Noise-exposed Groups Research Articles

Association of dietary factors with noise-induced hearing loss in Korean population: A 3-year national cohort study.

Noise-induced hearing loss (NIHL) is a hearing impairment (HI) caused by various clinical factors. Identifying the relationship between NIHL and nutrient consumption could help in reducing the prevalence of hearing loss. The aim of this study was to analyze the relationship between NIHL and dietary factors using data of the Korea National Health and Nutrition Examination survey (KNHANES). The data were collected from The Fifth KNHANES 2010-2012. The survey was taken by a total of 10,850 participants aged 20-65 years. Air conduction audiometry was measured at 500, 1000, 2000, and 4000 Hz in both ears. Metabolic syndrome, noise exposure, alcohol consumption, smoking, income level, marital status, and nutritional intake were evaluated. The differences between non-HI and HI participants in the noise-exposed group showed statistically significant differences in age, sex, marital and smoking status, alcohol consumption, and fasting glucose and triglyceride levels (p<0.05). In a multiple regression analysis of the noise-exposed group, age showed a significant association with HI (OR: 0.604; 95% CI: 0.538-0.678) after adjusting for confounders. In multivariate analysis for dietary factors affecting HI in noise-exposed groups, retinol (OR: 1.356; 95% CI: 1.068-1.722), niacin (OR: 1.5; 95% CI: 1.022-2.201), and carbohydrates (OR: 0.692; 95% CI: 0.486-0.985) showed a significant association with NIHL. Age was identified as the only factor significantly affecting NIHL. When the dietary factors of the noise-exposed group were analyzed, high intake of niacin and retinol and low intake of carbohydrates appeared to reduce the risk of hearing loss.

Protective effects of nanocurcumin against stress-induced deterioration in the intestine

The therapeutic activities of curcumin have long been investigated in some chronic and inflammatory diseases. This study was designed to investigate the protective effects of nanocurcumin on intestinal barrier function, apoptosis, and oxidative stress in rats exposed to traffic noise. Forty rats were divided into four groups: two traffic noise-exposed groups of animals that received either vehicle (NOISE) or nanocurcumin (NCUR + NOISE) and two control groups that either remained intact (CON) or received nanocurcumin (NCUR). Nanocurcumin injection (15 mg/Kg/ip) and traffic noise exposure were administered daily for two weeks. The relative protein expression of intestinal tight junctions, occludin, and ZO-1 and Bax/Bcl-2 ratio was measured to evaluate barrier integrity and apoptosis in intestinal samples, respectively. Plasma D-lactate concentration was examined as a criterion of intestinal permeability. Corticosterone, superoxide dismutase (SOD) activity, glutathione (GSH), total antioxidant capacity (TAC), and nitrite were measured in serum. The noise exposure increased Bax/Bcl-2 ratio, corticosterone, and oxidative stress in the NOISE animals. Nanocurcumin treatment improved the Bax/Bcl-2 ratio and reduced corticosterone and oxidative stress in the NCUR + NOISE animals. The expression of tight junction proteins was decreased while the concentration of D-lactate was increased in the NOISE animals. Nanocurcumin did not efficiently impact the expression of tight junction proteins and the D-lactate level in the NCUR + NOISE group. Nanocurcumin administration displayed antioxidant and anti-apoptotic roles in the noise-exposed rats, however, it did not affect the intestinal barrier integrity. We concluded that reduced apoptosis in the intestine might be related to the antioxidant activity of nanocurcumin and its modulatory effects on the HPA axis in the nanocurcumin-treated animals.

Does Exposure of Lead and Cadmium Affect the Endometriosis?

This study aimed to investigate the effects of blood lead levels (BLLs) and lead and cadmium exposure on endometriosis (EM). The study cohort consisted of female workers who underwent a lead-associated special medical examination between 1 January 2000 and 31 December 2004 (n = 26,542). The standard admission rate (SAR) and admission odds ratio (OR) for EM were calculated using the general population and noise-exposed groups, respectively, for the same period as the reference standards. The SAR for EM was 1.24 (95% confidence interval (CI): 1.03–1.48) in lead-exposed workers and 1.44 (95% CI: 1.11–1.85) in workers with BLLs < 5 μg/dL when compared with that of the general population. Admission ORs of EM in lead-exposed workers and those with BLLs < 5 μg/dL were statistically higher than those of noise-exposed workers (OR, 1.40; 95% CI, 1.15–1.70 and OR, 1.48; 95% CI, 1.11–1.98, respectively). The relative excess risk due to interaction of lead and cadmium was 0.33. Lead exposure was associated with EM admission. EM admission in lead-exposed workers with BLLs < 5 μg/dL was statistically higher than that of the general population and noise-exposed workers. Co-exposure to lead and cadmium has a synergistic effect with EM.

Alpha2-Adrenoblockers Regulate Development of Oxidative Stress and Cognitive Behaviour of Rats under Chronic Acoustic Stress Conditions.

Noise is a wide-spread stress factor in modern life produced by urbanization, traffic, and an industrialized environment. Noise stress causes dysfunction and neurotransmission impairment in the central nervous system, as well as changes in hormone levels. In this study, we have examined the level of α-Tocopherol (α-T) and malondialdehyde (MDA) in plasma and the erythrocytes’ membrane (EM), as well as the behavioral characteristics of a noise-induced stress model in rats. In addition, the modulating effect of α2-adrenoblockers, beditin, and mesedin on the aforementioned parameters has been investigated. For these purposes, albino male rats were divided into four groups: (1) untreated; (2) noise-exposed, (3) noise-exposed and beditin-treated (2 mg/kg, i.p.), and (4) noise-exposed and mesedin-treated (10 mg/kg, i.p.) animals. Noise-exposed groups were treated with 91dBA noise on 60 days with a daily duration of 8 h. Increased MDA and decreased α-T levels in plasma and EM were observed upon chronic high-level noise exposure. Locomotor and behavioral activity assessed with a Y-maze revealed disorientation and increased anxiety under chronic noise exposure. Prominently, α2-adrenoblockers alleviated both behavioral deficits and oxidative stress, providing evidence for the involvement of α2-adrenoceptor in the pathophysiology of noise-induced stress.

Noise-Induced Vascular Dysfunction, Oxidative Stress, and Inflammation Are Improved by Pharmacological Modulation of the NRF2/HO-1 Axis.

Vascular oxidative stress, inflammation, and subsequent endothelial dysfunction are consequences of traditional cardiovascular risk factors, all of which contribute to cardiovascular disease. Environmental stressors, such as traffic noise and air pollution, may also facilitate the development and progression of cardiovascular and metabolic diseases. In our previous studies, we investigated the influence of aircraft noise exposure on molecular mechanisms, identifying oxidative stress and inflammation as central players in mediating vascular function. The present study investigates the role of heme oxygenase-1 (HO-1) as an antioxidant response preventing vascular consequences following exposure to aircraft noise. C57BL/6J mice were treated with the HO-1 inducer hemin (25 mg/kg i.p.) or the NRF2 activator dimethyl fumarate (DMF, 20 mg/kg p.o.). During therapy, the animals were exposed to noise at a maximum sound pressure level of 85 dB(A) and a mean sound pressure level of 72 dB(A). Our data showed a marked protective effect of both treatments on animals exposed to noise for 4 days by normalization of arterial hypertension and vascular dysfunction in the noise-exposed groups. We observed a partial normalization of noise-triggered oxidative stress and inflammation by hemin and DMF therapy, which was associated with HO-1 induction. The present study identifies possible new targets for the mitigation of the adverse health effects caused by environmental noise exposure. Since natural dietary constituents can achieve HO-1 and NRF2 induction, these pathways represent promising targets for preventive measures.

Neuroanatomical changes of the medial prefrontal cortex of male pups of Wistar rat after prenatal and postnatal noise stress

Recent evidences showed that, noise stress causes abnormal changes in structure and function of central nervous system (CNS). The Current study was conducted to evaluate some stereological parameters of the medial prefrontal cortex (mPFC) of male pups of Wistar rat after prenatal and early postnatal noise stress. 18 pregnant Wistar rats were randomly divided into prenatal noise-exposed (NE) group, postnatal NE group, and controls. Male pups of NE groups were exposed to noise 100 dB at the frequency ranges of 500–8000 Hz, 4 h per day from gestational day one (GD1) to GD21 for the prenatal NE group, and from postnatal day one (PND1) to PND21 in the postnatal NE group. The Control group animals were maintained under standard condition without noise stimulation. Corticosterone level in plasma was measured using ELISA technique. Changes of the neurons and non-neurons cells number and volume of the mPFC were evaluated by stereological analysis. Tunnel assay was also used for detection of apoptotic cells. Increase in plasma corticosterone level, decrease in the number of neurons, and increase in the apoptotic cells number were observed in both NE groups. Decrease in volume of mPFC and also in non-neurons cells number was observed in the prenatal NE group. An increase in the non-neurons number was seen in the postnatal NE group. Data of the current comparative study showed that, noise stress during prenatal and early postnatal periods can induce the abnormal alteration in some stereological parameters of mPFC in male pups of Wistar rat. These negative alterations were more remarkable after prenatal noise stress.

Adverse effects of noise stress on glucose homeostasis and insulin resistance in Sprague-Dawley rats

Noise pollution remains a pervasive health hazard that people encounter especially in large commercial metropolis and has been implicated in many adverse non-auditory health conditions such as hypertension, atherosclerosis, vascular (endothelial) dysfunction and metabolic disorders. There is a growing body of evidence showing that chronic noise exposure is associated with an increased risk of hypercholesterol, adiposity and development of type 2 diabetes. The present study investigated the effect of noise stress on parameters of glucose homeostasis in male rats and possible recovery after noise cessation. Twenty-four (24) adult male Sprague-Dawley rats were designated into four groups (n = 6 per group). All rats except the control group were exposed to 95dB noise using a noise generator for 28 consecutive days. A group of rats was investigated immediately after 28 days of noise exposure (NE28), while others were left to recover from noise stress for 7 days (NER7) or 14 days (NER14). OGTT and ITT were performed using standard methods. Plasma levels of triglyceride (TRIG), total cholesterol (CHOL), low density lipoprotein (LDL) and high-density lipoprotein (HDL) were determined. Serum level of insulin, corticosterone (CORT) and corticosterone-releasing-factor (CRF) were determined using ELISA. Homeostasis model assessment-insulin resistance (HOMA-IR) and glycogen content in liver as well as gastrocnemius muscle were also determined.Although glucose tolerance remained unchanged in the noise-exposed groups, insulin sensitivity was however significantly reduced compared with control. There was significant increase (P < 0.05) in the level of CHOL, LDL and HDL. Noise also increased (P < 0.05) both insulin and CORT levels; and elicited a higher HOMA-IR index in NE28 rats. Hepatic and myocytic glycogen content were lower (P < 0.05) in NE28 rats relative to control. The reported changes above were reversed following a 14-day noise withdrawal period. Noise-induced insulin resistance may result from dysregulation of the stress axis and appears to be reversible with noise cessation.

Exposure of Developing Male Rats to One or Multiple Noise Sessions and Different Housing Conditions: Hippocampal Thioredoxin Changes and Behavioral Alterations.

Exposure of developing rats to noise has shown to induce hippocampal-related behavioral alterations that were prevented after a week of housing in an enriched environment. However, neither the effect of repeated exposures nor its impact on key endogenous antioxidants had been studied yet. Thus, the aim of the present work was to reveal novel data about hippocampal oxidative state through the measurement of possible age-related differences in the levels of hippocampal thioredoxins in rats exposed to noise at different developmental ages and subjected to different schemes and housing conditions. In addition, the possibility that oxidative changes could underlie hippocampal-related behavioral changes was also analyzed. Developing male Wistar rats were exposed to noise for 2 h, either once or for 5 days. Upon weaning, some animals were transferred to an enriched cage for 1 week, whereas others were kept in standard cages. One week later, auditory and behavioral assessments, as well as measurement of hippocampal thioredoxin, were performed. Whereas no changes in the auditory function were observed, significant behavioral differences were found, that varied according to the age, scheme of exposure and housing condition. In addition, a significant increase in Trx-1 levels was found in all noise-exposed groups housed in standard cages. Housing animals in an enriched environment for 1 week was effective in preventing most of these changes. These findings suggest that animals become less susceptible to undergo behavioral alterations after repeated exposure to an environmental challenge, probably due to the ability of adaptation to an unfavorable condition. Moreover, it could be hypothesized that damage to younger individuals could be more easily prevented by a housing manipulation.

CLINICAL AND AUDIOLOGICAL VALUES IN THE EARLY DIAGNOSIS OF HEARING IMPAIRMENTS AND RISK GROUPS AMONG SHIP REPAIR WORKERS

Introduction: The hazardous effect of industrial noise exposure on ship repair workers has been highlighted in a number of studies. However, no data are currently available for studying the effect of noise exposure on the auditory system and general health of ship repair workers. The aim: The study is focused on the early diagnosis of hearing impairments and identifying risk groups among the workers. Materials and methods: It was examined two groups of workers of approximately the same age and length of employment. The Group 1 included workers from the Azov Shiprepair Yard (Mariupol city, Ukraine) who were exposed to workplace noise impact of less than 80 dBA threshold level, the workplace noise level in the Group 2 was above 80 dBA. Audiometric testing was conducted in a sound-treated room using the MA 31 clinical audiometer (Germany). Results: Our findings indicate that all the noise-exposed groups of ship repair workers should be conducted audiometric testing. The hearing levels at the audiometric test frequencies of 4, 6 and 8 kHz, as well as differential thresholds at the audiometric test frequencies of 4 kHz by the Luscher-Zwislocki method should be taken into account. Such complaints as increased annoyance, sleep disorder, tinnitus aurium, hypertension should be considered as most hazardous. Conclusions: We recommend that the ship repair workers undergo routine medical check-ups and systematic prophylactic observation. All these preventive measures will contribute to the early detection of hearing impairments, thereby timely preventing the development and progression of occupational sensorineural hearing loss.

Prevalence of hypertension and noise-induced hearing loss in Chinese coal miners.

Owing to inconsistent epidemiologic evidence and the presence of confounding factors, the relation between occupational noise exposure and hypertension still remained unclear. We aimed to assess whether Chinese coal miners were at risk of developing hypertension and noise induced hearing loss (NIHL), and whether occupational noise exposure was a risk factor of hypertension. A questionnaire was designed to collect information from 738 study participants, all of whom were employees from the Datun Xuzhou Coal Company. The participants were divided into a noise-exposed group and a control group based on the noise level to which they were exposed in the workplace. The differences in the mean of systolic blood pressure (SBP) and diastolic blood pressure (DBP) were compared between the noise-exposed and control groups. Also the prevalence and age-adjusted odds ratio (OR) [95% confidence intervals (CIs)] of audiometric deficit and hypertension was compared in the study. Binary logistic regression was used to assess the relation between occupational noise level and hypertension while controlling for potential confounding factors. Hypertension was more prevalent in noise-exposed group than the control group, 29.2% vs. 21.2% (P=0.012). The noise-exposed group faced an increased risk of hypertension (age-adjusted OR =1.52, 95% CI =1.07-2.15) when the control group was used as reference. The mean values of SBP and DBP of the noise-exposed groups were significantly higher than the control group (P=0.006 and P=0.002 respectively). Hearing loss at low frequencies was significantly more prevalent in the noise-exposed group than the control group, 12.8% vs. 7.4% (P=0.015), while the noise-exposed group faced the increased risk of hearing loss at low frequencies (age-adjusted OR =1.81, 95% CI =1.10-2.96). LEX, 8h (OR =1.036, 95% CI =1.012-1.060) was an independent risk of hypertension when controlling for potential confounding factors. We found that the occupational noise had an effect on the hypertension and hearing loss of Chinese coal miners. And the occupational noise was an independent risk factor for hypertension and could increase the values of SBP and DBP.

Noise-induced damage to ribbon synapses without permanent threshold shifts in neonatal mice

Recently, ribbon synapses to the hair cells (HCs) in the cochlea have become a novel site of interest in the investigation of noise-induced cochlear lesions in adult rodents (Kujawa and Liberman, 2009; Lin et al., 2011; Liu et al., 2012; Shi et al., 2013). Permanent noise-induced damage to this type of synapse can result in subsequent degeneration of spiral ganglion neurons (SGNs) in the absence of permanent changes to hearing sensitivity. To verify whether noise exposure during an early developmental period produces a similar impact on ribbon synapses, the present study examined the damaging effects of noise exposure in neonatal Kunming mice. The animals received exposure to broadband noise at 105-decibel (dB) sound pressure level (SPL) for 2h on either postnatal day 10 (P10d) or postnatal day 14 (P14d), and then hearing function (based on the auditory brainstem response (ABR)) and cochlear morphology were evaluated during either postnatal weeks 3–4 (P4w) or postnatal weeks 7–8 (P8w). There were no significant differences in the hearing threshold between noise-exposed and control animals, which suggests that noise did not cause permanent loss of hearing sensitivity. However, noise exposure did produce a significant loss of ribbon synapses, particularly in P14d mice, which continued to increase from P4w to P8w. Additionally, a corresponding reduction in the amplitude of compound action potential (CAP) was observed in the noise-exposed groups at P4w and P8w, and the CAP latency was elongated, indicating a change in synaptic function.

Therapeutic Effect of Dexamethasone for Noise-induced Hearing Loss: Systemic Versus Intratympanic Injection in Mice.

Dexamethasone is commonly used clinically to treat noise-induced hearing loss (NIHL) because the drug exerts multiple anti-inflammatory effects. In the present study, we investigated the post-noise therapeutic effects of dexamethasone given systemically or via intratympanic injection in the mouse. Twenty-four C57BL/6J mice were used. Eighteen experimental mice were exposed to 110 dB sound pressure level white noise and then divided into three groups: the noise, intraperitoneal dexamethasone injection (IP), and intratympanic dexamethasone injection (IT) groups. Dexamethasone (3 mg/kg/d) was injected intraperitoneally for five successive days in the IP group. Intratympanic injections were given on post-noise days 1 and 4 in the IT group. We compared hearing levels, the architecture of the organ of Corti (OC), and the microscopic appearance of the medial olivocochlear efferent terminals (MOC ETs) among the groups. Both the IP and IT groups exhibited hearing recovery as revealed by auditory brainstem responses (ABRs), but recovery was not apparent in distortion product otoacoustic emissions (DPOAEs). OC degeneration as revealed by light microscopy was most extensive in the noise group and least extensive in the IP group. Scanning electron microscopy showed that the OC ultrastructure was better preserved in the IP than the IT group. Confocal microscopy showed that the ETs were shrunken in all noise-exposed groups as compared to the control group, but more shrunken in the dexamethasone-treated groups. Transmission electron microscopy showed that the MOC ET-outer hair cell (OHC) synapses were damaged in all noise-exposed groups, but the extent of degeneration was less in the IT than in the noise group. Dexamethasone exerts reliable therapeutic effects when used to treat NIHL. It seems that the protective effects may differ by the routes of administration as the OCs were better preserved in the IP group and the ET-OHC synapses were more intact in the IT group.

Noise and age-related hearing loss: A study of 40 123 gold miners in South Africa

Objective and design: This retrospective cohort study aimed to describe the differential effect of noise exposure and age-related hearing loss in a large sample of gold miners in South Africa. Study sample: Audiological data of 40 123 South African mine workers were investigated. Data of a non-noise-exposed control group (n = 6162) and group exposed to underground noise (≥ 85 dB A (TWA) (n = 33 961) were included. Within these two larger noise-exposed groups two homogenous exposure groups (HEG) were also selected for analyses, namely the driller group (n = 4399) and the administration group (administrative workers) (n = 2211). Participants were categorized in terms of noise exposure, age, and race. Results: Significantly different thresholds (worse for underground noise group) with respect to the median for all frequencies after adjusting for age was evident between the noise-exposed and control groups (ANCOVA). The largest differences in hearing thresholds between the noise-exposed and control groups were observed at 3 and 4 kHz in the age group 36 to 45 years. Administration and driller group differed significantly (driller group worse results) with respect to the mean LFA512 and HFA346 after adjusting for age (ANCOVA). Black males had significantly better high-frequency hearing compared with white male counterparts but significantly worse low-frequency hearing. Conclusion: Age was the most important influence on hearing thresholds for the noise and control groups. Race was shown to be a very significant factor determining susceptibility to NIHL and ARHL.

WDR1 expression in normal and noise-damaged Sprague-Dawley rat cochleae

WD40 repeat protein 1 (WDR1) has been suggested as a protective mechanism or a sign of regeneration in avian cochlea. However, its role in mammalian cochlea has yet to be determined. Hence, we investigated WDR1 expression in sound-overstimulated Sprague-Dawley rats. Rats were divided into three groups (the permanent and temporary threshold shift [PTS and TTS] groups and the control group) according to the extent of noise exposure and euthanized immediately, 3, or 7 days after noise exposure for cochlear harvest. Immunocytochemistry localized WDR1 to outer hair cells, Deiter's cells, outer sulcus cells, and Reissner's membrane in the control group, and the PTS and TTS groups exhibited stronger WDR1 expression in the same cochlear regions than the controls. Moreover, WDR1 expression in these noise-exposed groups was extended to inner hair cells and basal cells of the stria vascularis. The expression of WDR1 in the PTS and TTS groups showed differences in intensity and shifts of localization, based on exposure length and recovery duration. Contrary to the avian cochlea, hair cell regeneration does not naturally occur in the acoustically damaged mammalian cochlea. Therefore, elevated WDR1 expression after acoustic overstimulation in the current experiments may provide a mechanism for protection against noise exposure.

Increased activity of mitochondrial respiratory chain complex in noise-damaged rat cochlea

Conclusion: Functional changes of mitochondrial respiratory chain (MRC) and hearing threshold shifts were observed after noise exposure and the pattern was different depending on the extent of the noise damage. Objectives: The aim of this study was to reveal any functional changes of the MRC enzyme in outer hair cells after noise damage. Methods: Sprague-Dawley rats were used and divided into three groups including normal control group and noise exposure for 1 h and 5 h. White band noise was used with 120 dB SPL. We measured hearing threshold and activity of succinate dehydrogenase (SDH) before noise exposure, and immediately and 1, 3, 7, and 14 days after noise exposure in each group. Immunostaining using monoclonal anti-MRC complex V subunit α was performed. Transmission electron microscopy (TEM) was carried out. Results: The hearing threshold level changed depending on the exposure time in both the noise-exposed groups. In the 1 h group, hearing was improved after 1 day, and in the 5 h group, hearing was measured after 7 days. Changes in SDH activity were observed at the third day in the 1 h group and at the seventh day in the 5 h group. The expression level of MRC complex V was increased after noise exposure. TEM showed mitochondrial damage.

Epidemiological and clinical study of subjects occupationally exposed to noise

The role of occupational exposure to noise as a cardiovascular risk factor has not been established sufficiently. The present study investigated the blood pressure (BP) and electrocardiographic (ECG) changes in subjects exposed to different degrees of noise. The first group, comprising 105 males with a mean working life of 20.9 years, was occupationally exposed to mean 93 db(A). The second group, comprising 311 subjects, with a mean working life of 20.2 years, was occupationally exposed to a lower level of noise (15% on average). A control group included 150 clerical workers with a mean working life of 19.7 years not exposed to noise at work. The prevalence of hypertension in differences are statistically significant (p <0.02). The prevalence of orthostatic hypotension was significantly higher in the noise-exposed groups than in the controls (p<0.05). The incidence of electrocardiographic abnormalities in the three groups was 21.9%, 10.9%, and 7.9%, respectively, (p<0.01). These data demonstrate that subjects occupationally exposed to noise are at higher risk for developing certain cardiovascular disorders. The noise-related risk correlates with the intensity of noise and the duration of exposure.

Application of the Kurtosis Statistic to the Evaluation of the Risk of Hearing Loss in Workers Exposed to High-Level Complex Noise

Develop dose-response relations for two groups of industrial workers exposed to Gaussian or non-Gaussian (complex) types of continuous noises and to investigate what role, if any, the kurtosis statistic can play in the evaluation of industrial noise-induced hearing loss (NIHL). Audiometric and noise exposure data were acquired on a population (N = 195) of screened workers from a textile manufacturing plant and a metal fabrication facility located in Henan province of China. Thirty-two of the subjects were exposed to non-Gaussian (non-G) noise and 163 were exposed to a Gaussian (G) continuous noise. Each subject was given a general physical and an otologic examination. Hearing threshold levels (0.5-8.0 kHz) were age adjusted (ISI-1999) and the prevalence of NIHL at 3, 4, or 6 kHz was determined. The kurtosis metric, which is sensitive to the peak and temporal characteristics of a noise, was introduced into the calculation of the cumulative noise exposure metric. Using the prevalence of hearing loss and the cumulative noise exposure metric, a dose-response relation for the G and non-G noise-exposed groups was constructed. An analysis of the noise environments in the two plants showed that the noise exposures in the textile plant were of a Gaussian type with an Leq(A)8hr that varied from 96 to 105 dB whereas the exposures in the metal fabrication facility with an Leq(A)8hr = 95 dB were of a non-G type containing high levels (up to 125 dB peak SPL) of impact noise. The kurtosis statistic was used to quantify the deviation of the non-G noise environment from the Gaussian. The dose-response relation for the non-G noise-exposed subjects showed a higher prevalence of hearing loss for a comparable cumulative noise exposure than did the G noise-exposed subjects. By introducing the kurtosis variable into the temporal component of the cumulative noise exposure calculation, the two dose-response curves could be made to overlap, essentially yielding an equivalent noise-induced effect for the two study groups. For the same exposure level, the prevalence of NIHL is greater in workers exposed to non-G noise environments than for workers exposed to G noise. The kurtosis metric may be a reasonable candidate for use in modifying exposure level calculations that are used to estimate the risk of NIHL from any type of noise exposure environment. However, studies involving a large number of workers with well-documented exposures are needed before a relation between a metric such as the kurtosis and the risk of hearing loss can be refined.

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.

Prior Heat Acclimation Confers Protection against Noise-Induced Hearing Loss

Exposure to intense noise stress can cause a permanent noise-induced hearing loss which is thought to be due to elevation of reactive oxygen species in excess of the inherent antioxidant mechanisms of the cell. However, preconditioning to low levels of stress of one type can activate cellular mechanisms leading to the elevation of antioxidant levels so that the cell is then better able to tolerate subsequent severe stress of a different type. This has been called cross-tolerance. Here, we tested this hypothesis by acclimating rats to a moderate heat stress (30 days at 34°C). The rats were exposed to 113 dB SPL noise for 3 days (12 h/day) in three different groups: heat acclimated then noise exposed; noise exposed and then heat acclimated; heat acclimated, then noise exposed and then heat acclimated again. Permanent changes in auditory function – auditory nerve brainstem evoked responses (ABR) and distortion product otoacoustic emissions (DPOAEs) – were evaluated in each of these animals and compared with those in rats exposed to noise only and in control groups of rats. Statistical evaluation of the results showed that when assessed with ABR, each of the heat-acclimated, noise-exposed groups was protected from the noise, even the group that was heat-acclimated after the noise exposure. When assessed with DPOAE, protection was statistically apparent only in the group that was heat acclimated, then exposed to noise, and not in the other groups. Thus, heat acclimation provides protection against permanent noise-induced hearing loss.

The electrochemical and fluorescence detection of nitric oxide in the cochlea and its increase following loud sound

A nitric oxide (NO)-selective sensor (tip diameter 30 μm) was inserted into the perilymph of the basal turn of the guinea pig cochlea. The basal level and stimulation-induced changes of NO were measured. The mean (±S.E.M.) basal level of NO was 273±42.9 nM. Following perilymphatic perfusion of the artificial perilymph containing NO synthase (NOS) substrate L-arginine (100 μM) combined with cofactor (6 R)-5,6,7,8-tetrahydrobiopterin dihydrochloride (100 μM), a rapid and significant increase of NO to a mean concentration of 392±32.3 nM ( P<0.01, n=10) was recorded. In contrast, a significant decrease of mean NO concentration to 180±32.7 nM ( P<0.01, n=10) was observed following the perfusion of the NOS-inhibiting agent N G-nitro- L-arginine methyl ester (100 μM). No change in the NO concentration was found following the perfusion of either artificial perilymph or N G-monomethyl- D-arginine (100 μM) solution employed as controls. Broadband noise exposure (3 h/day at 120 dBA SPL) for three consecutive days produced an increase in NO concentration to 618±60.7 nM ( P<0.05, n=10) in the perilymph. In addition, by using specific dyes for NO, 4,5-diaminofluoresceine diacetate and for the reactive oxygen species (ROS), dihydrorhodamine 1,2,3, the distribution of NO in the whole mounts of the organ of Corti and the production of ROS in vivo in the organ of Corti were investigated in both control ( n=5) and noise-exposed ( n=5) animals. The more intense NO and ROS fluorescence was observed in both the inner and outer hair cells in the noise-exposed groups. It is proposed that both the basal level and the increase in NO concentration following the addition of substrate ( L-arginine) are produced by the constitutive NOS while the elevated NO and ROS following noise exposure indicate that NO may be involved in noise-induced hearing loss.