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PubMed1982

[Annoyance due to street traffic and aircraft noise].

Annoyance is an important criterion to assess the health-impairing effects of noise. Affected are especially communications, due to speech interference, as well as relaxation and sleep. The extent of annoyance increases with rising noise load in the street traffic as well as in the air traffic. Air-traffic noise in residential areas should lie below NNI-values of 35; values of above 45 NNI result in a heavy noise load and require sound-protection measures. Street-traffic noise in residential areas should not surpass an Leq value of 60 dB(A) in daytime and 50 dB(A) at night; Leq values of more than 65 dB(A) are qualified as considerable annoyance and are thus critical. In recreation areas the threshold limits should be 5 dB(A) below these values, whereas for shops and offices at main thoroughfares values higher by 5 dB(A) can be tolerated. The noise load should first of all be diminished by stricter regulations for vehicles as well as by measures regarding traffic organization. Furthermore, noise-conscious driving is recommended. Very great traffic noise also requires sound protection measures.

Aircraft↗
PubMed2006

Pilot survey of subway and bus stop noise levels.

Excessive noise exposure is a serious global urban health problem, adversely affecting millions of people. One often cited source of urban noise is mass transit, particularly subway systems. As a first step in determining risk within this context, we recently conducted an environmental survey of noise levels of the New York City transit system. Over 90 noise measurements were made using a sound level meter. Average and maximum noise levels were measured on subway platforms, and maximum levels were measured inside subway cars and at several bus stops for comparison purposes. The average noise level measured on the subway platforms was 86 +/- 4 dBA (decibel-A weighting). Maximum levels of 106, 112, and 89 dBA were measured on subway platforms, inside subway cars, and at bus stops, respectively. These results indicate that noise levels in subway and bus stop environments have the potential to exceed recommended exposure guidelines from the World Health Organization (WHO) and U.S. Environmental Protection Agency (EPA), given sufficient exposure duration. Risk reduction strategies following the standard hierarchy of control measures should be applied, where feasible, to reduce subway noise exposure.

Environmental Health↗
PubMed1990

Interaction of cisplatin and noise on the peripheral auditory system.

The potentiation of cisplatin ototoxicity by noise was explored in the chinchilla. The effects of exposure to cisplatin alone, noise alone or concurrent exposure to both agents were compared in terms of the threshold shift of the auditory evoked potential and the amount of hair cell loss. The combination of cisplatin plus noise produced significantly more hair cell loss and hearing loss at the high frequencies than did either the noise or cisplatin alone when the noise level was 85 dB SPL or higher; no interaction was seen when the noise level was 70 dB SPL. The amount of the interaction, when present, was constant regardless of the noise level. These results indicate that moderate to high levels of noise can exacerbate cisplatin ototoxicity.

Animals↗
PubMed2005

Effect of noise exposure on gap detection in rats.

The effects of intense (110-120 dB) noise exposure (broadband noise for one hour) on temporal resolution was estimated in rats by measuring the behavioural gap detection threshold (GDT). Changes in GDT after 120 dB noise exposure were compared with changes in the threshold and amplitude of middle latency responses (MLR) recorded in response to tone stimuli. GDT values increased from 1.6 to 4.3 or 7.8 ms after exposure to 110 or 115 dB SPL, respectively; GDT recovered to pre-exposure values in 3-7 days. Three main types of noise-induced changes were observed after 120 dB SPL exposure: (I) GDT changes similar to those following noise exposure to 115 dB SPL and maximal hearing threshold shifts (TSs) at high frequencies of about 45 dB; (II) more pronounced changes in GDT (up to 60 ms) with maximal hearing threshold shifts of about 65 dB and (III) a lack of reliable responses to gap during the first weeks post-exposure with maximal hearing threshold shifts of about 80 dB. An increased GDT was present two months after noise exposure in animals with types II and III post-exposure changes; enhanced MLR amplitudes were also found in most of these in the first post-exposure week. The pronounced deficit in gap detection in some rats after 120 dB SPL noise exposure may signal the presence of a noise-induced tinnitus.

Animals↗
PubMed2001

Susceptibility to noise exposure during postnatal development in rats.

Susceptibility to noise-induced hearing loss was studied during maturation in 20 female pigmented rats (strain Long-Evans). Young rats, 3, 4, 5 and 6-7 weeks old, were exposed for 1 h to a broad-band noise with an intensity of 120 dB SPL. The thresholds and amplitudes of middle latency responses (MLR) recorded from electrodes implanted on the surface of the auditory cortex were analyzed before and after noise exposure. The results were compared with data from our previous study, in which the effects of broad-band noise exposure on MLR were investigated in adult rats [Syka, J. and Rybalko, N. (2000) Hear. Res. 139, 59-68]. The hearing thresholds of 3-7 week old rats before noise exposure were within the normal adult range. Noise exposure in young rats produced an adult-like pattern with an elevation of hearing thresholds. One-two weeks post-exposure a recovery of MLR thresholds was observed, though full recovery only occurred in the low frequency range. Recovery of hearing thresholds in the high frequency range depended on the age of the animal at the time of exposure. In all animals aged less that 6-7 weeks, exposure resulted in a permanent threshold shift in the range of 4-32 kHz. The mean values of permanent threshold shifts at 16 kHz (the frequency of maximal hearing loss) were 53.0+/-4.5, 47.6+/-9.6, 37.5+/-7.5 and 27+/-10 dB for rats exposed at 3, 4, 5 and 6-7 weeks of age, respectively. Similar to adult rats, young rats exposed to noise exhibited an enhancement of MLR amplitudes. This amplitude enhancement was more pronounced in the high frequency range. In several rats exposed at 3-5 weeks of age, the recovery period to normal amplitudes was substantially prolonged and lasted 4-8 weeks in comparison with 1-2 weeks in adult rats. These results demonstrate a greater susceptibility to noise exposure in rats during the first 5 postnatal weeks.

Age Factors↗
PubMed2004

Consequences of noise- or styrene-induced cochlear damages on glutamate decarboxylase levels in the rat inferior colliculus.

Both noise and styrene can injure the cochlea, resulting in a reduction of incoming inputs from the cochlea to the central nervous system. In addition, styrene is known to have neurotoxic properties at high doses. The loss of inputs caused by noise has been shown to be compensated by a new equilibrium between excitatory and inhibitory influences within the inferior colliculus (IC). The main goal of this study was to determine whether styrene-induced hearing loss could also be counterbalanced by a GABAergic adjustment in the IC. For this purpose, rats were exposed to noise (97 dB SPL octave band noise centered at 8 kHz), or to a non-neurotoxic dose of styrene for 4 weeks (700 ppm, 6 h/day, 5 days/week). Auditory sensitivity was tested by evoked potentials, and cochlear damage was assessed by hair cell counts. Glutamate decarboxylase (GAD) was dosed in the IC by indirect competitive enzyme-linked immunosorbent assay. Both noise and styrene caused PTSs that reached 27.0 and 14.6 dB respectively. Outer hair cell (OHC) loss caused by noise did not exceed 9% in the first row, on the other hand OHC loss induced by styrene reached 63% in the third row. Only the noise caused a decrease of GAD of 37% compared to that measured in the controls. No significant modification of GAD concentration has been shown after styrene exposure. Thus, central compensation for cochlear damage may depend on the nature of the ototoxic agent. Unless styrene directly affects IC function, it is reasonable to assume that noise causes a modification of inhibitory neurotransmission within the structure because of impairment of afferent supply to the auditory brainstem. The present findings suggest that central compensation for cochlear damage can preferably occur when afferent fibers are altered.

Animals↗
PubMed1997

Chronic strychnine administration into the cochlea potentiates permanent threshold shift following noise exposure.

To investigate whether elimination of the medial efferent system influences permanent threshold shift following noise exposure, we developed an animal model in which strychnine was chronically delivered into the cochlea via an osmotic pump. Pigmented female guinea pigs were allocated into three groups: group I was treated with strychnine (50 microM, 0.5 microl/h, 14 days) in the left ear and exposed to noise (105 dB SPL broadband, 3 h) 3 weeks after the cessation of the strychnine perfusion; group II received strychnine in the left ear but no noise exposure; group III was treated with Ringer's solution in the left ear and exposed to noise. Animals in group II developed no hearing loss after the strychnine perfusion. The operated ears in group I demonstrated greatest hearing threshold shift 3 h after noise exposure. Hearing recovered during 2 weeks after noise exposure in both operated and non-operated ears in groups I and III. Two weeks after noise exposure, the operated ears in group I showed significantly greater threshold shift at 12, 16, and 20 kHz compared to the operated ears in group III and non-operated ears in groups I and III. These findings suggest that chronic strychnine administration into the cochlea inactivates the medial efferents without changing hearing threshold and that the medial efferents help to protect against permanent threshold shift following noise exposure.

Animals↗
PubMed1998

Effects of noise on inferior colliculus evoked potentials and cochlear anatomy in young and aged chinchillas.

Like many aging humans, the aging chinchilla tends to lose high-frequency sensitivity at a faster rate than low-frequency sensitivity. This feature, combined with its excellent low-frequency hearing, makes the chinchilla attractive as an animal model for studying the relationship between noise-induced hearing loss (NIHL) and age-related hearing loss (AHL). In the present study, we examined susceptibility to noise in 15 aged (10-15 years old) and 15 young chinchillas. Two levels of noise were used, with the aim of determining whether age-related differences exist in the magnitude and rate of recovery from temporary threshold shifts produced by a moderate-level (95 dB) noise exposure, or in susceptibility to permanent threshold shifts and cochlear damage caused by a high-level (106 dB) noise exposure. Thresholds and response amplitudes at 0.5, 1, 2, 4, 8 and 16 kHz were determined from evoked potentials recorded from the inferior colliculus. Cochlear histology was performed on animals exposed to high-level noise. The results suggest that older animals are equally vulnerable to moderate-level noise, but may be slightly more vulnerable to high-level noise. For moderate-level exposures, there appears to be a simple additive relationship (in dB) between AHL and NIHL. For high-level exposures, the relationship may be more complex.

Acoustic Stimulation↗
PubMed2005

[Measuring noise].

High levels of noise encountered both in leisure activities and at workplaces can be somewhat annoying, but they can also cause hearing damage. In order to lessen these risks, some physical characteristics of the sound phenomenon need to be understood. The level of a sound is given in dB, a logarithmic unit in which simple addition is not available : 100 dB + 100 dB = 103 dB. The highest level of noise which can be tolerated by the human ear is considered to be 120 dB. Another component of sound characteristics is the frequency, which describes the height of a sound. The frequency is given in Hz, the human hearing field is comprised in the range of 20 to 20,000 Hz. Regarding the sensitivity of the ear, depending on the frequency, acusticians use a weighed dB, called dB(A), which takes into account a lower risk to hearing below 500 Hz and above 6 kHz. They also integrate the energy measured during a period of time to take the fluctuation of usual noise levels into account. So that currently, the levels of noise are often given in LAeq (equivalent to the level of continuous noise given in dBA). For moderate levels of noise, another weighted filter is used in sound level meters : the C curve, because low frequencies, although they are less dangerous for the ear, are more disturbing. In every day life, we sometimes have noise levels reaching 100 dB, and even 120 dB (fire alarms). Amplified music can reach 110 dBA, but a French regulation limits the output of PCPs (Walkmans) to 100 dB and the levels in concerts and discotheques to 105 dBA. At the workplace, the maximum level of noise allowed by French Law is 90 dBA for an 8 hour exposure, and 140 dB for peaks. In order to improve the protection of all workers in the EC, a recent European Directive will decrease the maximum level to 87 dBA before March 2006.

Hearing Loss, Noise-Induced↗
PubMed2001

The effect of noise on serum and urinary magnesium and catecholamines in humans.

We have studied whether a short-term exposure to loud noise was able to modify urinary catecholamine excretion and serum concentration and urinary excretion of magnesium and other related electrolytes. In 25 healthy volunteers, blood and urine concentrations of magnesium, calcium, phosphorus and creatinine, and urinary catecholamines were measured before and after exposure to noise in an industrial plant. Samples were collected at 08:00 h on the day of the experiment and soon after noise exposure (at 20:00 h). Two further urine samples were collected the following day and 2 days after the experiment, always at 08:00 h in the morning. The sound energy average level was 98 dB(A), but peak levels reached 108 dB(A). Urinary catecholamines were determined by high-performance liquid chromatography. Serum magnesium and calcium were significantly increased after exposure to noise, whereas phosphorus displayed a similar but non-significant trend (P = 0.065). Multivariate analysis of variance (ANOVA) showed significant differences both among subjects (P < 0.001) and after exposure (P < 0.001). Adrenaline, noradrenaline and dopamine values were not significantly different after exposure to noise (P > 0.05). Urinary magnesium levels were significantly different across time (P = 0.017). Urinary calcium levels were not significantly different across time (P = 0.36). Urinary phosphate values were increased after exposure to noise (P = 0.007); urinary creatinine was not changed after exposure (P > 0.05). Our study shows that noise induces significant increases of serum calcium and magnesium, with a borderline increase of serum phosphorus; this in turn is reflected in a significantly increased urinary excretion of magnesium and phosphate after exposure, which lasts for the following 2 days. Urinary calcium and creatinine were not modified by noise. The difference in catecholamine values did not reach statistical significance. Thus, we failed to substantiate a significant correlation between catecholamine secretion and magnesium metabolism, as others had suggested.

Adult↗
PubMed2005

Joint effects of smoking, noise exposure and age on hearing loss.

BACKGROUND: Smoking has been shown to have adverse effects on hearing, but it's unclear whether smoking interacts with known causes of hearing loss such as noise exposure and ageing. AIMS: To examine the hypothesis that smoking, noise and age jointly affect hearing acuity. METHODS: This cross-sectional study was carried out in 535 male adult workers of a metal processing factory. Pure-tone audiometric tests were utilized to assess hearing loss. Noise exposure assessment was based on a job exposure matrix constructed with industrial hygienist scoring and job titles. Each participant answered questionnaires about socio-demographic, life-style, occupational and health-related data. Analysis of the possible underlying biological model was undertaken assessing departures from additivity using measures of the size of the interaction present. RESULTS: Age and occupational noise exposures were, separately, positively associated with hearing loss. For all the factors combined the estimated effect on hearing loss was higher than the sum of the effects from each isolated variable, especially for smoking and noise among those 20-40 years of age, and for smoking and age among those non-exposed to occupational noise. CONCLUSIONS: The synergistic effect of smoking, noise exposure and age on hearing loss, found in this study, is consistent with the biological interaction. Furthermore, it is possible that distinct ototoxic substances in the chemical composition of mainstream smoke may synergistically affect hearing when in combination with noise exposure, which needs to be examined in future studies.

Adult↗
PubMed2004

Hearing loss and perceptions of noise in the workplace among rural Australians.

OBJECTIVE: To compare measured hearing levels of individuals regularly exposed to noise in their workplace to self-reported and family-reported hearing loss. To compare the attitudes and preventative actions adopted by individuals who are more aware of the potential for hearing loss to less aware individuals. DESIGN: The project examined the perceptions of rural workers concerning noise, noise exposure and hearing. The subjects completed a 'Noise at Work' questionnaire and some demographic data at the time of audiometric testing. SETTING: The subjects were recruited when attending their rural health clinic for audiometric testing. PARTICIPANTS: Participants comprised 113 men and 23 women (20-65 years, mean = 39.6, SD = 11.4) working across a range of activities at different levels in their workplaces. The range in current employment was from 0.5 to 45 years (mean = 13.8, SD = 10.7). RESULTS: Hearing tests were compared with perceptions of noise annoyance, hearing damage risk and preventative action. Self- and family-reported hearing loss and conversational difficulties in noise correlated well with measured audiograms. Perceptions of workplace noise tended to be more positive if people felt they had hearing problems. There was no difference in preventative action between those who did and did not feel they had hearing problems. Both groups rated barriers to action and lack of self-efficacy in a similar negative way. CONCLUSIONS: There is a need for specific training to ensure that rural workers have skills to take more positive action in reducing noise exposure at work.

Adult↗
PubMed2006

The kurtosis metric as an adjunct to energy in the prediction of trauma from continuous, nonGaussian noise exposures.

Data from an earlier study [Hamernik et al. (2003). J. Acoust. Soc. Am. 114, 386-395] were consistent in showing that, for equivalent energy [Leq= 100 dB(A)] and spectra, exposure to a continuous, nonGaussian (nonG) noise could produce substantially greater hearing and sensory cell loss in the chinchilla model than a Gaussian (G) noise exposure and that the statistical metric, kurtosis, computed on the amplitude distribution of the noise could order the extent of the trauma. This paper extends these results to Leq= 90 and 110 dB(A), and to nonG noises that are generated using broadband noise bursts, and band limited impacts within a continuous G background noise. Data from nine new experimental groups with 11 or 12 chinchillas/group is presented. Evoked response audiometry established hearing thresholds and surface preparation histology quantified sensory cell loss. At the lowest level [Leq=90 dB(A)] there were no differences in the trauma produced by G and nonG exposures. For Leq >90 dB(A) nonG exposures produced increased trauma relative to equivalent G exposures. Removing energy from the impacts by limiting their bandwidth reduced trauma. The use of noise bursts to produce the nonG noise instead of impacts also reduced the amount of trauma.

Animals↗
PubMed1979

Development of noise and vibration ride comfort criteria.

A laboratory investigation was directed at the development of criteria for the prediction of ride quality in a noise-vibration environment. The stimuli for the study consisted of octave bands of noise centered at 500 and 2000 Hz and vertical floor vibrations composed of either 5 Hz sinusoidal vibration, or random vibrations centered at 5 Hz and with a 5 Hz bandwidth. The noise stimuli were presented at A-weighted sound pressure levels ranging from ambient to 95 dB and the vibration and acceleration levels ranging from 0.02--0.13 grms. Results indicated that the total subjective discomfort response could be divided into two subjective components. One component consisted of subjective discomfort to vibration and was found to be a linear function of vibration acceleration level. The other component consisted of discomfort due to noise which varied logarithmically with noise level (power relationship). However, the magnitude of the noise discomfort component was dependent upon the level of vibration present in the combined environment. Based on the experimental results, a model of subjective discomfort that accounted for the interdependence of noise and vibration was developed. The model was then used to develop a set of criteria (constant discomfort) curves that illustrate the basic design tradeoffs available between noise and vibration.

Adult↗
PubMed1982

Spectral analysis of impulse noise for hearing conservation purposes.

Damage-risk criteria for impulse noise does not presently take the spectrum of the impulse into account; however, it is known that the human auditory system is spectrally tuned. The present paper advocates the extension to impulse noise of the noise dose concept which is widely used for continuous noise. This approach is based upon sound exposure instead of sound pressure. An A-weighting filter or an octave band analysis can then be used to take the spectral content of the impulses into account. The equipment needed for applying these procedures for impulse noise is an integrating sound level meter or a digital Fourier processor. Generalized spectral methods have been evaluated by means of an impulse simulation applied to a mathematical model of the human hearing mechanism. The results of this simulation agree with the most recent experiments on impulse noise and fully support the proposed rating methods. This conclusion must be emphasized as it leads the derivation of a uniform procedure for predicting loudness and damage risk for hearing which is applicable for continuous noise as well as for impulse noise.

Environmental Exposure↗
PubMed1989

The effect of traffic noise on sleep of young adults in their homes.

The disturbance of sleep by traffic noise is a major problem area in noise pollution. Extensive laboratory tests using multichannel electroencephalograms (EEG) have been carried out by many workers to determine the general response of people when exposed to noise during sleep. An experimental technique for obtaining results in people's homes has been developed using a simplified one-channel EEG. The responses of six people in the age range 19-24 were measured. A significant correlation was found between sleep disturbance and traffic noise when the noise is expressed in EPNdB. In the home experiments the subjects appeared to be approximately 10 dB less sensitive to noises than laboratory subjects for similar noise exposure. There also appeared to be some adaptation to the noise exposure; however, only one subject was tested for a period of 20 days and was insufficient to give definite results on adaptation.

Adaptation, Physiological↗
PubMed1990

An alternative mathematical description of the relationship between noise exposure and hearing loss.

Retrospective investigation of large populations has provided means for determining quantitative relationships between the hearing levels of non-noise-exposed populations and age, and between the hearing levels of noise-exposed populations and age and noise exposure. In the latter case, noise exposures have been predominantly steady state over many years and no way of measuring the effects of noise alone, excluding the effects of age, has ever been demonstrated. In the following paper, attention is confined to the problem of developing a mathematical description of an existing set of empirically determined hearing level data; questions of audiology are not of concern here. It is shown that the mathematical analysis traditionally used to determine the contribution of noise exposure alone to hearing level is not unique; an alternative formulation is possible and indeed is demonstrated. Whereas the traditional formulation leads to the conclusion that noise-induced hearing loss scales on the integral of sound pressure squared with time, and thus, to the equal energy hypothesis, the alternative formulation leads to the conclusion that noise-induced hearing loss scales on the integral of pressure with time. Since either formulation adequately describes the data, and the equal energy hypothesis has never been adequately substantiated, use of the latter hypothesis to extend the findings of steady-state exposures to application for unsteady exposures is not justified. The alternative formulation presented here is recommended for consideration.

Adolescent↗
PubMed1992

Speech reception in quiet and in noisy conditions by individuals with noise-induced hearing loss in relation to their tone audiogram.

Tone thresholds and speech-reception thresholds were measured in 200 individuals (400 ears) with noise-induced hearing loss. The speech-reception thresholds were measured in a quiet condition and in noise with a speech spectrum at levels of 35, 50, 65, and 80 dBA. The tone audiograms could be described by three principal components: hearing loss in the regions above 3 kHz, from 1 to 3 kHz and below 1 kHz; the speech thresholds could be described by two components: speech reception in quiet and speech reception in noise at 50-80 dBA. Hearing loss above 1 kHz was related to speech reception in noise; hearing loss at and below 1 kHz to speech reception in quiet. The correlation between the speech thresholds in quiet and in noise was only R = 0.45. An adequate predictor of the speech threshold in noise, the primary factor in the hearing handicap, was the pure-tone average at 2 and 4 kHz (PTA2,4, R = 0.72). The minimum value of the prediction error for any tone-audiometric predictor of this speech threshold was 1.2 dB (standard deviation). The prediction could not be improved by taking into account the critical ratio for low-frequency noise nor by its upward spread of masking. The prediction error is due to measurement error and to a factor common to both ears. The latter factor is ascribed to cognitive skill in speech reception. Hearing loss above 10 to 15 dB HL (hearing level) already shows an effect on the speech threshold in noise, a noticeable handicap is found at PTA2,4 = 30 dB HL.

Adult↗