Noise exposure levels predict blood levels of the inner ear protein prestin.

Serological biomarkers of inner ear proteins are a promising new approach for studying human hearing. Here, we focus on the serological measurement of prestin, a protein integral to a human's highly sensitive hearing, expressed in cochlear outer hair cells (OHCs). Building from recent nonhuman studies that associated noise-induced OHC trauma with reduced serum prestin levels, and studies suggesting subclinical hearing damage in humans regularly engaging in noisy activities, we investigated the relation between serum prestin levels and environmental noise levels in young adults with normal clinical audiograms. We measured prestin protein levels from circulating blood and collected noise level data multiple times over the course of the experiment using body-worn sound recorders. Results indicate that serum prestin levels have a negative relation with noise exposure: individuals with higher routine noise exposure levels tended to have lower prestin levels. Moreover, when grouping participants based on their risk for a clinically-significant noise-induced hearing loss, we found that prestin levels differed significantly between groups, even though behavioral hearing thresholds were similar. We discuss possible interpretations for our findings including whether lower serum levels may reflect subclinical levels of OHC damage, or possibly an adaptive, protective mechanism in which prestin expression is downregulated in response to loud environments.

IGF-1 Haploinsufficiency Causes Age-Related Chronic Cochlear Inflammation and Increases Noise-Induced Hearing Loss.

Insulin-like growth factor 1 (IGF-1) deficiency is an ultrarare syndromic human sensorineural deafness. Accordingly, IGF-1 is essential for the postnatal maturation of the cochlea and the correct wiring of hearing in mice. Less severe decreases in human IGF-1 levels have been associated with other hearing loss rare genetic syndromes, as well as with age-related hearing loss (ARHL). However, the underlying mechanisms linking IGF-1 haploinsufficiency with auditory pathology and ARHL have not been studied. Igf1-heterozygous mice express less Igf1 transcription and have 40% lower IGF-1 serum levels than wild-type mice. Along with ageing, IGF-1 levels decreased concomitantly with the increased expression of inflammatory cytokines, Tgfb1 and Il1b, but there was no associated hearing loss. However, noise exposure of these mice caused increased injury to sensory hair cells and irreversible hearing loss. Concomitantly, there was a significant alteration in the expression ratio of pro- and anti-inflammatory cytokines in Igf1+/- mice. Unbalanced inflammation led to the activation of the stress kinase JNK and the failure to activate AKT. Our data show that IGF-1 haploinsufficiency causes a chronic subclinical proinflammatory age-associated state and, consequently, greater susceptibility to stressors. This work provides the molecular bases to further understand hearing disorders linked to IGF-1 deficiency.

Cochlear Glucocorticoid Receptor and Serum Corticosterone Expression in a Rodent Model of Noise-induced Hearing Loss: Comparison of Timing of Dexamethasone Administration.

Glucocorticoid (GC) is a steroid hormone secreted from the adrenal cortex in response to stress, which acts by binding to cytoplasmic glucocorticoid receptors (GRs). Dexamethasone (DEX) is a synthetic GC exhibiting immunosuppressive effects in both human and rodent models of hearing loss. While clinical evidence has shown the effectiveness of DEX for treatment of various inner ear diseases, its mechanisms of action and the optimal timing of treatment are not well understood. In the present study, intergroup comparisons were conducted based on the time point of treatment with DEX: (1) pretreatment; (2) posttreatment; and (3) pre&post-noise. The pre&post DEX treatment group showed a significant improvement in threshold shift at 1 day post-noise exposure as compared to the TTS (transient threshold shift)-only group at 8 and 16 kHz. Both TTS and PTS (permanent threshold shift) significantly reduced cochlear GR mRNA expression and increased serum corticosterone and cochlear inflammatory cytokines. The pre&post DEX treatment group showed a significant decrease in serum corticosterone level as compared to other DEX treatment groups and TTS-treated group at 3 days after acoustic trauma. Our results suggest that the timing of DEX administration differentially modulates systemic steroid levels, GR expression and cochlear cytokine expression.

Betaine-homocysteine S-methyltransferase deficiency causes increased susceptibility to noise-induced hearing loss associated with plasma hyperhomocysteinemia.

Betaine-homocysteine S-methyltransferases (BHMTs) are methionine cycle enzymes that remethylate homocysteine; hence, their malfunction leads to hyperhomocysteinemia. Epidemiologic and experimental studies have revealed a correlation between hyperhomocysteinemia and hearing loss. Here, we have studied the expression of methionine cycle genes in the mouse cochlea and the impact of knocking out the Bhmt gene in the auditory receptor. We evaluated age-related changes in mouse hearing by recording auditory brainstem responses before and following exposure to noise. Also, we measured cochlear cytoarchitecture, gene expression by RNA-arrays and quantitative RT-PCR, and metabolite levels in liver and plasma by HPLC. Our results indicate that there is an age-dependent strain-specific expression of methionine cycle genes in the mouse cochlea and a further regulation during the response to noise damage. Loss of Bhmt did not cause an evident impact in the hearing acuity of young mice, but it produced higher threshold shifts and poorer recovery following noise challenge. Hearing loss was associated with increased cochlear injury, outer hair cell loss, altered expression of cochlear methionine cycle genes, and hyperhomocysteinemia. Our results suggest that BHMT plays a central role in the homeostasis of cochlear methionine metabolism and that Bhmt2 up-regulation could carry out a compensatory role in cochlear protection against noise injury in the absence of BHMT.-Partearroyo, T., Murillo-Cuesta, S., Vallecillo, N., Bermúdez-Muñoz, J. M., Rodríguez-de la Rosa, L., Mandruzzato, G., Celaya, A. M., Zeisel, S. H., Pajares, M. A., Varela-Moreiras, G., Varela-Nieto, I. Betaine-homocysteine S-methyltransferase deficiency causes increased susceptibility to noise-induced hearing loss associated with plasma hyperhomocysteinemia.

Noise-induced trauma produces a temporal pattern of change in blood levels of the outer hair cell biomarker prestin.

Biomarkers in easy-to-access body fluid compartments, such as blood, are commonly used to assess health of various organ systems in clinical medicine. At present, no such biomarkers are available to inform on the health of the inner ear. Previously, we proposed the outer-hair-cell-specific protein prestin, as a possible biomarker and provided proof of concept in noise- and cisplatin-induced hearing loss. Our ototoxicity data suggest that circulatory prestin changes after inner ear injury are not static and that there is a temporal pattern of change that needs to be further characterized before practical information can be extracted. To achieve this goal, we set out to 1) describe the time course of change in prestin after intense noise exposure, and 2) determine if the temporal patterns and prestin levels are sensitive to severity of injury. After assessing auditory brainstem thresholds and distortion product otoacoustic emission levels, rats were exposed to intense octave band noise for 2 h at either 110 or 120 dB SPL. Auditory function was re-assessed 1 and 14 days later. Blood samples were collected at baseline, 4, 24, 48, 72 h and 7 and 14 days post exposure and prestin concentrations were measured using enzyme-linked immunosorbent assay (ELISA). Functional measures showed temporary hearing loss 1 day after exposure in the 110 dB SPL group, but permanent loss through Day 14 in the 120 dB SPL group. Prestin levels temporarily increased 5% at 4 h after 120 dB SPL exposure, but not in the 110 dB SPL group. There was a gradual decline in prestin levels in both groups thereafter, with prestin being below baseline on Day 14 by 5% in the 110 dB group (NS) and more than 10% in the 120 dB SPL group (p = 0.043). These results suggest that there is a temporal pattern of change in serum prestin level after noise-induced hearing loss that is related to severity of hearing loss. Circulatory levels of prestin may be able to act as surrogate biomarker for hearing loss involving OHC loss.

Analysis of serum microRNA expression in male workers with occupational noise-induced hearing loss.

Occupational noise-induced hearing loss (ONIHL) is a prevalent occupational disorder that impairs auditory function in workers exposed to prolonged noise. However, serum microRNA expression in ONIHL subjects has not yet been studied. We aimed to compare the serum microRNA expression profiles in male workers of ONIHL subjects and controls. MicroRNA microarray analysis revealed that four serum microRNAs were differentially expressed between controls (n=3) and ONIHL subjects (n=3). Among these microRNAs, three were upregulated (hsa-miR-3162-5p, hsa-miR-4484, hsa-miR-1229-5p) and one was downregulated (hsa-miR-4652-3p) in the ONIHL group (fold change >1.5 and Pbon value <0.05). Real time quantitative PCR was conducted for validation of the microRNA expression. Significantly increased serum levels of miR-1229-5p were found in ONIHL subjects compared to controls (n=10 for each group; P<0.05). A total of 659 (27.0%) genes were predicted as the target genes of miR-1229-5p. These genes were involved in various pathways, such as mitogen-activated protein kinase (MAPK) signaling pathway. Overexpression of miR-1229-5p dramatically inhibited the luciferase activity of 3' UTR segment of MAPK1 (P<0.01). Compared to the negative control, HEK293T cells expressing miR-1229-5p mimics showed a significant decline in mRNA levels of MAPK1 (P<0.05). This preliminary study indicated that serum miR-1229-5p was significantly elevated in ONIHL subjects. Increased miR-1229-5p may participate in the pathogenesis of ONIHL through repressing MAPK1 signaling.

Analysis of serum microRNA expression in male workers with occupational noise-induced hearing loss

Occupational noise-induced hearing loss (ONIHL) is a prevalent occupational disorder that impairs auditory function in workers exposed to prolonged noise. However, serum microRNA expression in ONIHL subjects has not yet been studied. We aimed to compare the serum microRNA expression profiles in male workers of ONIHL subjects and controls. MicroRNA microarray analysis revealed that four serum microRNAs were differentially expressed between controls (n=3) and ONIHL subjects (n=3). Among these microRNAs, three were upregulated (hsa-miR-3162-5p, hsa-miR-4484, hsa-miR-1229-5p) and one was downregulated (hsa-miR-4652-3p) in the ONIHL group (fold change >1.5 and Pbon value <0.05). Real time quantitative PCR was conducted for validation of the microRNA expression. Significantly increased serum levels of miR-1229-5p were found in ONIHL subjects compared to controls (n=10 for each group; P<0.05). A total of 659 (27.0%) genes were predicted as the target genes of miR-1229-5p. These genes were involved in various pathways, such as mitogen-activated protein kinase (MAPK) signaling pathway. Overexpression of miR-1229-5p dramatically inhibited the luciferase activity of 3′ UTR segment of MAPK1 (P<0.01). Compared to the negative control, HEK293T cells expressing miR-1229-5p mimics showed a significant decline in mRNA levels of MAPK1 (P<0.05). This preliminary study indicated that serum miR-1229-5p was significantly elevated in ONIHL subjects. Increased miR-1229-5p may participate in the pathogenesis of ONIHL through repressing MAPK1 signaling.

Outer Hair Cell Molecular Protein, Prestin, as a Serum Biomarker for Hearing Loss: Proof of Concept.

HYPOTHESIS: At present there are no serum biomarkers available to monitor cochlear health in those at risk of hearing loss. Outer hair cells (OHCs) play an important role in cochlear function and are one of the cellular elements most vulnerable to damage, such as acoustic trauma. We hypothesized that an OHC-specific protein can serve as a biomarker for OHC damage in circulation. METHODS: After assessing auditory function, rats were exposed to intense octave band noise for 2 to 3 hours. Auditory function was assessed 14 days after trauma. Blood samples were collected and prestin concentration was measured using enzyme-linked immunosorbent assay. RESULTS: Circulating prestin was detectable in all control and noise-exposed animals. At 14 days after trauma, however, noise-exposed rats demonstrated statistically significant decrease in prestin concentrations compared with control animals. CONCLUSION: This work, for the first time, provides proof of concept that an otologic serum biomarker level can change after acoustic trauma and hearing loss. Our approach represents an entirely novel strategy in hearing diagnostics and has both research and clinical potential. Further work is needed to map out the temporal course of change in serum prestin concentrations after inner ear trauma, better define the relationship of serological and functional changes, and explore application to other etiologies of hearing loss (e.g., ototoxins).

[Association between serum magnesium ion level and risk of noise-induced hearing loss].

Objective: To investigate the association between serum magnesium ion level and risk of noise-induced hearing loss (NIHL) . Methods: Acohort study was performed for 7 445 workers exposed to noise in the steelmaking and steel rolling workshops of an iron and steel enterprise in Henan Province, China. The follow-up time was from January 1, 2006 to December 31, 2015. The workers with a binaural average high-frequency hearing threshold of ≥40 dB (HL) were enrolled as case group, and those with a binaural average high-frequency hearing threshold of <35 dB (HL) and a binaural average speech frequency of ≤25 dB (HL) were enrolled as control group. After being matched for age, working years of noise exposure, sex, and type of work at a ratio of 1∶1, 187 workers each were enrolled in the case group and the control group. Flame atomic absorption spectrometry was used to measure the serum magnesium ionlevel. Aconditional logistic regression analysis was performed to investigate the association of serum magnesium ion level, body mass index, cumulative noise exposure (CNE) , smoking, drinking, hypertension, and physical exercise with NIHL, as well as the association between serum magnesium ion level and risk of NIHL after the adjustment for covariants. Results: There was no significant difference in the serum magnesium ion level between the case group and the control group (24.63±7.92 mg/m(3) vs 24.91±7.33 mg/m(3), P>0.05) . Smoking (OR=1.687, 95%CI 1.090-2.613) was a risk factor for NIHL, and physical exercise (OR=0.509, 95%CI 0.325-0.796) reduced the risk of NIHL. In the workers with CNE>98 dB (A) ·year, the risk of NIHL in the workers with higher CNE was 1.305 times (95%CI 1.051-1.620) that in those with lower CNE. After the adjustment for CNE, smoking, and physical exercise, there was no significant difference in the influence of serum magnesium ion level on the risk of NIHL between the two groups (P>0.05) . Conclusion: Serum magnesium ion level may not be associated with NIHL. Increased CNE and smoking may increase the risk of NIHL and physical exercise may reduce the risk of NIHL.

Analysis of plasma microRNA expression profiles in male textile workers with noise-induced hearing loss.

BACKGROUND: Circulating microRNAs (miRNAs) have attracted interests as non-invasive biomarkers of physiological and pathological conditions, which may be applied in noise-induced hearing loss (NIHL). However, no epidemiology studies have yet examined the potential effects of NIHL or noise exposure on miRNA expression profiles. OBJECTIVES: We sought to identify permanent NIHL-related miRNAs and to predict the biological functions of the putative genes encoding the indicated miRNAs. METHODS: In the discovery stage, we used a microarray assay to detect the miRNA expression profiles between pooled plasma samples from 10 noise-exposed individuals with normal hearing and 10 NIHL patients. In addition, we conducted a preliminary validation of six candidate miRNAs in the same 20 workers. Subsequently, three miRNAs were selected for expanded validation in 23 non-exposed individuals with normal hearing and 46 noise-exposed textile workers which including 23 noise-exposed workers with normal hearing and 23 NIHL patients. Moreover, we predicted the biological functions of the putative target genes using a Gene Ontology (GO) function enrichment analysis. RESULTS: In the discovery stage, compared with the noise exposures with normal hearing, 73 miRNAs demonstrated at least a 1.5-fold differential expression in the NIHL patients. In the preliminary validation, compared with the noise exposures, the plasma levels of miR-16-5p, miR-24-3p, miR-185-5p and miR-451a were all upregulated (P < 0.001) in the NIHL patients. In the expanded validation stage, compared with the non-exposures, the plasma levels of miR-24, miR-185-5p and miR-451a were all significantly downregulated (P < 0.001) in the exposures. And compared with the noise exposures, the plasma levels of miR-185-5p and miR-451a were slightly elevated (P < 0.001) in the NIHL patients, which were consistent with the results of preliminary validation and microarray analysis. CONCLUSION: The two indicated plasma miRNAs may be biomarkers of indicating responses to noise exposure. However, further studies are necessary to prove the causal association between miRNAs changes and noise exposure, and to determine whether these two miRNAs are clear biomarkers to noise exposure.

Increased endothelial progenitor cell circulation and VEGF production in a rat model of noise-induced hearing loss.

CONCLUSIONS: The vascular endothelial growth factor (VEGF)-mediated mechanism of endothelial progenitor cell (EPC) mobilization, migration, and differentiation may occur in response to noise-induced acoustic trauma of the cochlea, leading to the protection of cochlear function. OBJECTIVE: The purpose of this study was to analyze changes in the cochlear vessel under an intensive noise environment. METHODS: Sixty male Sprague-Dawley rats were randomly divided into six groups. Acoustic trauma was induced by 120 dB SPL white noise for 4 h. Auditory function was evaluated by the auditory brainstem response threshold. Morphological changes of the cochleae, the expression of VEGF, and the circulation of EPCs in the peripheral blood were studied by immunohistochemistry, Western blotting analysis, scanning electron microscopy, and flow cytometry. RESULTS: Vascular recovery of the cochlea began after noise exposure. The change in the number of EPCs was consistent with the expression of VEGF at different time points after noise exposure. We propose that VEGF evokes specific permeable and chemotactic effects on the vascular endothelial cells. These effects can mobilize EPCs into the peripheral blood, leading the EPCs to target damaged sites and to exert a neoangiogenic effect.

Increased vitamin plasma levels in Swedish military personnel treated with nutrients prior to automatic weapon training.

Noise-induced hearing loss (NIHL) is a significant clinical, social, and economic issue. The development of novel therapeutic agents to reduce NIHL will potentially benefit multiple very large noise-exposed populations. Oxidative stress has been identified as a significant contributor to noise-induced sensory cell death and NIHL, and several antioxidant strategies have now been suggested for potential translation to human subjects. One such strategy is a combination of beta-carotene, vitamins C and E, and magnesium, which has shown promise for protection against NIHL in rodent models, and is being evaluated in a series of international human clinical trials using temporary (military gunfire, audio player use) and permanent (stamping factory, military airbase) threshold shift models (NCT00808470). The noise exposures used in the recently completed Swedish military gunfire study described in this report did not, on average, result in measurable changes in auditory function using conventional pure-tone thresholds and distortion product otoacoustic emission (DPOAE) amplitudes as metrics. However, analysis of the plasma samples confirmed significant elevations in the bloodstream 2 hours after oral consumption of active clinical supplies, indicating the dose is realistic. The plasma outcomes are encouraging, but clinical acceptance of any novel therapeutic critically depends on demonstration that the agent reduces noise-induced threshold shift in randomized, placebo-controlled, prospective human clinical trials. Although this noise insult did not induce hearing loss, the trial design and study protocol can be applied to other populations exposed to different noise insults.

Effect of vitamin E supplementation on carbogen-induced amelioration of noise induced hearing loss in man.

The study explores the effect of occupational noise on oxidative stress status and prophylactic effect of Vitamin E and carbogen (5% CO 2 +95%O 2 ) breathing in alleviating the oxidative damage and conserving the hearing in human volunteers exposed to intense occupational noise. Plasma total antioxidant status, blood glutathione (GSH), malondialdehyde (MDA), antioxidant enzyme activities of GSH peroxidase (EC 1.11.1.9, GPx), superoxide dismutase (EC 1.15.1.1; SOD) in erythrocytes, nitric oxide and nitric oxide synthase in plasma were assessed before and after 6 days of administration of Vitamin E and Carbogen. Results of the study indicate that the exposure to noise for 6 days increased blood concentration of MDA, decreased concentrations of reduced GSH, antioxidant enzyme activity of SOD and plasma total antioxidant status in control (noise) group. Vitamin E- supplemented group showed decline in oxidative stress reflected by significant decrease in blood concentration of MDA and increase in antioxidant enzyme activity of erythrocyte SOD. Results of audiometric studies revealed that breathing of carbogen prevented the development of temporary threshold shift; thereby reducing the risk of noise induced hearing loss.

The association between impaired fasting glucose and noise-induced hearing loss.

OBJECTIVES: This study was performed to determine whether there is an association between impaired fasting glucose and noise-induced hearing loss. METHODS: The study subjects were workers in one automobile manufacturing company. The data were obtained from results of health examinations during 2005 and 2009. The factors analyzed were age, smoking and alcohol history, work duration, environmental noise level, hearing thresholds, blood pressure, serum creatinine, initial hearing threshold and fasting glucose. RESULTS: The hearing thresholds at 4,000 Hz frequencies for both ears were significantly higher in 2009 than those in 2005. The changes in the hearing thresholds of the subjects with an impaired fasting glucose (100-125 mg/dl) and diabetes (≥126 mg/dl) were greater than those of the normal (<100 mg/dl) group. After adjusting for variables such as age, smoking and alcohol history, environmental noise, hypertension and serum creatinine, fasting glucose was found to be a significant variable. Impaired fasting glucose (100-125 mg/dl) was significant (ß=1.339, p=0.002) for the right ear, whereas it was not significant (ß=0.639, p=0.121) for the left ear. CONCLUSIONS: Impaired fasting glucose, as well as diabetes, might be risk factors for hearing loss in individuals with exposure to certain noise levels. The results of this study suggest that impaired fasting glucose should be considered a risk factor for hearing loss.

The association between low levels of lead in blood and occupational noise-induced hearing loss in steel workers.

As the use of leaded gasoline has ceased in the last decade, background lead exposure has generally been reduced. The aim of this study was to examine the effect of low-level lead exposure on human hearing loss. This study was conducted in a steel plant and 412 workers were recruited from all over the plant. Personal information such as demographics and work history was obtained through a questionnaire. All subjects took part in an audiometric examination of hearing thresholds, for both ears, with air-conducted pure tones at frequencies of 500, 1000, 2000, 3000, 4000, 6000 and 8000 Hz. Subjects' blood samples were collected and analyzed for levels of manganese, copper, zinc, arsenic, cadmium and lead with inductive couple plasma-mass spectrometry. Meanwhile, noise levels in different working zones were determined using a sound level meter with A-weighting network. Only subjects with hearing loss difference of no more than 15 dB between both ears and had no congenital abnormalities were included in further data analysis. Lead was the only metal in blood found significantly correlated with hearing loss for most tested sound frequencies (p<0.05 to p<0.0001). After adjustment for age and noise level, the logistic regression model analysis indicated that elevated blood lead over 7 microg/dL was significantly associated with hearing loss at the sound frequencies of 3000 through 8000 Hz with odds ratios raging from 3.06 to 6.26 (p<0.05-p<0.005). We concluded that elevated blood lead at level below 10 microg/dL might enhance the noise-induced hearing loss. Future research needs to further explore the detailed mechanism.

[Contributions of endothelin in the process of the noise-induced injury of inner ear].

OBJECTIVE: To study the pathological alteration of the cochlear microcirculation and the role of endothelin (ET) in the process of the noise-induced injury of inner ear. METHODS: Thirty rats were randomly divided into five groups: control group and 1, 4, 8, 15 d noise exposure groups (115 dB, white noise, 8 h daily). The cilium of hair cell was observed by scanning electron microscope, the cochlear microcirculation was determined by stretched preparation of the stria vascularis. The level of ET in plasma was measured through radio-immunity. The distribution of ET-1, ETA, ETB, in cochlea were detected through immunohistochemistry staining. RESULTS: In the 4, 8, 15 d group, severe ischemia appeared on the capillary of stria vascularis and the cilium of hair cell displayed significantly disorder. The level of ET in plasma rose temporarily in the 4 d group. ET-1 activity distributed widely in the rat cochlea, there was no significant difference between the control group and the noise exposure groups. ETA expressed in the plasma of the intermediate cells and the capillary walls in the stria vascularis. The control group and the 1 d group showed weak positive staining, while the 4, 8, 15 d groups showed strong positive. The ETB, activity distributed on the endothelial cells of the capillary of stria vascularis and the alteration of the staining intensity was similar to the manifestation of ETA. CONCLUSIONS: Severe disturbance of the cochlear circulation occurred during the course of the noise injury to the inner ear. At the same time, the activity of the ET system of the cochlea stepped up significantly. It coincided with the ischemia of the stria vascularis. These findings suggest that ET may play an important role in the process of the cochlear microcirculation disorder caused by noise.

Comparative analysis of serum homocysteine, folic acid and Vitamin B12 levels in patients with noise-induced hearing loss.

OBJECTIVE: The aim of the present study was to determine the levels of homocysteine, folic acid, and Vitamin B12 in subjects with noise-induced hearing loss. Furthermore, possible links between these parameters and noise-induced hearing loss were aimed to be evaluated. METHODS: In the present study, blood samples were obtained from all subjects after overnight fasting for biochemical analysis. We examined the levels of homocysteine, Vitamin B12 and folic acid levels in subjects with noise-induced hearing loss. Twenty-eight male patients with noise-induced hearing loss (mean age 37 +/- 5 year) were included in the study group whereas the control group was composed of 32 healthy male volunteers (mean age 36 +/- 4 year). RESULTS: It was found that homocysteine levels of subjects with noise-induced hearing loss as significantly high compared to healthy controls (P < 0.05). On the other hand, Vitamin B12 and folic acid levels of patients with noise-induced hearing loss were determined to be significantly low compared to the controls (P < 0.05 and < 0.01, respectively). CONCLUSION: Our findings indicate that there might be a link between increased homocysteine levels and noise-induced hearing loss. Since increased homocysteine levels cause elevated levels of free radicals in addition to its atherogenic and thrombogenic effects. Further experimental studies are needed to decipher how this relationship is linked.

[The levels of vitamins A, E, B12 and folic acid in noise-induced hearing loss]. / Gürültüye bagli isitme kayipli hastalarda vitamin A, E, B12 ve folik asit düzeyleri.

OBJECTIVES: To investigate the levels of vitamin A, E, B12, folic acid in employees with hearing loss due to noise. PATIENTS AND METHODS: Employees in a local hydroelectric powerhouse who suffered from hearing loss due to noise were included in the study. Study and control groups were composed of 28 employees (mean age 37+/-5 years) and 30 voluntary subjects (mean age 36+/-4 years), respectively. All the subjects in patient and control groups were males. Blood samples were obtained from all subjects and vitamin A, E, B12 and folic acid levels were measured. RESULTS: Level of vitamin B12 was found low in the patient group and normal in the control group and these were found statistically significant (p<0.005). There were no significant differences between vitamin A, E and folic acid levels. CONCLUSION: We think that measurement of vitamin B12 in routine control of the people who are working in noisy environment may be useful.

Correlation between blood group and noise-induced hearing loss.

OBJECTIVE: To investigate the correlation between blood group and noise-induced hearing loss (NIHL). MATERIAL AND METHODS: The study was conducted in 176 factory workers who had been exposed to a noise level of 85-90 dB for 8 h a day for a period of > or = 10 years. Pure-tone audiometric measurements were performed in a standard silent room. The blood groups of the workers were obtained from the factory files. RESULTS: NIHL was found in 23 (32.0%), 35 (58.3%), 10 (38.5%) and 7 (38.9%) persons with blood groups A, O, B and AB, respectively. NIHL was determined to be significantly more frequent in workers with blood group O. CONCLUSION: We suggest that people with blood group O are more prone to develop NIHL.

Airbags and permanent auditory deficits. A real correlation?

OBJECTIVES: To evaluate the relationship between airbag-induced noise and individual metabolic risk factors in determining persistent hypoacusia in drivers after road accidents. METHODOLOGY: We selected 22 patients previously involved in a car accident with deployment of airbags. Patients underwent general and audiological clinical history, tonal audiometric examination, vocal audiometric examination, impedance meter examination and blood tests. RESULTS: We divided patients, according to audiometric data, into 2 groups: group A with no residual otological disturbances (6 subjects) and group B with persistent hypoacusia (16 subjects). Blood parameters were into physiological levels in all group A patients; on the contrary 12 (subgroup B1) out of 16 group B patients had altered blood levels of glucose, urea and cholesterol, with mean values of 155.8 +/- 38.6 mg/dl, 48.2 +/- 8.3 mg/dl and 250.8 +/- 28.1 mg/dl, respectively, revealing statistically significant differences in these parameters when compared with the other 4 hypoacusic cases (Sub-group B2) and with the normal subjects (Group A) (p < 0.01 for glucose, p < 0.05 for urea and p < 0.001 for cholesterol). CONCLUSIONS: Our findings confirm the transitory otological damage due to airbag deployment: the intensity of the acoustic wave hitting the ear after airbag deployment is responsible for a temporary rise in the acoustic threshold but the persistence of an auditory deficit can be due to co-factors able to interfere with the acute acoustic trauma recovery processes through a metabolic, angiopathic, neuropathic or unknown mechanism. Moreover, also the age of the patients could affect in a significant way the recovery from the acoustic trauma.