REVIEW

CURRENT
OPINION Noise-induced hearing loss: an occupational
medicine perspective
Emily Z. Stucken a and Robert S. Hong a,b

Purpose of review
Up to 30 million workers in the United States are exposed to potentially detrimental levels of noise.
Although reliable medications for minimizing or reversing noise-induced hearing loss (NIHL) are not
currently available, NIHL is entirely preventable. The purpose of this article is to review the epidemiology
and pathophysiology of occupational NIHL. We will focus on at-risk populations and discuss prevention
programs. Current prevention programs focus on reducing inner ear damage by minimizing environmental
noise production and through the use of personal hearing protective devices.
Recent findings
NIHL is the result of a complex interaction between environmental factors and patient factors, both genetic
and acquired. The effects of noise exposure are specific to an individual. Trials are currently underway
evaluating the role of antioxidants in protection from, and even reversal of, NIHL.
Summary
Occupational NIHL is the most prevalent occupational disease in the United States. Occupational noise
exposures may contribute to temporary or permanent threshold shifts, although even temporary threshold
shifts may predispose an individual to eventual permanent hearing loss. Noise prevention programs are
paramount in reducing hearing loss as a result of occupational exposures.
Keywords
hearing protection programs, occupational noise exposure, occupational noise-induced hearing loss

INTRODUCTION in the United States are exposed to potentially det-

&&

Hearing loss is the most widespread disability in rimental levels of noise [2 ,7].
Westernized society. Noise exposure is the most The effects of occupational noise exposure place
common preventable cause of hearing loss; some a tremendous burden on both the individual and
estimate that one-third of all cases of hearing loss society. The financial burden to society is significant
can be attributed to noise exposure [1]. Occu- and continues to rise, with an estimated $242.4
pational exposure to noise makes up a great pro- million annual expenditure in compensation for
portion of patients affected by noise-induced work-related hearing loss in the United States
&&

hearing loss (NIHL), making NIHL the most preva- [2 ]. Following military service, workers affected
lent occupational disease in the United States [2 ].
&&
by NIHL make up the most populated disability
Occupational noise exposure has been documented classification. In 2010, the United States Depart-
since at least the 18th century, when it was noted ment of Veterans Affairs compensated more than
that copper miners developed hearing loss as a result 1.4 million veterans for service-connected NIHL and
&&
of the noise from hammering on metal [3 ].

a
SCOPE OF THE PROBLEM Michigan Ear Institute, Farmington Hills and bDepartment of Otolaryng-
ology, Wayne State University, Detroit, Michigan, USA
Worldwide, 1.3 billion people are affected by hear-
Correspondence to Robert S. Hong MD, PhD, Michigan Ear Institute,
ing loss [4]. It is estimated that 10% of the world’s 30055 Northwestern Highway, Suite #101, Farmington Hills, MI 48334,
&&
population are at risk for NIHL [2 ]. Within the USA. Tel: +1 248 865 4444; fax: +1 248 865 6161; e-mail: rhong@
United States, 16–24% of hearing losses can be [Link]
attributed to occupational noise exposures [5,6]. Curr Opin Otolaryngol Head Neck Surg 2014, 22:388–393
In fact, it is estimated that 22–30 million workers DOI:10.1097/MOO.0000000000000079

[Link] Volume 22  Number 5  October 2014

Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
 Noise-induced hearing loss Stucken and Hong

sounds, and communicate with other workers.

KEY POINTS One study of 46 550 workers exposed to noise found
 Occupational NIHL is the most prevalent occupational a statistically significant increase in risk for injury
disease in the United States. requiring hospitalization with each decibel of hear-
ing loss. The hazard ratio for injury was 1.01 for each
 Occupational NIHL can result in psychosocial isolation decibel of hearing loss [10]. Another study evaluated
and an increased risk of dementia in the elderly
1062 workers in a tractor manufacturing plant. In
population, as well as an increased risk of injury, heart
disease, and stroke. this study, workers exposed to sound intensities
more than 85 dBA averaged over 8 h had a 1.52 fold
 The effects of noise on an individual’s hearing threshold increased risk of injury compared with workers
are dependent on a complex interaction between exposed to less than 85 dBA [11]. Undiagnosed hear-
genetic and environmental factors that is unique to
ing loss has been associated with an excess mortality
an individual.
of 10–20% over the course of 20 years [12].
 The most important way to mitigate occupational NIHL NIHL has also been associated with a number of
is through prevention programs that emphasize nonauditory sequelae. The most prevalent of these
exposure reductions and the use of personal hearing are annoyance, cognitive impairment, sleep disturb-
protective devices. &&
ance, and adverse cardiovascular health [2 ]. A
 Antioxidant compounds have shown promise as theory has been proposed that noise exposure leads
preventive and possible therapeutic agents against to stimulation of the autonomic nervous system and
NIHL. endocrine system, leading to increased stress hor-
mone release and elevations in blood pressure and
heart rate. This, in turn, may lead to an increased
risk of hypertension, ischemic heart disease, and
tinnitus, resulting in more than $1.2 billion of stroke [13,14]. Epidemiological studies have dem-
&&
compensation [3 ]. onstrated a higher prevalence of cardiovascular dis-
Workers most at risk for occupational NIHL ease and mortality in populations exposed to high
include those employed in construction, manufac- noise levels [15–21].
turing, mining, agriculture, utilities, transportation,
and the military, as well as musicians. A retrospec-
tive cohort study evaluated audiograms of 1 million PATHOPHYSIOLOGY
employees exposed to loud noise and found the jobs NIHL may be inflicted by short bursts of loud sound
at highest risk for hearing loss were mining, wood
&&
or continuously elevated noise levels [2 ]. Such
product manufacturing, construction of buildings, exposures lead to cochlear hair cell damage, damage
and real estate and rental leasing. Within this group to surrounding supporting cells, and ultimately
of 1 million noise-exposed workers, hearing loss was degeneration of associated auditory nerve fibers.
more prevalent among men than women, and the The level of inner ear damage and associated hearing
risk of hearing loss increased with age [8]. loss are correlated to the intensity and duration of
The consequences of occupational NIHL to the
&&
noise exposure [3 ].
individual can be dire. Hearing loss limits an indi- Sublethal levels of noise damage may lead clin-
vidual’s ability to communicate with the surround- ically to temporary threshold shifts, in which an
ing world, which can lead to increased social stress, individual experiences depressed sensorineural
depression, embarrassment, poor self-esteem, and hearing that usually recovers within 24–48 h. More
relationship difficulties. Obstacles in communi- severe damage leads to a permanent threshold shift,
cation are exacerbated by difficult listening situ- clinically manifested as an irreversible decrease in
ations, such as environments with excessive hearing thresholds. Recent evidence suggests that
background noise. Hearing loss can affect attention even temporary threshold shifts from which an
&&
and cognition [2 ]. In older adults, a mild hearing individual recovers are not innocuous, as such
loss is associated with a two times increased risk of insults may accelerate the process of age-related
dementia, whereas a severe hearing loss is associated hearing loss [22–24].
with a five times increased risk of dementia [9]. The amount of hearing loss inflicted by a speci-
Associated aural fullness and tinnitus can also be fied noise exposure is variable and specific to an
extremely troublesome for some people. individual. Like many disease processes, the patho-
Occupational NIHL has been associated with an physiology of NIHL represents a complex inter-
increased risk for work-related injuries. Excessive action between genetic and environmental
noise hampers the ability to hear warning signals, factors. Some authors have estimated that up to
monitor equipment, respond to environmental 50% of individual variations in hearing loss due

1068-9508 ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins [Link] 389

Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
 Auditory and vestibular science

to noise exposure may be attributed to hereditary reasons for this have not been scientifically born
&&
factors [25]. In addition, other patient-related fac- out [3 ]. Some have hypothesized that a right-
tors such as age, preexisting sensorineural hearing handed machine operator may be more likely to
loss, hypertension, diabetes mellitus, smoking look over their right shoulder, leaving the left ear
history, and use of ototoxic medications may alter turned toward a machine engine. In hunters or
the amount of damage incurred to the inner ear as a others who shoot firearms, hearing loss tends to
result of noise [1]. be more severe in the ear closest to the barrel of
Noise exposure typically affects the hair cells the gun; the opposite ear is relatively protected by
near the basal turn of the cochlea, leading to a the head-shadow effect. Musicians may have dis-
characteristic decrease in hearing thresholds crepancies based on their location within the band
between 3 kHz and 6 kHz. This pattern of hearing or orchestra. Brass players generally produce the
loss will produce a distinctive dip at 4 kHz on pure- greatest amount of noise [26], and musicians seated
tone audiometry, often termed the ‘noise notch’ with one side closer to a noise-producing instru-
(Fig. 1). The natural resonance frequencies of the ment may have greater exposure in that ear.
outer ear, in particular the ear canal, appear to
emphasize the damage to this frequency region.
The lower frequencies, including the main speech PREVENTION PROGRAMS
frequencies, are often spared initially. With pro- At the present time, occupational NIHL is not a
gressive damage, however, the noise notch will reversible disease. It is, however, entirely prevent-
flatten as thresholds decrease at the surrounding able. A focus is placed, therefore, on prevention of
&&
frequencies [3 ]. Individuals with severe hearing NIHL before permanent damage to the inner ear can
loss as a result of noise exposure may have audio- occur. Prevention strategies may be focused on
grams that are indistinguishable from other causes reducing noise levels in an occupational environ-
of hearing loss. ment or on reducing the amount of environmental
Occupational NIHL is typically bilateral and noise that is transmitted to an individual’s inner ear
symmetric. There may be, however, some asymme- system. Many countries have implemented legal
try in hearing loss, particularly if there is differential standards regarding occupational noise exposure
exposure to sound between the two ears. When a and the need for protection above a certain exposure
discrepancy is present, occupational NIHL is com- level. In the United States, occupational noise
monly more severe in the left ear, although the exposure is regulated by the Occupational Safety

Frequency in hertz
125 250 500 1000 2000 4000 8000 16000
–20

–10

10
Hearing level in db (ANSI-69)

20

30

40

50

60

70

80

90

100

110

120

FIGURE 1. Pure-tone audiogram demonstrating the classic ‘noise notch’ at 4 kHz.

390 [Link] Volume 22  Number 5  October 2014

Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
 Noise-induced hearing loss Stucken and Hong

and Health Administration (OSHA, a division of the Table 1. Comparison of Occupational Safety and Health
United States Department of Labor) and the Administration and National Institute for Occupational
National Institute for Occupational Safety and Safety and Health regulations for noise exposure
Health (NIOSH, a division of the United States
Centers for Disease Control and Prevention within Maximum exposure duration
the United States Department of Health and Human Maximum exposure OSHA HCA (1983) NIOSH (1998)
Services). These two governing bodies work together level in dBA regulations recommendations
to develop and enforce workplace safety regulations 85 8h
in the prevention of occupational NIHL. 88 4h
To monitor occupational noise exposures, noise
90 8h 2 h, 31 min
levels must be quantified and expressed as a numeri-
95 4h 47 min, 37 s
cal value that can be subjected to standardized
97 3h 30 min
regulations. For regulatory purposes, noise levels
are generally measured in the dBA scale and 100 2h 15 min
expressed as an 8-h time-weighted average (TWA). 105 1h 4 min, 43 s
The dBA scale is a decibel scale in which the low 110 30 min 1 min, 29 s
frequencies are relatively de-emphasized. This scale 115 15 min or less 28 s
is applied when measuring occupational noise
exposure because high-frequency noise exposures
cause greater threshold shifts than low-frequency as possible through engineering or scheduling
exposures of equivalent intensity [1]. OSHA and changes to decrease noise levels in the workplace
NIOSH have both set forth regulatory guidelines [28]. Mechanisms to reduce noise production and
for acceptable occupational noise exposures and exposure through engineering and administrative
recommendations for hearing conservation pro- controls may provide the most effective means for
grams. OSHA regulations carry the weight of law; reducing workers’ exposure to noise, but often these
however, NIOSH recommendations are more strin- mechanisms are unrealistic or impossible to impose.
gent and are thought to be backed by stronger When the on-the-job environmental noise levels
scientific evidence [27]. Under OSHA criteria, the cannot be brought down to acceptable standards,
maximum 8-h noise exposure is 90 dBA. For noise every employee must be provided with appropriate
above 90 dBA, exposure time must be reduced by personal hearing protective devices and instructed
50% for every 5 dB increase (e.g., maximum allow- on their use. It may be that current regulations,
able exposure time for 95 dBA noise is 4 h, etc). This which are based upon recovery of pure-tone
is referred to as the 5-dB trading rule or 5-dB thresholds following noise exposure, will, in the
exchange rate. In contrast, NIOSH recommen- future, need to take into account the recently
dations are calculated using a 3-dB exchange rate, reported findings that even recovery of thresholds
in which exposure time must be halved for every following temporary threshold shifts does not truly
3 dB elevation in noise levels. In addition, NIOSH indicate an undamaged ear [22–24].
sets the recommended 8-h TWA exposure at 85 dBA Personal hearing protective devices include
rather than 90 dBA [27]. These changes lead to con- both earmuffs and earplugs. Expandable foam plugs
siderably more protective regulations for workers, as provide similar noise attenuation to earmuffs,
is demonstrated in Table 1. although other types of earplugs provide less pro-
OSHA mandates that a hearing conservation tection. Advertised attenuation levels of hearing
program be provided for workers who are exposed protective devices range from 15 to 28 dB when
to noise more than 85 dB over an 8-h TWA. This tested in a laboratory setting. In real workplace
hearing conservation program must include the conditions, most earmuffs and expandable foam
following elements: first, employers must measure plugs will provide 10–15 dB attenuation. The use
noise levels on the premises; second, free hearing of earmuffs and plugs together improves attenu-
protective devices must be provided if noise exceeds ation by 5–10 dB over either device alone. A pro-
exposure limits; third, employees must be trained tective effect of 10–15 dB is relevant to a noise-
regarding noise exposure and the use of personal exposed worker, as 10 dB of attenuation will bring
hearing protective devices; fourth, employees must noise levels into the acceptable range in more than
be provided with baseline and annual audiograms to 90% of exposed workers [27]. Data have shown that
assess their hearing; and fifth, records of all test earplugs may not provide the advertised level of
results must be kept and made available to employ- protection if employees are not instructed on their
ees [27]. With regard to noise regulation, noise proper use [1]. The most important variable in pre-
sources or the environment must be altered as much venting occupational NIHL with personal hearing

1068-9508 ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins [Link] 391

Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
 Auditory and vestibular science

protective devices is consistent use of the device. did demonstrate that N-acetyl cysteine significantly
Data suggest that personal hearing protective devi- reduced the incidence of temporary threshold
&
ces are effective in preventing NIHL [29 ,30–32]; shift [45]. Interestingly, variability in response to
however, studies have demonstrated that many this compound was associated with genetic poly-
workers do not regularly use these devices [33–37]. morphisms. Those workers with the glutathione S-
Nonuse of hearing protective devices tends to be transferases null genotype demonstrated increased
more prevalent in certain occupations, particularly responses to the treatment compound.
among agricultural workers [38]. Musicians represent Another compound, D-methionine, may soon
another class of workers many of whom do not undergo clinical trials with the United States Army
regularly use hearing protective devices [26]. for its use as an otoprotective agent [26]. D-meth-
Studies evaluating the success of hearing pro- ionine is an ingredient of yogurt and cheese that has
tection programs have demonstrated conflicting shown a protective effect against NIHL in animal
results. A Cochrane Review of 15 studies including studies [46,47]. This agent was effective even when
79 986 participants found that the regular use of administered after the noise exposure. Each of these
personal hearing protective devices as part of a compounds has shown promise in preventing or
strong hearing loss prevention program was associ- reversing the effects of NIHL, and hopefully in the
&
ated with less hearing loss [29 ]. Other studies have future will add to the armamentarium of protective
demonstrated significant continued hearing loss tools against occupational NIHL.
even in the presence of a hearing loss prevention
program. Groenewold et al. [39] studied audiometric
CONCLUSION
data from 19 911 workers who were exposed to
significant noise, stratified into groups on the basis Occupational NIHL is the most prevalent occu-
of survey responses into those workers who never pational disease in the United States. The burden
used hearing protection and those who always used of disease is felt both by the affected individual and
hearing protection. Data did not show any signifi- by society. Treatment strategies are in the develop-
cant difference in OSHA threshold shifts between mental stages; before they become universally avail-
the two groups, although there was a significant able, the mainstay of care is in prevention.
trend toward increased risk for high frequency Prevention programs to reduce occupational NIHL
threshold shift without use of protective devices. can be effective, but they require compliance with
OSHA and NIOSH standards and consistent use of
personal hearing protective devices.
FUTURE DIRECTIONS
Research into the underlying disease processes has Acknowledgements
produced some headway in achieving preventive Special thanks to Christopher Turner for helpful com-
and therapeutic treatments for occupational NIHL. ments on this manuscript.
Several authors have theorized that oxidative stress This work has not been published previously in any form,
plays a role in the pathogenesis of NIHL on a micro- and is not under consideration for publication elsewhere.
cellular level [40,41]. Accordingly, several antioxi-
dant compounds have been explored for their Conflicts of interest
protective properties. In a study looking at the treat- The authors have no conflicts of interest or disclosures to
ment effect of the antioxidant compound magnes- report. No grant funding or support has been received in
ium after impulse noise, magnesium-treated guinea producing this manuscript.
pigs had improved hair cell preservation compared
with groups treated with methylprednisolone and
with placebo [42]. REFERENCES AND RECOMMENDED
The antioxidant precursor of glutathione, READING
Papers of particular interest, published within the annual period of review, have
N-acetyl-L-cysteine, has been shown to have protec- been highlighted as:
& of special interest
tive effects against noise exposure in chinchilla && of outstanding interest

studies [43]. Human studies on such compounds

are preliminary and have had conflicting results. 1. National Institutes of Health. Consensus Development Conference State-
ment: Noise and Hearing Loss. Bethesda, MD; U.S. Department of Health &
One trial in which 31 normal-hearing participants Human Services; 1990.
were treated with N-acetyl cysteine as a protective 2. Basner M, Babisch W, Davis A, et al. Auditory and nonauditory effects of noise
on health. Lancet 2014; 383:1325–1332.
mechanism against nightclub music exposure &&

A detailed discussion of the effects of NIHL and their implications for public health.
did not demonstrate a protective effect [44]. A 3. Hong O, Kerr M, Poling G, Dhar S. Understanding and preventing noise-
induced hearing loss. Dis Mon 2013; 59:110–118.
double-blind, placebo-controlled crossover study, &&

An excellent review of the mechanisms and effects of NIHL, as well as prevention

however, performed on 53 noise-exposed workers programs.

392 [Link] Volume 22  Number 5  October 2014

Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
 Noise-induced hearing loss Stucken and Hong

4. Vos T, Flaxman AD, Naghavi M, et al. Years lived with disability (YLDs) for 26. Sliwinska-Kowalska M, Davis A. Noise-induced hearing loss. Noise Health
1160 sequelae of 289 diseases and injuries 1990-2010:a systematic ana- 2012; 14:274–280.
lysis for the Global Burden of Disease Study 2010. Lancet 2012; 380:2163– 27. Gelfand, SA. The effects of noise and industrial audiology. In: Essentials of
2196. Audiology, New York: Thieme, 2001. 33; 501-541.
5. Nelson DI, Nelson RY, Concha-Barrientos M, Fingerhut M. The global burden 28. U.S. Department of Labor (USDL), Occupational Safety and Health Admin-
of occupational noise-induced hearing loss. Am J Ind Med 2005; 48:446– istration (OSHA). Occupational noise exposure: hearing conservation amend-
458. ment; final rule. Fed Regist 1983; 48:9738-85.
6. Tak S, Calvert GM. Hearing difficulty attributable to employment by industry 29. Verbeek JH, Kateman E, Morata TC, et al. Interventions to prevent occupa-
and occupation: An analysis of the National Health Interview Survey – United & tional noise-induced hearing loss. Cochrane Database Syst Rev 2012;
States, 1997 to 2003. J Occup Environ Med 2008; 50:46–56. 10:CD006396.
7. National Institute for Occupational Safety and Health (NIOSH). National A thorough evidence-based review of the efficacy and utility of prevention pro-
Occupational Research Agenda. Cincinnati, OH: National Institute of Occu- grams for occupational hearing loss.
pational Safety and Health Publications 1996. 96-115. 30. Hong O. Hearing loss among operating engineers in American construction
8. Masterson EA, Tak S, Themann CL, et al. Prevalence of hearing loss in the industry. Int Arch Occup Environ Health 2005; 78:565–574.
United States by industry. Am J Ind Med 2013; 56:670–681. 31. Brink LI, Talbott EO, Burks JA, Palmer CV. Changes over time in audiometric
9. Lin FR. Hearing loss in older adults: who’s listening? JAMA 2012; thresholds in a group of automobile stamping and assembly workers with a
307:1147–1148. hearing conservation program. Am Ind Hyg Assoc J 2002; 63:482–487.
10. Girard SA, Leroux T, Courteau M, et al. Occupational noise exposure and 32. Hessel PA. Hearing loss among construction workers in Edmonton, Alberta,
noise-induced hearing loss are associated with work-related injuries leading Canada. J Occup Environ Med 2000; 42:57–63.
to admission to hospital. Inj Prev 2014. [Epub ahead of print] 33. Neitzel R, Seixas N. The effectiveness of hearing protection among construc-
11. Amjad-Sardrudi H, Dormohammadi A, Golmohammadi R, Poorolajal J. Effect tion workers. J Occup Environ Hyg 2005; 2:227–238.
of noise exposure on occupational injuries: a cross-sectional study. J Res 34. Hong O, Ronis DL, Lusk SL, Kee GS. Efficacy of a computer-based hearing
Health Sci 2012; 12:101–104. test and tailored hearing protection intervention. Int J Behav Med 2006;
12. Karpa MJ, Gopinath B, Beath K, et al. Associations between hearing impair- 13:304–314.
ment and mortality risk in older persons: the Blue Mountains Hearing Study. 35. Kerr MJ, Savik K, Monsen KA, Lusk SL. Effectiveness of computer-based
Ann Epidemiol 2010; 20:452–459. tailoring versus targeting to promote use of hearing protection. Can J Nurs
13. Babisch W. Cardiovascular effects of noise. In: Nriagu Jo, editor. Encyclo- Res 2007; 39:80–97.
pedia of environmental health. Burlington: Elsevier; 2011. pp. 532–542. 36. McCullagh M, Lusk SL, Ronis DL. Factors influencing use of hearing protec-
14. Lusk S, Gillespie B, Hagerty BM, Ziemba RA. Acute effects of noise on blood tion among farmers: a test of the pender health promotion model. Nurs Res
pressure and heart rate. Arch Environ Health 2004; 59:392–399. 2002; 51:33–39.
15. Van Kempen EE, Kruize H, Boshuizen HC, et al. The association between 37. Hong O, Chin DL, Ronis DL. Predictors of hearing protection behavior among
noise exposure and blood pressure in ischemic heart disease: a meta- firefighters in the United States. Int J Behav Med 2013; 20:121–130.
analysis. Environ Health Perspect 2002; 110:307–317. 38. Depczynski J, Challinor K, Fragar L. Changes in the hearing status and noise
16. Tomei G, Fioravanti M, Cerratti D, et al. Occupational exposure to noise and injury prevention practices of Australian farmers from 1994 to 2008.
the cardiovascular system: a meta-analysis. Sci Total Environ 2010; J Agromedicine 2011; 16:127–142.
408:681–689. 39. Groenewold MR, Masterson EA, Themann CL, Davis RR. Do hearing pro-
17. Davies H, van Kamp IV. Noise and cardiovascular disease: a review of the tectors protect hearing? Am J Ind Med 2014. [Epub ahead of print]
literature. Noise Health 2012; 14:287–291. 40. Le Prell CG, Dolan DF, Bennett DC, Boxer PA. Nutrient plasma levels
18. Huss A, Spoerri A, Egger M, Roosli M; Swiss National Cohort Study Group. achieved during treatment that reduces noise-induced hearing loss. Transl
Aircraft noise, air pollution, and mortality from myocardial infarction. Epide- Res 2011; 158:54–70.
miology 2010; 21:829–836. 41. Le Prell CG, Spankovich C. Healthy diets and dietary supplements: recent
19. Sorensen M, Hvidberg M, Andersen ZJ, et al. Road traffic noise and stroke: a changes in how we might think about hearing conservation. In: Griefahn B, ed.
prospective cohort study. Eur Heart J 2011; 32:737–744. 10th International Congress on Noise as a Public Health Problem of the
20. Gan WQ, Davies HW, Koehoorn M, Brauer M. Association of long-term International Commission on Biological Effects of Noise, London, UK, 2011.
exposure to community noise and traffic-related air pollution with coronary [Link] [Accessed 25 April 2014].
heart disease mortality. Am J Epidemiol 2012; 175:898–906. 42. Abaamrane L, Raffin F, Gal M, et al. Long-term administration of magnesium
21. Sorensen M, Andersen ZJ, Nordsborg RB, et al. Road traffic noise and incident after acoustic trauma caused by gunshot noise in guinea pigs. Hear Res
myocardial infarction: a prospective cohort study. PLoS One 2012; 7:e39283. 2009; 247:137–145.
22. Kujawa SG, Liberman MC. Acceleration of age-related hearing loss by early 43. Kopke RD, Jackson RL, Coleman JK, et al. NAC for noise: from the bench top
noise exposure: evidence of a misspent youth. J Neurosci 2006; 26:2115– to the clinic. Hear Res 2007; 226:114–125.
2123. 44. Kramer S, Dreisbach L, Lockwood J, et al. Efficacy of the antioxidant N-
23. Campo P, Venet T, Rumeau C, et al. Impact of noise or styrene exposure on acetylcysteine (NAC) in protecting ears exposed to loud music. J Am Acad
the kinetics of presbycusis. Hear Res 2011; 280:122–132. Audiol 2006; 17:265–278.
24. Kujawa SG, Liberman MC. Adding insult to injury: cochlear nerve degenera- 45. Lin CY, Wu JL, Shih TS, et al. N-acetylcysteine against noise-induced
tion after ‘‘temporar’’ noise-induced hearing loss. J Neurosci 2009; temporary threshold shift in male workers. Hear Res 2010; 269:42–47.
29:14077–14085. 46. Samson J, Wiktorek-Smagur A, Politanski P, et al. Noise-induced time-
25. Sliwinska-Kowalska M. Contribution of genetic factors to noise-induced dependent changes in oxidative stress in the mouse cochlea and attenuation
hearing loss. In: Griefahn B, ed. 10th international congress on noise as a by D-methionine. Neuroscience 2008; 152:146–150.
public health problem of the international commission on biological effects of 47. Campbell K, Claussen A, Meech R, et al. D-methionine (D-met) significantly
noise, London, UK, 2011. [Link] [Accessed rescues noise-induced hearing loss: timing studies. Hear Res 2011;
25 April 2014]. 282:138–144.

1068-9508 ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins [Link] 393

Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.