Noise-induced hearing loss

Hearing loss affects 30 million people in the United States; of these, 21 million are over the age of 65 years. This disorder may have several causes: heredity, noise, aging, and disease. Hearing loss from noise has been recognized for centuries but was generally ignored until some time after the Industrial Revolution. Hearing loss from occupational exposure to hazardous noise was identified as a compensable disability by the United States courts in 1948 to 1959. Development of noisy jet engines and supersonic aircraft created additional claims for personal and property damage in the 1950s and 1960s. These conditions led to legislation for noise control in the form of the Occupational Safety and Health Act of 1970 and the Noise Control Act of 1972. Protection of the noise-exposed employee was also an objective of the Hearing Conservation Act of 1971. Subsequent studies have confirmed the benefits of periodic hearing tests for workers exposed to hazardous noise and of otologic evaluation as part of the hearing conservation process. Research studies in laboratory animals, using scanning electron microscopical techniques, have demonstrated that damage to the inner ear and organ of hearing can occur even though subjective (conditioned) response to sound stimuli remains unaffected. Some investigators have employed an epidemiologic approach to identify risk factors and to develop profiles to susceptibility to noise-induced hearing loss. The need for joint involvement of workers and employers in the reduction and control of occupational noise hazards is evident.     

Noise-induced autoimmune sensorineural hearing loss

Typically, autoimmune sensorineural hearing loss has been described as a slowly progressive, asymmetric hearing loss that is responsive to medications traditionally used in the treatment of other autoimmune conditions. These medications include steroids and cytotoxic drugs. Inciting factors in autoimmune inner ear disease are rarely cited. We describe a case of episodic sudden hearing loss triggered consistently by environmental noise. The hearing loss was responsive to steroids at the time of each occurrence and was determined to be autoimmune. This case raises questions about the relationship between autoimmune inner ear disease and sensitivity to environmental noise that warrant further research.     

Noise-induced hearing loss and tinnitus]

The presence of subjective tinnitus is an important aspect in the evaluation of hearing loss induced by noise. Tinnitus due to this condition is characterised by a frequency of 3,000 Hz or above and is closely related to the frequency range of maximal hearing loss. Tinnitus below 1,000 Hz is not induced by noise, and indicates the presence of a different cause for the hearing loss. This type of tinnitus should not be regarded as an occupational disease: it requires extensive investigation.     

Noise-induced hearing loss in iron-deficient rats

The role of iron deficiency in noise-induced hearing loss (NIHL) was evaluated in 64 rats of four different experimental groups. Iron-deficient rats (ID-rats) and normal rats (N-rats) were simultaneously exposed to a steady state white noise (20-10,000 Hz) at 110 dB SPL for 30 min. Unexposed ID- and N-rats served as controls. In N-rats the temporary threshold shifts (TTS) would have completely disappeared if the animals were allowed to survive for 72 h. No permanent threshold shift (PTS) was seen in any of the N-rats. The ultrastructural correlates in N-rats are stereocilia disarray and mitochondria swelling in outer hair cells (OHCs). The TTS in ID-rats were larger than those in the N-rats, and most ID-rats with larger threshold shifts showed varying degrees of PTSs at 11 days post-exposure. The ultrastructural correlates of NIHL in ID-rats are obvious pathology of the stereocilia, such as segmental coalescence of stereocilia of many continuous OHCs and fusion of the tips of stereocilia of OHCs, and a significant reduction of mitochondria as well as slight degeneration of nucleus in the OHCs. It is concluded that iron deficiency can provide a pathological basis for NIHL.     

Noise-induced hearing loss in children.

Occupational noise exposure remains the most commonly identified cause of noise-induced hearing loss (NIHL), but potentially hazardous noise can be encountered during leisure-time activities. NIHL in the pediatric population has received scant attention. This study focuses on 114 children and adolescents (ages 19 and under: 90.3% males) who were diagnosed as having probable NIHL on the basis of history and audiometric configuration. In 42 children the loss was unilateral, while the remaining 72 had sensorineural losses of varying configurations in the contralateral ear. The mean age of referral for evaluation was 12.7 years (range 1.2 to 19.8, SD 4.21), although 26% of these losses were diagnosed in children aged 10 years and younger. Such irreversible, but potentially preventable losses, should be given high priority on the public health agenda. Comprehensive, age-appropriate educational programs must be developed for elementary and secondary students and their parents to acquaint them with potentially hazardous noise sources in their environment.     

Noise-induced hearing loss in shipyard workers with unilateral conductive hearing loss

In a study of 6500 workers in the shipbuilding industry, 8 subjects were found to have unilateral conductive hearing impairment established before the noise exposure period and without recurrent attacks of acute or chronic infection or clinical diagnosis of otosclerosis. All subjects demonstrated a more pronounced sensorineural hearing loss at 4.0 kHz in the ear with normal middle ear function. The results show the value of even a small permanent conductive hearing loss for protection against noise-induced hearing loss. The observations are discussed in relation to the role of individual variations in sound transmission, the value of the acoustic reflex in noise-induced hearing loss and the efficiency of continuous use of hearing protectors.     

Noise-induced hearing loss in rats with renal hypertension

Genetically hypertensive rats have been found in previous studies to be more susceptible than normotensive rats to the formation of lesions of the inner ear as a result of excess noise. The present study was designed to investigate whether or not that susceptibility is a direct result of the high blood pressure. Hypertension was induced in 28 Sprague-Dawley rats by placing a 0.25 mm wide silver clip on one renal artery. Systolic blood pressure was measured indirectly by a tail-cuff technique 3 weeks after the operation and again after noise exposure. The animals were kept for one month in noise conditions (100 dB L_eq (lin)) simulating those in an industrial milieu. The frequency range was adjusted to correlate to the hearing range of the rat. Auditory sensitivity was assessed electrophysiologically by recording auditory brain stem responses to pulses of $\text{1}\text{3}\text{-octave}$ filtered full-cycle sine waves. The results showed no correlation between hearing loss and systolic blood pressure. There was no difference between the audiograms obtained from rats with a systolic pressure below 160 mmHg and those obtained from rats with systolic pressures of between 170 and 255 mmHg. These results do not support the hypothesis that high blood pressure is a mechanism underlying noise-induced hearing loss.     

Noise-induced hearing loss and portable radios with headphones

Portable radio/cassette players with headphones have gained increasing popularity in recent years. Volume settings are often increased to override environmental noise, perhaps placing the listener at risk for noise-induced hearing loss (NIHL). A total of 190 public college students in NYC were studied via a self-administered questionnaire regarding the volume setting used and weekly exposure in hours to these units. Three popular models were tested using a Bruel and Kjaer sound level meter, octave band filter and artificial ear. Sound levels were measured at various frequencies (250-8000 Hz) and an overall measurement obtained using the "A"-weighted scale. Based on OSHA criteria for permissible noise dose (i.e. intensity X duration) in the work place, auditory risk criteria were developed. Of all students who used such radios 31.4% equalled or exceeded the maximum allowable dose permitted by these criteria (41.2% of the males and 29.2% of females). This sex-related difference in risk, while not statistically significant, warrants further investigation. Of the total 'at risk' group 50% exceeded the risk criteria by more than 100%. These results suggest that portable radios with headphones may be capable of causing permanent hearing loss in a large proportion of radio users.     

Noise-induced hearing loss in the noise-toughened auditory system

The auditory system, toughened by an interrupted noise exposure, has been shown in several reports to be less affected by (or protected from) a subsequent high-level noise exposure. Exposure to 115 dB peak SPL, 1 kHz narrow band (400 Hz) transients presented l/s, 6 h/day, to four groups of chinchillas produced a 10-28 dB toughening effect across the 0.5-8.0 kHz test frequency range. Following either a 30 day or an 18 h recovery period the animals were exposed to the same impulses but presented at 121 or 127 dB peak SPL for five uninterrupted days, thus producing an asymptotic threshold shift (ATS) condition. Comparisons between toughened and untoughened control subjects showed: (1) During the 121 dB exposure there was a statistically significant reduction of 10-25 dB in ATS across the entire test frequency range. Thirty days following the 121 dB exposure there were no significant differences in the postexposure permanent effects on thresholds and sensory cell loss. (2) During the 127 dB exposure only the group with the 30 day interval between the toughening and traumatic exposures showed a small (approximately 10 dB), statistically significant, frequency-specific (8 kHz), reduction in ATS. Thirty days following the 127 dB exposure a statistically significant protective effect on threshold was measured only at 16.0 kHz. However, both toughened groups showed less inner hair cell loss at and above 1.0 kHz, while only the group with the 18 h interval between the toughening and traumatic exposures showed less outer hair cell loss at and above 1.0 kHz. There were no systematic differences in the response of the toughened animals that could be attributed to the 30 day or 18 h post-toughening interval.     

Noise-induced hearing loss in snorers and their bed partners

OBJECTIVE: As habitual snoring affects a large percentage of the population and is associated with various medical and social complications, we examined whether loud snoring is also associated with noise-induced hearing loss for the snorers and/or their bed partners. PATIENT SELECTION: Healthy adults between the ages of 35 and 55 years with subjective symptoms of severe snoring were screened to exclude those with a past history of noise exposure (e.g., factory workers, army personnel), use of ototoxic medications, and previously diagnosed hearing disorder. MAIN OUTCOME MEASURES: Behavioural audiograms and otoacoustic emission testing were used to evaluate the subjects' hearing. RESULTS: Although all of the snorers did not demonstrate consistent hearing loss patterns, all four bed partners of snorers in our study demonstrated a unilateral high-frequency pattern of hearing loss consistent with noise-induced hearing loss. Furthermore, the affected ear in every case was the one that was claimed to be chronically exposed to snoring noise. CONCLUSIONS: The findings suggest that there may be a relationship between snoring and noise-induced hearing loss in the bed partners of chronic snorers. Further investigation of this association may enable the population at risk to identify early hearing loss in order that appropriate management of noise exposure and snoring can be recommended, including preventive measures and medical and surgical therapies.     

Noise-induced hearing loss in normotensive and spontaneously hypertensive rats

Hearing loss was investigated in normotensive (N) and spontaneously hypertensive (SH) rats after prolonged exposure to a simulated industrial noise environment. Exposure was initiated in a group of young rats (3 months old) and continued up to 18 months of age, and in a group of old rats (15 months old) and followed up to 18 months of age. Hearing thresholds were determined behaviorally with a conditioned suppression technique before and after 1, 2, 3 and, for some groups, also after 15 months of exposure. A frequency-modulated noise band sweeping from 3 to 30 kHz at a frequency of 0.5 Hz was presented 10 hours daily at a level of 100 dB L_eq (lin). The results showed that young N and SH rats not exposed to noise had identical hearing thresholds. Noise exposure induced a significantly greater hearing loss in SH rats than in N rats; SH animals were more susceptible to noise than were young ones; no difference was seen between males and females. The histology of the inner ears of the rats was examined by light microscopy after the end of the experiment. The young noise-exposed N rats showed no abnormal loss of hair cells in spite of the fact that they sustained hearing losses of 30–40 dB. The SH rats showed a significantly greater loss of hair cells than did the N rats. The stereocilia were found to be fused on a large number of inner hair cells in the basal turns of both N and SH animals. It was concluded that SH and N rats constitute an interesting model for the investigation of biological mechanisms behind individual differences in susceptibility to noise-induced hearing loss.     

噪声性耳聋:基础研究进展和展望

噪声性耳聋是一种十分常见的感音性聋。其发病原因是噪声引起耳蜗内组织机械损伤,进而引起一系列组织生物、病理及分子改变。这些因素相互作用造成以毛细胞为主的耳蜗组织损伤,进而导致听觉敏感度及分辨力下降,并可引发耳鸣、声耐受能力下降等症状,极大地影响患者的生活质量。因此,噪声性耳聋的防治具有十分重要的临床及社会意义。近年来,噪声性耳聋研究领域出现了许多令人瞩目的新进展,这些进展对认识噪声性耳聋的发病机制和寻找有效的防治方法具有十分重要的意义,并为今后的研究指明了方向,本文对此进行简要综述。     

Noise-induced hearing loss in chinchillas pre-treated with glutathione monoethylester and R-PIA

The protective effects of glutathione monoethylester (GEE) and GEE in combination with R-N6-phenylisopropyladenosine (R-PIA) were evaluated in the chinchilla when exposed to impulse (145 dB pSPL) or continuous (105 dB SPL, 4 kHz OB) noise. Six groups of 10 chinchillas were used as subjects. Before exposure to noise, the subjects were anesthetized, a 30 microl drop of drug was placed on the round window (GEE [50, 100, 150 mM], GEE 50 mM and R-PIA). Forty minutes later the subject was exposed to either impulse or continuous noise. The 50 mM treatment provided significant protection from impulse noise, but not from continuous noise exposure. The combination provided significant protection from both the continuous and impulse noise. In a separate set of experiments, glutathione (GSH) levels were measured in the perilymph. All the drug treatments elevated GSH levels. The results are discussed in terms of antioxidant treatments as a prophylactic measure against noise-induced hearing loss.