Lifetime Noise Exposure Research Articles

Acoustic Middle-Ear-Muscle-Reflex Thresholds in Humans with Normal Audiograms: No Relations to Tinnitus, Speech Perception in Noise, or Noise Exposure

The acoustic middle-ear-muscle reflex (MEMR) has been suggested as a sensitive non-invasive measure of cochlear synaptopathy, the loss of synapses between inner hair cells and auditory nerve fibers. In the present study, clinical MEMR thresholds were measured for 1-, 2-, and 4-kHz tonal elicitors, using a procedure shown to produce thresholds with excellent reliability. MEMR thresholds of 19 participants with tinnitus and normal audiograms were compared to those of 19 age- and sex-matched controls. MEMR thresholds did not differ significantly between the two groups at any frequency. These 38 participants were included in a larger sample of 70 participants with normal audiograms. For this larger group, MEMR thresholds were compared to a measure of spatial speech perception in noise (SPiN) and a detailed self-report estimate of lifetime noise exposure. MEMR thresholds were unrelated to either SPiN or noise exposure, despite a wide range in both measures. It is possible that thresholds measured using a clinical paradigm are less sensitive to synaptopathy than those obtained using more sophisticated measurement techniques; however, we had good sensitivity at the group level, and even trends in the hypothesized direction were not observed. To the extent that MEMR thresholds are sensitive to cochlear synaptopathy, the present results provide no evidence that tinnitus, SPiN, or noise exposure are related to synaptopathy in the population studied.

Effects of lifetime noise exposure on the middle-age human auditory brainstem response, tinnitus and speech-in-noise intelligibility

Recent animal studies have shown that the synapses between inner hair cells and the dendrites of the spiral ganglion cells they innervate are the elements in the cochlea most vulnerable to excessive noise exposure. Particularly in rodents, several studies have concluded that exposure to high level octave-band noise for 2 h leads to an irreversible loss of around 50% of synaptic ribbons, leaving audiometric hearing thresholds unaltered. Cochlear synaptopathy following noise exposure is hypothesized to degrade the neural encoding of sounds at the subcortical level, which would help explain certain listening-in-noise difficulties reported by some subjects with otherwise ‘normal’ hearing. In response to this peripheral damage, increased gain of central stages of the auditory system has been observed across several species of mammals, particularly in association with tinnitus. The auditory brainstem response (ABR) wave I amplitude and waves I-V amplitude ratio have been suggested as non-invasive indicators of cochlear synaptopathy and central gain activation respectively, but the evidence for these hearing disorders in humans is inconclusive. In this study, we evaluated the influence of lifetime noise exposure (LNE) on the human ABR and on speech-in-noise intelligibility performance in a large cohort of adults aged 29 to 55. Despite large inter-subject variability, results showed a moderate, but statistically significant, negative correlation between the ABR wave I amplitude and LNE, consistent with cochlear synaptopathy. The results also showed (a) that central gain mechanisms observed in animal studies might also occur in humans, in which higher stages of the auditory pathway appear to compensate for reduced input from the cochlea; (b) that tinnitus was associated with activation of central gain mechanisms; (c) that relevant cognitive and subcortical factors influence speech-in-noise intelligibility, in particular, longer ABR waves I-V interpeak latencies were associated with poorer performance in understanding speech in noise when central gain mechanisms were active; and (d) absence of a significant relationship between LNE and tinnitus, central gain activation or speech-in-noise performance. Although this study supports the possible existence of cochlear synaptopathy in humans, the great degree of variability, the lack of uniformity in central gain activation and the significant involvement of attention in speech-in-noise performance suggests that noise-induced cochlear synaptopathy is, at most, one of several factors that play a role in humans' speech-in-noise performance.

The Physiological Bases of Hidden Noise-Induced Hearing Loss: Protocol for a Functional Neuroimaging Study.

BackgroundRodent studies indicate that noise exposure can cause permanent damage to synapses between inner hair cells and high-threshold auditory nerve fibers, without permanently altering threshold sensitivity. These demonstrations of what is commonly known as hidden hearing loss have been confirmed in several rodent species, but the implications for human hearing are unclear.ObjectiveOur Medical Research Council–funded program aims to address this unanswered question, by investigating functional consequences of the damage to the human peripheral and central auditory nervous system that results from cumulative lifetime noise exposure. Behavioral and neuroimaging techniques are being used in a series of parallel studies aimed at detecting hidden hearing loss in humans. The planned neuroimaging study aims to (1) identify central auditory biomarkers associated with hidden hearing loss; (2) investigate whether there are any additive contributions from tinnitus or diminished sound tolerance, which are often comorbid with hearing problems; and (3) explore the relation between subcortical functional magnetic resonance imaging (fMRI) measures and the auditory brainstem response (ABR).MethodsIndividuals aged 25 to 40 years with pure tone hearing thresholds ≤20 dB hearing level over the range 500 Hz to 8 kHz and no contraindications for MRI or signs of ear disease will be recruited into the study. Lifetime noise exposure will be estimated using an in-depth structured interview. Auditory responses throughout the central auditory system will be recorded using ABR and fMRI. Analyses will focus predominantly on correlations between lifetime noise exposure and auditory response characteristics.ResultsThis paper reports the study protocol. The funding was awarded in July 2013. Enrollment for the study described in this protocol commenced in February 2017 and was completed in December 2017. Results are expected in 2018.ConclusionsThis challenging and comprehensive study will have the potential to impact diagnostic procedures for hidden hearing loss, enabling early identification of noise-induced auditory damage via the detection of changes in central auditory processing. Consequently, this will generate the opportunity to give personalized advice regarding provision of ear defense and monitoring of further damage, thus reducing the incidence of noise-induced hearing loss.

Impaired speech perception in noise with a normal audiogram: No evidence for cochlear synaptopathy and no relation to lifetime noise exposure

In rodents, noise exposure can destroy synapses between inner hair cells and auditory nerve fibers (“cochlear synaptopathy”) without causing hair cell loss. Noise-induced cochlear synaptopathy usually leaves cochlear thresholds unaltered, but is associated with long-term reductions in auditory brainstem response (ABR) amplitudes at medium-to-high sound levels. This pathophysiology has been suggested to degrade speech perception in noise (SPiN), perhaps explaining why SPiN ability varies so widely among audiometrically normal humans. The present study is the first to test for evidence of cochlear synaptopathy in humans with significant SPiN impairment. Individuals were recruited on the basis of self-reported SPiN difficulties and normal pure tone audiometric thresholds. Performance on a listening task identified a subset with “verified” SPiN impairment. This group was matched with controls on the basis of age, sex, and audiometric thresholds up to 14 kHz. ABRs and envelope-following responses (EFRs) were recorded at high stimulus levels, yielding both raw amplitude measures and within-subject difference measures. Past exposure to high sound levels was assessed by detailed structured interview. Impaired SPiN was not associated with greater lifetime noise exposure, nor with any electrophysiological measure. It is conceivable that retrospective self-report cannot reliably capture noise exposure, and that ABRs and EFRs offer limited sensitivity to synaptopathy in humans. Nevertheless, the results do not support the notion that noise-induced synaptopathy is a significant etiology of SPiN impairment with normal audiometric thresholds. It may be that synaptopathy alone does not have significant perceptual consequences, or is not widespread in humans with normal audiograms.

Effects of age and noise exposure on the representation of amplitude modulation

Age and lifetime noise exposure were used as predictors for electrophysiological and psychophysical measures of amplitude modulation processing. Frequency-following responses (FFRs) were recorded from 61 listeners (20 young, 23 middle-aged, 18 elderly) to 0.6- and 2-kHz, 75-dB SPL, carrier tones amplitude modulated at 100 Hz. A pink noise highpass-filtered at 3 kHz was included to mask basal cochlear contributions to the FFR. Sinusoidal amplitude modulation detection (AMD) thresholds were measured for the same listeners for a 2-kHz carrier (40 and 80 dB SPL) and for three modulation frequencies (25, 50, and 100 Hz). The carrier was presented in notched pink noise to limit off-frequency listening. Lifetime noise exposure was estimated using a structured interview. A regression model was used to determine the independent contributions of age and noise exposure, while controlling for audiometric threshold. FFR amplitude for the 0.6 kHz carrier showed a marked age-related decline. Age was also associated with a significant increase in AMD thresholds. Lifetime noise exposure was not significantly associated with either FFR amplitude or AMD threshold. The results suggest that age is a stronger predictor of modulation processing deficits than lifetime noise exposure.

The Noise Exposure Structured Interview (NESI): An Instrument for the Comprehensive Estimation of Lifetime Noise Exposure.

Lifetime noise exposure is generally quantified by self-report. The accuracy of retrospective self-report is limited by respondent recall but is also bound to be influenced by reporting procedures. Such procedures are of variable quality in current measures of lifetime noise exposure, and off-the-shelf instruments are not readily available. The Noise Exposure Structured Interview (NESI) represents an attempt to draw together some of the stronger elements of existing procedures and to provide solutions to their outstanding limitations. Reporting is not restricted to prespecified exposure activities and instead encompasses all activities that the respondent has experienced as noisy (defined based on sound level estimated from vocal effort). Changing exposure habits over time are reported by dividing the lifespan into discrete periods in which exposure habits were approximately stable, with life milestones used to aid recall. Exposure duration, sound level, and use of hearing protection are reported for each life period separately. Simple-to-follow methods are provided for the estimation of free-field sound level, the sound level emitted by personal listening devices, and the attenuation provided by hearing protective equipment. An energy-based means of combining the resulting data is supplied, along with a primarily energy-based method for incorporating firearm-noise exposure. Finally, the NESI acknowledges the need of some users to tailor the procedures; this flexibility is afforded, and reasonable modifications are described. Competency needs of new users are addressed through detailed interview instructions (including troubleshooting tips) and a demonstration video. Limited evaluation data are available, and future efforts at evaluation are proposed.

Subcortical amplitude modulation encoding deficits suggest evidence of cochlear synaptopathy in normal-hearing 18-19 year olds with higher lifetime noise exposure.

Noise exposure and aging can damage cochlear synapses required for suprathreshold listening, even when cochlear structures needed for hearing at threshold remain unaffected. To control for effects of aging, behavioral amplitude modulation (AM) detection and subcortical envelope following responses (EFRs) to AM tones in 25 age-restricted (18-19 years) participants with normal thresholds, but different self-reported noise exposure histories were studied. Participants with more noise exposure had smaller EFRs and tended to have poorer AM detection than less-exposed individuals. Simulations of the EFR using a well-established cochlear model were consistent with more synaptopathy in participants reporting greater noise exposure.

Effects of noise exposure on young adults with normal audiograms II: Behavioral measures

An estimate of lifetime noise exposure was used as the primary predictor of performance on a range of behavioral tasks: frequency and intensity difference limens, amplitude modulation detection, interaural phase discrimination, the digit triplet speech test, the co-ordinate response speech measure, an auditory localization task, a musical consonance task and a subjective report of hearing ability. One hundred and thirty-eight participants (81 females) aged 18–36 years were tested, with a wide range of self-reported noise exposure. All had normal pure-tone audiograms up to 8 kHz. It was predicted that increased lifetime noise exposure, which we assume to be concordant with noise-induced cochlear synaptopathy, would elevate behavioral thresholds, in particular for stimuli with high levels in a high spectral region. However, the results showed little effect of noise exposure on performance. There were a number of weak relations with noise exposure across the test battery, although many of these were in the opposite direction to the predictions, and none were statistically significant after correction for multiple comparisons. There were also no strong correlations between electrophysiological measures of synaptopathy published previously and the behavioral measures reported here. Consistent with our previous electrophysiological results, the present results provide no evidence that noise exposure is related to significant perceptual deficits in young listeners with normal audiometric hearing. It is possible that the effects of noise-induced cochlear synaptopathy are only measurable in humans with extreme noise exposures, and that these effects always co-occur with a loss of audiometric sensitivity.

The effects of noise exposure and musical training on suprathreshold auditory processing and speech perception in noise

Recent animal research has shown that exposure to single episodes of intense noise causes cochlear synaptopathy without affecting hearing thresholds. It has been suggested that the same may occur in humans. If so, it is hypothesized that this would result in impaired encoding of sound and lead to difficulties hearing at suprathreshold levels, particularly in challenging listening environments. The primary aim of this study was to investigate the effect of noise exposure on auditory processing, including the perception of speech in noise, in adult humans. A secondary aim was to explore whether musical training might improve some aspects of auditory processing and thus counteract or ameliorate any negative impacts of noise exposure. In a sample of 122 participants (63 female) aged 30–57 years with normal or near-normal hearing thresholds, we conducted audiometric tests, including tympanometry, audiometry, acoustic reflexes, otoacoustic emissions and medial olivocochlear responses. We also assessed temporal and spectral processing, by determining thresholds for detection of amplitude modulation and temporal fine structure. We assessed speech-in-noise perception, and conducted tests of attention, memory and sentence closure. We also calculated participants' accumulated lifetime noise exposure and administered questionnaires to assess self-reported listening difficulty and musical training. The results showed no clear link between participants' lifetime noise exposure and performance on any of the auditory processing or speech-in-noise tasks. Musical training was associated with better performance on the auditory processing tasks, but not the on the speech-in-noise perception tasks. The results indicate that sentence closure skills, working memory, attention, extended high frequency hearing thresholds and medial olivocochlear suppression strength are important factors that are related to the ability to process speech in noise.

Auditory Brainstem Response Altered in Humans With Noise Exposure Despite Normal Outer Hair Cell Function.

Recent animal studies demonstrated that cochlear synaptopathy, a partial loss of inner hair cell-auditory nerve fiber synapses, can occur in response to noise exposure without any permanent auditory threshold shift. In animal models, this synaptopathy is associated with a reduction in the amplitude of wave I of the auditory brainstem response (ABR). The goal of this study was to determine whether higher lifetime noise exposure histories in young people with clinically normal pure-tone thresholds are associated with lower ABR wave I amplitudes. Twenty-nine young military Veterans and 35 non Veterans (19 to 35 years of age) with normal pure-tone thresholds were assigned to 1 of 4 groups based on their self-reported lifetime noise exposure history and Veteran status. Suprathreshold ABR measurements in response to alternating polarity tone bursts were obtained at 1, 3, 4, and 6 kHz with gold foil tiptrode electrodes placed in the ear canal. Wave I amplitude was calculated from the difference in voltage at the positive peak and the voltage at the following negative trough. Distortion product otoacoustic emission input/output functions were collected in each participant at the same four frequencies to assess outer hair cell function. After controlling for individual differences in sex and distortion product otoacoustic emission amplitude, the groups containing participants with higher reported histories of noise exposure had smaller ABR wave I amplitudes at suprathreshold levels across all four frequencies compared with the groups with less history of noise exposure. Suprathreshold ABR wave I amplitudes were reduced in Veterans reporting high levels of military noise exposure and in non Veterans reporting any history of firearm use as compared with Veterans and non Veterans with lower levels of reported noise exposure history. The reduction in ABR wave I amplitude in the groups with higher levels of noise exposure cannot be accounted for by sex or variability in outer hair cell function. This change is similar to the decreased ABR wave I amplitudes observed in animal models of noise-induced cochlear synaptopathy. However, without post mortem examination of the temporal bone, no direct conclusions can be drawn concerning the presence of synaptopathy in the study groups with higher noise exposure histories.

Tinnitus with a normal audiogram: Relation to noise exposure but no evidence for cochlear synaptopathy

In rodents, exposure to high-level noise can destroy synapses between inner hair cells and auditory nerve fibers, without causing hair cell loss or permanent threshold elevation. Such “cochlear synaptopathy” is associated with amplitude reductions in wave I of the auditory brainstem response (ABR) at moderate-to-high sound levels. Similar ABR results have been reported in humans with tinnitus and normal audiometric thresholds, leading to the suggestion that tinnitus in these cases might be a consequence of synaptopathy. However, the ABR is an indirect measure of synaptopathy and it is unclear whether the results in humans reflect the same mechanisms demonstrated in rodents. Measures of noise exposure were not obtained in the human studies, and high frequency audiometric loss may have impacted ABR amplitudes. To clarify the role of cochlear synaptopathy in tinnitus with a normal audiogram, we recorded ABRs, envelope following responses (EFRs), and noise exposure histories in young adults with tinnitus and matched controls. Tinnitus was associated with significantly greater lifetime noise exposure, despite close matching for age, sex, and audiometric thresholds up to 14 kHz. However, tinnitus was not associated with reduced ABR wave I amplitude, nor with significant effects on EFR measures of synaptopathy. These electrophysiological measures were also uncorrelated with lifetime noise exposure, providing no evidence of noise-induced synaptopathy in this cohort, despite a wide range of exposures. In young adults with normal audiograms, tinnitus may be related not to cochlear synaptopathy but to other effects of noise exposure.

Tinnitus and leisure noise

Objective: To study the relationship of life-time noise exposure and experience of tinnitus. Design: Audiometric measures included otoscopy, pure tone air- and bone-conduction hearing threshold levels (HTL) and otoacoustic emissions (OAEs). Participants completed questionnaires including demographic information, past hearing health, history of participation in loud leisure activities, and attitudes to noise. Study sample: A representative sample (1435) of the young (11–35 years old) Australian population. Results: Of the sample, 63% indicated they experienced tinnitus in some form. There was no correlation of tinnitus experience with HTL or OAE amplitudes. Although median octave band HTLs for those who experienced tinnitus “all the time” were slightly higher for those who did not, neither group exhibited HTLs outside clinically-normal values. Of those who experienced tinnitus a direct correlation was found between frequency of experience of tinnitus and increasing cumulative, life-time noise exposure. Those who experienced tinnitus were more likely to report noticing deterioration in their hearing ability over time and to report difficulty hearing in quiet and/or noisy situations. Conclusions: Experience of tinnitus was found throughout this young population but not associated with HTLs or variation in OAE amplitudes. Males experienced ‘permanent’ tinnitus at significantly greater rate than females.

Long‐term self‐reported exposure to occupational noise is associated with BMI‐defined obesity in the US general population

Evidence is emerging about the risk of obesity associated with traffic noise. The present study aimed to explore the association between self-reported occupational noise exposure and body mass index (BMI)-defined obesity in the US general population. This study is based on the 2014 National Health Interview Survey. Information regarding self-reported occupational lifetime noise exposure was linked to self-reported BMI, adjusting for other covariates. The multivariate models yielded OR = 1.46 (95% CI: 1.27, 1.68) for obesity, and 0.97 kg/m2 (95% CI: 0.57, 1.36) higher BMI among participants exposed to high level of noise for ≥15 years, in comparison to never exposed participants. Moderation analysis revealed that among those less than 55 years of age noise had significantly stronger adverse effect. Those without cancer and diabetes also experienced stronger adverse effect. Self-reported exposure to occupational noise was associated with increased odds of obesity and continuously measured BMI. Am. J. Ind. Med. 59:1009-1019, 2016. © 2016 Wiley Periodicals, Inc.

Comparison of two dose-response relationship of noise exposure evaluation results with high frequency hearing loss.

Background:Complex noise and its relation to hearing loss are difficult to measure and evaluate. In complex noise measurement, individual exposure results may not accurately represent lifetime noise exposure. Thus, the mean LAeq,8 h values of individuals in the same workgroup were also used to represent LAeq,8 h in our study. Our study aimed to explore whether the mean exposure levels of workers in the same workgroup represented real noise exposure better than individual exposure levels did.Methods:A cross-sectional study was conducted to establish a model for cumulative noise exposure (CNE) and hearing loss in 205 occupational noise-exposed workers who were recruited from two large automobile manufacturers in China. We used a personal noise dosimeter and a questionnaire to determine the workers’ occupational noise exposure levels and exposure times, respectively. A qualified audiologist used standardized audiometric procedures to assess hearing acuity after at least 16 h of noise avoidance.Results:We observed that 88.3% of workers were exposed to more than 85 dB(A) of occupational noise (mean: 89.3 ± 4.2 dB(A)). The personal CNE (CNEp) and workgroup CNE (CNEg) were 100.5 ± 4.7 dB(A) and 100.5 ± 2.9 dB(A), respectively. In the binary logistic regression analysis, we established a regression model with high-frequency hearing loss as the dependent variable and CNE as the independent variable. The Wald value was 5.014 with CNEp as the independent variable and 8.653 with CNEg as the independent variable. Furthermore, we found that the figure for CNEg was more similar to the stationary noise reference than CNEp was. The CNEg model was better than the CNEp model. In this circumstance, we can measure some subjects instead of the whole workgroup and save manpower.Conclusions:In a complex noise environment, the measurements of average noise exposure level of the workgroup can improve the accuracy and save manpower.

Pure tone hearing thresholds and leisure noise: Is there a relationship?

This paper reports on the examination of the relationship between self-reported historical noise exposure during leisure activities and audiological indicators: Measured hearing threshold levels (HTLs) and otoacoustic emissions (OAEs). The research was conducted by a cross-sectional survey of 1,432 individuals whose ages ranged from 11 years to 35 years. Methodology included a comprehensive audiometric assessment including otoscopy, pure tone audiometry (PTA) (air- and bone-conduction), OAEs, and tympanometry. A comprehensive questionnaire gathered information on demographics, hearing health status, and participation in work, nonwork, and leisure activities. Using the history of work, nonwork, and leisure noise exposure, a cumulative lifetime noise exposure was estimated. No correlation was found between cumulative lifetime noise exposure and audiometric PTA or OAE parameters.

Task-Based Noise Exposures for Farmers Involved in Grain Production

Few studies have been done examining noise exposures associated with agricultural tasks. This study was conducted to address that research gap by calculating the noise exposures for tasks and equipment associated with grain production and assessing the variability in those exposures. An additional aim of this study was to identify tasks and equipment that could be targeted for intervention strategies as a means toward reducing the total noise exposures of farmers and farm workers. Through the use of personal noise dosimetry and direct observation, over 30,000 one-minute noise exposure measurements and corresponding task and equipment data were collected on 18 farms and compiled into a task-based noise exposure database. Mean noise exposures were calculated for 23 tasks and 18 pieces of equipment. The noise exposures for the tasks and equipment ranged from 78.6 to 99.9 dBA and from 80.8 to 96.2 dBA, respectively, with most of the noise exposures having a large standard deviation and maximum noise exposure level. Most of the variability in the task and equipment noise exposures was attributable to within-farm variations (e.g., work practices, distance from noise sources). Comparisons of the mean noise exposures for the agricultural tasks and equipment revealed that most were not statistically different. Grain production tasks and equipment with high mean noise exposures were identified. However the substantial variability in the noise exposures and the occurrence of intense noise measurements for nearly every task and piece of equipment indicate that targeting a few specific tasks or equipment for intervention strategies would reduce lifetime noise exposure but would not completely eliminate exposure to hazardous noise levels.

Relationship Between Styrene Exposure and Hearing Loss: Review of Human Studies

Styrene is an aromatic solvent belonging to the alkylbenzene family. Occupational exposure to styrene occurs mainly in the manufacturing of fiberglass-reinforced polyester products, e.g. reinforced plastics and composites. Since 1988, nine studies have been published on the relationship between occupational exposure to styrene and hearing loss. All studies were the cross-sectional epidemiological studies or clinical studies from occupational health clinics. A total of more than 1000 workers exposed to styrene, both with and without concurrent noise exposure, were examined using different outcome measures for hearing loss. Exposure assessment was usually based on styrene measurements in the breathing zone during several hours of one working day. Some of the studies employed also the biological monitoring of styrene exposure based on determination of its urinary metabolites. The current exposures to styrene varied between 2 and 35 ppm. In some studies, lifetime exposure was calculated using company records and questionnaire data. The current exposure to noise was estimated by noise dosimetry or standard noise measurements. Lifetime noise exposure was assessed using questionnaire data and occupational noise estimates. In many studies, noise-exposed groups were used as controls together with the unexposed workers. Of the nine studies, seven show some effects on the auditory system that were associated with styrene-alone exposure. These effects are examined using different outcome measures such as pure tone audiometry, high frequency hearing loss, and central hearing tests. In some studies, an increased risk for hearing loss was associated with exposure estimates.

The association of noise sensitivity with coronary heart and cardiovascular mortality among Finnish adults

The association of coronary heart and cardiovascular mortality with noise sensitivity was studied. We also investigated how this association is affected by self-reported lifetime noise exposure. In 1988 a case-control study, based on the Finnish Twin Cohort, was carried out to investigate the relationship between noise and hypertension (n=1495). Potential confounders were obtained from questionnaire in 1981 for the same individuals. Data on deaths and causes of death were obtained from record linkage to the nationwide register of death certificates. All deaths that occurred among the study population during the 15 years of follow-up were classified as being due to all causes (n=382), to cardiovascular diseases (n=193), including the number of deaths due to coronary heart diseases (n=111) and to other causes than cardiovascular diseases (n=189). Cardiovascular mortality (Hazard ratio 1.80, 95% CI 1.07-3.04) was significantly increased among noise-sensitive women. Among men, there were no statistically significant effects. Noise sensitivity may be a risk factor for cardiovascular mortality in women.

Somatic and Psychological Characteristics of Noise-Sensitive Adults in Finland

The authors examined the relationship of noise sensitivity with health status and psychological factors in individuals <70 yr of age in Finland. Subjects (n = 1,355) were selected from a 1988 case-control study, based on the Finnish Twin Cohort, that assessed noise sensitivity, lifetime noise exposure, and hypertension. Other health status and psychological factors were obtained from a questionnaire that had been administered to the same individuals in 1981. Statistical analysis showed that noise sensitivity was associated significantly with hypertension, emphysema, use of psychotropic drugs (i.e., sleeping pills, tranquilizers, and pain relievers), stress, smoking, and hostility, even after adjustment for lifetime noise exposure. These results indicate that noise sensitivity has both psychological and somatogenic components.

Effects of coexposure to noise and mixture of organic solvents on hearing in dockyard workers.

Questionnaire and audiometric data of 701 dockyard workers (517 noise and organic solvent mixture-exposed and 184 noise-only-exposed) were referred to 205 control subjects not exposed to either noise or solvents. The odds ratio (OR) of hearing loss was significantly increased by approximately 3 times in the noise-only group and by almost 5 times in the noise and solvent group. A moderate effect of solvent ototoxicity, in addition to noise, was observed on hearing threshold at a frequency 8 kHz. ORs for hearing loss were 1.12 for each increment of 1 year of age, 1.07 for every decibel of lifetime noise exposure (dB-A), and 1.004 for each increment of the index of lifetime exposure to solvents. The results suggest an additive damaging effect of coexposure to noise and organic solvents to the auditory organ.