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Perfect hearing is crucial to the practice of various professions, such as instrument makers, musicians, sound engineers, and other professions not related to music, such as sonar technicians. For people of these occupational groups, we propose the term "professional ear user" (PEU) in analogy to "professional voice user". PEUs have special requirements for their hearing health, as they have well-known above-average auditory perceptual abilities on which they are professionally dependent.The purpose of this narrative review is to summarize selected aspects of the prevention, diagnosis, and treatment of ear disorders in PEUs.Prevention of hearing disorders and other ear diseases includes protection from excessive sound levels, avoidance of ototoxins and nicotine, and a safe manner of cleaning the outer auditory canal. Diagnosing hearing disorders in PEUs can be challenging, since subclinical but relevant changes in hearing cannot be reliably objectified by conventional audiometric methods. Moreover, the fact that a PEU is affected by an ear disease may influence treatment decisions. Further, physicians must be vigilant for non-organic ear diseases in PEUs. Lastly, measures to promote comprehensive ear health in PEUs as part of an educational program and to maintain ear health by means of a specialized otolaryngology service are discussed. In contrast to existing concepts, we lay the attention on the entirety of occupational groups that are specifically dependent on their ear health in a professional setting. In this context, we suggest avoiding a sole focus on hearing disorders and their prevention, but rather encourage the maintenance of a comprehensive ear health.HINTERGRUND: Ein vollständig intaktes Hörvermögen ist zentral für die Ausübung verschiedener Berufe wie Instrumentenbaumeister, Musiker, Tonmeister sowie für weitere Berufsgruppen ohne Bezug zu Musik wie beispielsweise Sonar-Techniker. Für Personen all dieser Berufsgruppen schlagen wir in Analogie zum „Professional Voice User“ den Begriff „Professional Ear User“ (PEU) vor. PEU haben spezielle Anforderungen an ihre Ohrgesundheit, da sie über eine überdurchschnittliche auditive Wahrnehmungsfähigkeit verfügen, von der sie beruflich abhängig sind.Die vorliegende narrative Übersichtsarbeit hat zum Ziel, die sich daraus ergebenden speziellen Aspekte der Prävention, Diagnostik und Therapie von Ohrerkrankungen bei PEU zusammenzufassen.Die Prävention von Hörstörungen und weiteren Ohrerkrankungen umfasst den Schutz vor zu hohen Schallpegeln, die Vermeidung von Ototoxinen oder Nikotin sowie die korrekte Durchführung einer Gehörgangsreinigung. Die Abklärung von Hörstörungen kann sich bei PEU herausfordernd gestalten, da subklinische, jedoch einschränkende Veränderungen des Hörvermögens mit konventionellen audiometrischen Methoden nicht zuverlässig objektiviert werden können. Schließlich kann das Vorliegen einer Ohrerkrankung bei einem PEU Therapieentscheidungen beeinflussen. Weiter muss bei PEU auch eine hohe Wachsamkeit bezüglich nichtorganischer Ohrerkrankungen bestehen. Abschließend werden Möglichkeiten diskutiert, um bei PEU eine umfassende Ohrgesundheit im Rahmen eines edukativen Programms zu fördern und mittels einer spezialisierten ohrenärztlichen Sprechstunde zu erhalten. Im Gegensatz zu bestehenden Konzepten ist der Fokus dabei auf die Gesamtheit der Berufsgruppen gerichtet, welche in professionellem Rahmen speziell von der Ohrgesundheit abhängig sind. Außerdem soll der Schwerpunkt hierbei nicht nur auf Hörstörungen und deren Prävention, sondern auch auf der Erhaltung einer ganzheitlichen Ohrgesundheit liegen.

Hearing loss is frequently induced by occupational noise exposure and leads to rising hearing thresholds as well as reduced otoacoustic emissions (OAE), mostly caused by metabolic hair cell decompensation.Primary endpoint is the increase in average pure tone thresholds after noise exposure, secondary endpoints are loss of distortion product and click-evoked OAE as well as reduction of their contralateral suppression.The present study design describes the verification of the anti-oxidant and neuroprotective properties of EGb 761® by evaluation of cochlear protection from noise impact as well as its safety and tolerance in 202 healthy male participants distributed equally to verum and placebo groups in a double-blind manner. Participants were assessed, medicated, exposed to noise, and then examined at timepoints up to 10 min and 4 weeks thereafter.This summary of the verification study protocol highlights the complexity of diligent and precise planning according to the European Medicines Agency criteria for controlled trials (EudraCT). Key points are the intervention rationale, definitions of in- and exclusion criteria, estimation of subject numbers, and examination method setting in terms of optimum endpoint description.

Due to demographic change and altered recreational behavior, a rapid increase in hearing deficits is expected in the next 20-30 years. Consequently, the risk of age-related loss of speech discrimination, tinnitus, hyperacusis, or-as recently shown-dementia, will also increase. There are increasing indications that the loss of specific hearing fibers in humans and animals is involved in various hearing disorders. This fiber loss can be caused by cochlear synaptopathy or deafferentation and does not necessarily lead to clinically measurable threshold changes. Animal experiments have shown that reduced auditory nerve activity due to acoustic trauma or aging can be centrally compensated by disproportionately elevated and faster auditory brainstem responses (ABR). The analysis of the suprathreshold amplitudes of auditory evoked brain stem potentials and their latency in combination with non-invasive imaging techniques such as magnetic resonance imaging can help to identify the central compensatory ability of subjects and to assign defined hearing deficits.

New research in animal models indicates that even at lower intensities, noise exposure can induce defects in the synapses of the auditory pathway. However, only very high levels of noise exposure lead to mechanical hair cell damage with lesions of the inner ear and measurable hearing loss (audiogram; distortion product otoacoustic emissions, DPOAE). This paper revises the literature, starting with a case study.A 41-year-old patient suffered from hearing loss and tinnitus in the right ear following a car accident with airbag deployment. Hearing loss recovered partially, tinnitus and difficulties in speech discrimination persisted. Audiometry showed typical high-frequency hearing loss (40 dB) and tonal tinnitus (8 kHz). Although DPOAE and ABR potentials (auditory brainstem response, wave III and V) were completely normal 6 months after the accident, there was no detectable cochlear action potential (CAP) in electrocochleography (ECochG).These findings indicate recovery of initial hair cell damage, whereas synaptic transformation remains reduced and slight hearing loss and poor speech perception in complex listening situations persist. This phenomenon has been described as "hidden hearing loss" in newer literature. Although similar retrocochlear lesions in the auditory pathway could be detected in animal models, valid data in humans are currently lacking because no adequate diagnostic methods are available.Noise trauma initially results in hair cell damage. After recovery, hearing loss may persist, which can be due to synaptic lesions in the first neuron. An adequate testbattery has to be developped.

A noise trauma induces central nervous system pathologies, which generate deficits in hearing and perception of sound.Are degenerative mechanisms in the central auditory system a direct impact of overstimulation or an effect of acoustic deprivation?Detection of cell death in a mouse model of noise-induced hearing loss at different times after single or repeated noise exposure.A single noise exposure (3 h, 115 dB SPL, 5-20 kHz) induces acute (≤1 day) and long-term (observation period 14 days) degeneration, particularly in subcortical structures. Repeated noise trauma is followed by pathologies in the auditory thalamus and cortex.Noise has a direct impact on basal structures of the central auditory system; a protection of cortical areas is possibly due to inhibitory neuronal projections. Degenerative mechanisms in higher structures of the pre-damaged system point to an increased impairment of complex processing of acoustic information.

Noise is an important socioeconomic problem in industrialized countries. Development of efficient treatment options for the audiological phenomena resulting from noise-induced hearing loss requires in-depth understanding of the underlying damage mechanisms causing peripheral and central nervous changes. Mechanical damage, ischemia and excitotoxicity are mainly responsible for noise-induced cell death and biophysical changes in the cochlea. Auditory synaptopathy is an additional consequence. Besides these cochlear pathologies, noise exposure leads to extensive changes within the central auditory pathway. Overstimulation causes early cell loss in the ventral cochlear nucleus just after noise exposure, which is in accordance with enhancement of apoptotic mechanisms within the corresponding timeframe. In contrast to the cell loss in lower auditory structures due to overstimulation, the later significant reduction of cell density in higher auditory structures is due to sensory deprivation. Changes in network homeostasis seem to partially compensate structural losses by modulation of spontaneous activity. However, central nervous processing of auditory information is permanently impaired by the neuroplastic changes. Unfortunately, the various noise-induced peripheral and central pathologies are difficult to treat. New therapeutic approaches are required, particularly for treatment of central nervous processing disorders and auditory synaptopathy, which contribute to audiological phenomena such as tinnitus, hyperacusis and poor speech perception in noise.

High-intensity noise exposure from impulse and blast noise events often leads to acute hearing loss and may cause irreversible permanent hearing loss as a long-term consequence. Here, a treatment regime was developed to limit permanent damage based on a preclinical animal model of acute noise trauma. To develop clinical trials for the treatment of acute noise traumas using approved drugs. The otoprotective potential of glucocorticoids applied locally to the inner ear was examined. A series of experiments with different impulse noise exposures were performed. Permanent hearing loss and hair cell density were assessed 14 days after exposure. Hearing and hair cell preservation were investigated as a function of the glucocorticoid dose. After impulse noise exposure, local application to the round window of the cochlea of high-dose prednisolone (25 mg/ml) or methylprednisolone (12.5 mg/ml) resulted in a statistically significant reduction in hearing loss compared with the control group. The local application of high doses of the drugs to the round window of the cochlea appears to be an effective treatment for acute noise trauma.

High-intensity noise exposure from impulse and blast noise events often leads to acute hearing loss and may cause irreversible permanent hearing loss as a long-term consequence. Here, a treatment regime was developed to limit permanent damage based on a preclinical animal model of acute noise trauma.To develop clinical trials for the treatment of acute noise traumas using approved drugs. The otoprotective potential of glucocorticoids applied locally to the inner ear was examined.A series of experiments with different impulse noise exposures was performed. Permanent hearing loss and hair cell density were assessed 14 days after exposure. Hearing and hair cell preservation were investigated as a function of glucocorticoid dose.After impulse noise exposure, local application of high-dose prednisolone (25 mg/ml) or methylprednisolone (12.5 mg/ml) to the round window of the cochlea resulted in a statistically significant reduction in hearing loss compared to the control group.Local application of high doses of the drugs to the round window of the cochlea appears to be an effective treatment for acute noise trauma.

In recent decades, acoustic shock and explosion traumas have increased in frequency in the general population. Beside the use of fireworks and firearms, airbag ignitions and explosions caused by terror or suicidal acts are also relevant. Depending on duration and strength of the sound pressure affecting the human ear, isolated inner ear damage or additional ear drum perforation and interruption of the middle ear ossicle chain can result. By means of otoscopy, pure tone audiometry, measurement of otoacoustic emissions, and other neurootological examinations, the severity of the trauma can be determined. With prompt and adequate therapy, permanent hearing loss can be minimized. In particular, the measurement of otoacoustic emissions allows conclusions to be made on the functionality of the outer hair cells which are damaged first in most cases. Histological investigations on noise-exposed cochleas show extensive damage to the outer hair cells in the frequency range between 1.0 and 4.0 kHz, which correlates well with audiometric measurements.

The ENT physician and specialist in musician's medicine is consistently confronted with the issue of hearing protection, since musicians exposed to high sound levels due to their profession, and who are often concerned about their hearing, refer to him. Furthermore, this topic has gained more relevance since a noise exposure limit for professional musicians was issued in February 2008 by the EC guidelines for occupational health and safety regarding "Noise" (2003/10/EC). The present article gives an outline of the recent state of knowledge about sound pressure levels, hearing risks, as well as the use of hearing protection for musicians.

During an orchestral performance musicians are exposed to high noise levels, which may exceed the intensity which could evoke hearing impairment after many years of exposure. From experience the degree of hearing loss in musicians is in general less than would be expected from the levels of exposure. The likelihood that an orchestral musician would develop a noise-induced hearing loss is much lower than for an industrial worker in a noise-intense factory. On the other hand it has to be considered that it is imperative for musicians to have non-impaired hearing to practise their profession. In some cases a sudden onset of hearing loss is traced to the noise stress of a loud performance. In such cases, the high noise levels predominantly produced by brass instruments or drums were assumed to be the cause. This publication presents five cases of expert opinions, where previous expert opinions had assumed noise or a blast trauma as the cause for the hearing loss. By careful analysis, a noise or a blast trauma was not regarded as probable in any of the cases. Interestingly, three of the five musicians had a normal contralateral hearing. In one case normal bilateral hearing was observed without the typical c(5) notch although the musician had been subject to noise stress in an orchestra for years.

The bulletin for occupational disease no. 2301 in the annex of the Occupational Disease Act, noise-induced hearing impairment, ("Merkblatt zu der Berufskrankheit Nr. 2301 der Anlage zur Berufskrankheiten-Verordnung: Lärmschwerhörigkeit") states that sound events with an intensity exceeding 137 dB (C) may cause immediate mechanical damage to the inner ear. Up to now a distinction has been made between prevention and actual damage potential for the risks caused by sounds with extremely high peak levels. In the field of prevention the unweighted sound pressure peak level of 140 dB, which is now 137 dB(C,peak) according to the LärmVibrationsArbSchV, was applied as the trigger threshold for measures; in contrast actual hearing impairment was not found until 150-160 dB. This article compiles the current state of knowledge and demonstrates that in the area of the reasons mentioned here for acute hearing impairment, no scientifically based new findings exist especially with reference to publications listed in the bulletin.

The effect of an incorrect audiological medical assessment of noise trauma deafness can be substantial. The impact will be demonstrated using a case example. The reasons for incorrect assessment are often insufficient examination conditions or simulation and aggression of the subject. The results of a study on this topic will be presented.A total of 61 patients who underwent a psycho-acoustic medical assessment were grouped into 1 of 4 categories ranging from category 0 for no simulation or aggravation to category III for severe simulation and aggravation. For category III reliable and valid thresholds of pure tone audiometry can only be achieved using objective audiological measurements. The frequency, extent and socio-economic factors were evaluated.Of the 61 individuals 26 showed no simulation or aggravation behavior (category 0), 10% were grouped into category III and 48% into categories I and II. The tendency to simulation and aggravation increased with the patients' age, the level of education and the frequency of medical examinations prior to this investigation.Simulation and aggravation is a more frequent phenomenon than previously assumed (approximately 58% of all audiological examinations). The effect in terms of economical damage could be substantial. The usage of a well-defined classification is highly recommended in order to improve the quality of medical assessment in ENT.

We present the case of a 43-year-old patient with sensorineural hearing loss and the finding of an aberrant internal carotid artery in the left tympanic cavity that was causing pulsatile tinnitus. The aberrant vessel was initially invisible on magnetic resonance imaging (MRI) and was confirmed by high-resolution computed tomography and MR angiography (MRA). Recognition of an aberrant course of an internal carotid artery often requires a combination of MRI and MRA to establish the diagnosis and rule out other differential diagnoses.

In the past hearing aid fitting frequently turned out to be a problem in patients with noise-induced hearing loss. Selective amplification in the high frequency range and at the same time natural sound and appropriate wearing comfort (open fitting) could not be achieved in numerous cases. Today these problems can be tackled by modern hearing aid technology providing us with efficient feedback suppression algorithms making open fittings possible for many more patients. This development is particularly beneficial for patients with noise-induced hearing loss. Unfortunately, open fitting is in opposition to wearing hearing aids at noisy workplaces. Tight fittings, however, can be used at work if a special listening program for noisy conditions is available. This dilemma is discussed and possible solutions are pointed out.

The DPOAE-threshold, estimated from extrapolated I/O functions, allows an objective assessment of the mechanical sensitivity of the inner ear. In children, the specificity of this diagnostic tool is impaired by conductive hearing loss.In this study, we propose an individual optimization of the primary tone level ratio. This procedure allows the detection of a conductive hearing loss that can be accounted for when estimating the DPOAE-threshold. By means of a simulation using DPOAE-data from 22 normally hearing subjects, the effects of this procedure on the estimation of the DPOAE-threshold are examined.An individually optimized DPOAE stimulation distinctly improves the signal-to-noise ratio of the DPOAE which enables an estimation of the DPOAE-threshold for sound conductive losses up to 15 dB. The DPOAE-threshold only worsens in individual cases.An individually optimized stimulation paradigm may improve the specificity of inner ear diagnostics with the DPOAE-threshold. A clinical evaluation of the method in children, however, is necessary.

An investigation was made to reveal whether suspicion of occupational hearing loss can be satisfactorily determined by an otolaryngologist or workplace audiological measurement. These were compared with a formal audiometrical assessment at a university clinic.A retrospective study was made of 95 cases of noise induced hearing loss. A total of 78 individuals were investigated by an otolaryngologist and 70 by workplace audiometry. Using workplace audiometry, 27% of the tests showed a reduction in working capacity of at least 20%. In only five of these was a specialist opinion sought within a year. In 50%, this took longer than 5 years. A comparison of audiometric data from expert opinion revealed that there was conformity in only 47% with workplace audiometry and 48% with otolaryngologist testing. In some cases (27% workplace and 33% ENT practice), the measured hearing loss and calculation of disability exceeded that determined by the experts.The results of workplace audiometry demonstrated that hearing loss was frequently reported only after the workers had received a disability of at least 20%. Possible reasons for discrepancies in audiological testing might be the exaggeration of hearing loss by the worker, insufficient recovery time after noise exposure, or inexperienced audiologists. Our data show that audiometric testing in workplace audiometry, as well as in ENT practice, often reveal a higher disability rating compared to formal audiological (university) assessment, even if these discrepancies do not reach statistical significance.

The initial and permanent effects of leisure noise (toy pistols, rock music) compared to broadband noise were examined in 68 guinea pigs. Auditory threshold shifts at 1.5, 2, 3, 4, 6, 8, 12 und 16 kHz were registered before and immediately after exposure as well as on days 1, 2, 3, 5,7 and 21 post-exposure using the auditory brain stem response (ABR) technique. In order to examine cilia and hair cell damage in eight cochlear frequency regions (0,4 kHz, 0,4-0,8 kHz, 0,8-1.5 kHz, 1.5-3 kHz, 3-5 kHz, 5-11.5 kHz, 11.5-26 kHz und26 kHz), cytocochleograms were performed immediately after exposure and on days 1, 7 and 21.Frequency dependent functional or morphological damage was found which depended on the type of trauma tested. All results were highly significant ( P0.001). The results show that partial recovery of hearing occurred within 3 days of acute acoustic trauma induced by toy pistols and within 1 day after exposure to rock music or broadband noise. There was no further recovery of hearing within the following 18 and 20 days, respectively. Furthermore, permanent threshold shifts after exposure to rock music or broadband noise were not associated with cilia and/or hair cell damage.

Information campaigns are regarded useful to prevent adolescents from hearing-damage due to loud music. This study examined whether adolescents who are informed on the risk of a hearing-damage, exhibit preventive behavior when attending discotheques.253 pupils (age 14 to 19 years) were interviewed about their disco attending habits and about their information on the risk associated with listening to loud music.About 85% of the sample were informed about the risk. Informed and uninformed pupils did not significantly differ in the frequency of disco attendance nor in the frequency of using ear-plugs. However, significantly more informed pupils experienced disco music as too loud (p0.05).Information influences the subjective appraisal of loudness perception, but has little effect on preventive behavior. Instead, experimental forms of educational campaigns may be more effective. Additional provisions (lowering sound levels in discotheques) are necessary.

Rupture of the round window membrane as a special cause of inner ear deafness is widely accepted after changing pressure levels, e.g. in diving. However, even without a barotrauma before, the spontaneous rupture of the round window membrane is suspected occasionally in patients with sudden hearing loss and/or vertigo and tinnitus. To carry through the tympanotomy is decided by ENT surgeons often in cases of progressive hearing loss despite infusion therapy. Perilymph fistulas have been detected relatively seldom, compared to the number of reported operations by several authors. However, covering the round niche with connective tissue leads to the improvement of symptoms sometimes even in cases without microscopical evidence of fistula. Within the last 3 years 14 patients suffering sudden hearing loss of one ear underwent tympanotomy in our department. Of these patients 8 reached restitution of the hearing ability. Especially 2 patients with sudden deafness caused by spontaneous rupture of the round window membrane are reported in the following article. Perilymph fistulas were detected in these cases by IV-application of fluorescein and fluorescence endoscopy of the middle ear. Both patients obtained a normal hearing curve within 1 week after surgical intervention and obliteration of the round niche.

Explosive amusement and deterrent articles such as New Year's Eve cannons and rockets, toy pistols, and blank guns are not at all harmless items. Their potential dangerousness is often extremely underestimated. Two damaging mechanisms are important: during explosions, high pressures and temperatures develop and a considerable sound pressure level can be measured. If the explosion happens near the human body (intentionally or inadvertently), not only superficial lesions can occur, but also (mainly due to contact shots) serious, deep-seated tissue damage, especially in the head and neck region with its endangered sense organs such as eye and ear, the vessels and nerves supplying the brain, the speech- and voice-forming apparatus, and in particular the face, can be the consequence. Their mutilation can lead to serious and extensive interpersonalchanges. Accidents are published in the relevant otological and forensic medical papers, but nevertheless it seems important to us to point out the dangerousness of these readily available items.

Proof of cochlear hearing loss is an essential prerequisite for the diagnosis of noise deafness. For this purpose, the Königsteiner instruction leaflet (Königsteiner Merkblatt) recommends among other items the SISI test.The results of the SISI test at 1 and 4 kHz were analysed for 100 expert opinions of noise (200 ears).10% of the subjects showed at 1 and 4 kHz a positive and 44% a negative result. At 1 kHz, 46% indicated a negative result and at 4 kHz a positive result. In the group with a negative SISI test at both frequencies, 74% demonstrated characteristics of pseudohypacusis. There was no correlation between a retrocochlear hearing disorder and a negative SISI test.Our analysis demonstrated that the negative SISI test is more often evidence of pseudohypacusis rather than a retrocochlear disorder. Consequently, the validity of a negative SISI test is limited.

Airbag inflation is associated with a loud noise. This very short noise has a peak amplitude of 170 dB sound pressure level and can make otologic injuries. We report a case of acoustic trauma after airbag inflation. The 24-year-old man has hearing loss both side in the 3000- to 6000-Hz range and in the deep-frequency. The possibility of acoustic trauma from airbag noise are probably much more common and need more attention in the clinic.

Air bags are among the latest developments in extensive automobile safety systems. They successfully have saved the lives of car occupants in road accidents. Many additional injuries caused by air bags from minor to severe have been reported. With the help of two acceleration sensors, the electronic tuner amplifier records the vehicle's deceleration. This is the adequate trigger for air bag deployment, which creates an intense noise of up to 170 dB sound pressure level. This noise level can cause cochlear damage. We present two patients with otologic symptoms after spontaneous air bag deployment.

Sound overexposure is known to cause damage to cochlear structures and can induce permanent or temporary hearing loss and tinnitus. Perhaps the most sensitive of these structures to sound overexposure are the tip links. In this paper the electrophysiological effects of pharmacological destruction of the tip links of outer hair cells was investigated. Outer hair cells treated with elastase (20 U/mL) or BAPTA (5 mM) no longer responded to sinusoidal stimuli. In contrast to common belief, transduction channels opened due to loss of tip links. Such opened channels can allow K+ and Ca2+ to enter the cell from the endolymphatic space and cold lead to permanent depolarization. This influx of cations caused by loss of tip links, together with the subsequent hair-cell depolarization, might be a source of sensorineural hearing loss and tinnitus associated with acoustic trauma.

The study presents an analysis of 20 cases of acute acoustic trauma caused by toy pistols. The problem generally involves boys within the age range from 6 to 11 years. Half of the incidents involved attacks with toy pistols used as weapons. Auditory damage appeared in two types, each of which had a notch in the audiogram at the frequency range between 10 and 14 kHz. In children, a shot close to one ear can damage both ears. Great differences in the severity of tinnitus were apparent. The most severe cases of tinnitus were observed in the children with no or minor permanent auditory damage. Children experiencing long periods of uninterrupted tinnitus suffer significantly. This is not only detrimental to family life, but also to the performance of the children at school. The total expenses of treatment for these 20 cases were estimated to be approximately 80,000 DM (40,000 Euro).

Although noise in general can induce hearing loss, environmental noise represents an important risk for children, teenagers and young adults. Epidemiological investigations now support the occurrence of an increasing number of irreversible hearing losses in these groups. Major causes of hearing loss are toys (guns), explosives and electroacoustically amplified music delivered by head sets or heard in discotheques and open air concerts. Clinical indications are discussed.

Starter's pistols are often bought for self-defense, but can also be used for criminal activities (e.g. assaults, etc.). When a starter's pistol is loaded with blank cartridges and is fired, a powerful shooting noise results. The level of the noise produced is high enough to cause acoustic trauma. For legal examinations and giving an expert opinion further information is needed about the power of such noise. We examined how high peak sound pressure levels were of the gunshots of blank cartridges and whether there existed any directional characteristics from the noise emissions. In all, 15 different models of starter's pistols of 8 different calibres were examined. In addition to blank cartridges, 8 mm tear gas cartridges were also examined. Four transducers were situated in the horizontal plane around the muzzle: 0 degree (shooting direction), 45 degrees, 90 degrees, and 180 degrees (towards the firer). The distances between the transducers and the muzzle were 25 cm, 50 cm, 100 cm, and 200 cm. At a distance of 1 m and in the 0 degree shooting direction the peak sound pressure levels of nearly all weapons tested exceeded 160 dB. At a shooting distance of 25 cm the peak sound pressure levels reached 181 dB. In addition, we observed a directional characteristic concerning the emission of noise: pistols produced higher peak sound pressure levels to the front than backwards towards the firer.

In order to understand the repeated occurrences of auditory impairments caused by toy pistols, an analysis of the circumstances involved was performed at Justus-Liebig University of Giessen. The acoustic impact of toy pistols on the ear was determined with a special measuring system for impulse noise. Results were compared with the acoustic impacts of the G3 common rifle of the German military on the ear of the soldier. It was apparent that all of the five randomly selected types of toy pistols were much louder than the military rifle, if fired close to the ear. The current standard of the European Union related to the safety of toys (EN 71-1) tolerates peaks of impulse noise from toy pistols that are actually illegal for workplaces without auditory protection. Measurements showed that the toy pistols tested were even louder than that tolerated by the EU standard. Problems related to acute acoustic trauma caused by these toys are discussed using recent examples. In order to prevent such injuries, we suggest limiting the loudness of the "worst case" instead of using unrealistic measurements.