disease, stress, and impaired cognitive performance. 125 110 100 90 80 70 60 50 40 30 20 10 0 Frequency (Hz) Hearing level (dB) 250 tfe L th giR 500 8000 4000 1000 2000 Fig. 10.2.5.1  Audiogram typical of noise-​induced hearing loss with a dip at 4 kHz frequency. Red circles, right ear; blue crosses, left ear.