Distortion Product Otoacoustic Emissions Amplitudes Research Articles

Noise Exposure and Distortion Product Otoacoustic Emission Suprathreshold Amplitudes: A Genome-Wide Association Study

Background: Although several candidate-gene association studies have been conducted to investigate noise-induced hearing loss (NIHL) in humans, most are underpowered, unreplicated, and account for only a fraction of the genetic risk. Mouse genome-wide association studies (GWASs) have revolutionized the field of genetics and have led to the discovery of hundreds of genes involved in complex traits. The hybrid mouse diversity panel (HMDP) is a collection of classic inbred and recombinant inbred strains whose genomes have been either genotyped at high resolution or sequenced. To further investigate the genetics of NIHL, we report the first GWAS based on distortion product otoacoustic emission (DPOAE) measurements and the HMDP. Methods: A total of 102 strains (n = 635) from the HMDP were evaluated based on DPOAE suprathreshold amplitudes before and after noise exposure. DPOAE amplitude variation was set at 60 and 70 dB SPL of the primary tones for each frequency separately (8, 11.3, 16, 22.6, and 32 kHz). These values provided an indirect assessment of outer hair cell integrity. Six-week-old mice were exposed for 2 h to 10 kHz octave-band noise at 108 dB SPL. To perform local expression quantitative trait locus (eQTL) analysis, gene expression microarray profiles were generated using cochlear RNA from 64 hybrid mouse strains (n = 3 arrays per strain). Results: Several new loci were identified and positional candidate-genes associated with NIHL were prioritized, especially after noise exposure (1 locus at baseline and 5 loci after exposure). A total of 35 candidate genes in these 6 loci were identified with at least 1 probe whose expression was regulated by a significant cis-eQTL in the cochlea. After careful analysis of the candidate genes based on cochlear gene expression, 2 candidate genes were prioritized: Eya1 (baseline) and Efr3a (post-exposure). Discussion and Conclusion: For the first time, an association analysis with correction for population structure was used to map several loci for hearing traits in inbred strains of mice based on DPOAE suprathreshold amplitudes before and after noise exposure. Our results identified a number of novel loci and candidate genes for susceptibility to NIHL, especially the Eya1 and Efr3a genes. Our findings validate the power of the HMDP for detecting NIHL susceptibility genes.

A Wirelessly Controlled Scalable 3D-Printed Microsystem for Drug Delivery.

Here we present a 3D-printed, wirelessly controlled microsystem for drug delivery, comprising a refillable microreservoir and a phase-change peristaltic micropump. The micropump structure was inkjet-printed on the back of a printed circuit board around a catheter microtubing. The enclosure of the microsystem was fabricated using stereolithography 3D printing, with an embedded microreservoir structure and integrated micropump. In one configuration, the microsystem was optimized for murine inner ear drug delivery with an overall size of 19 × 13 × 3 mm3. Benchtop results confirmed the performance of the device for reliable drug delivery. The suitability of the device for long-term subcutaneous implantation was confirmed with favorable results of implantation of a microsystem in a mouse for six months. The drug delivery was evaluated in vivo by implanting four different microsystems in four mice, while the outlet microtubing was implanted into the round window membrane niche for infusion of a known ototoxic compound (sodium salicylate) at 50 nL/min for 20 min. Real-time shifts in distortion product otoacoustic emission thresholds and amplitudes were measured during the infusion, demonstrating similar results with syringe pump infusion. Although demonstrated for one application, this low-cost design and fabrication methodology is scalable for use in larger animals and humans for different clinical applications/delivery sites.

Hidden or subclinical cochleopathy in idiopathic subjective tinnitus: extended high frequency audiometry and otoacoustic emission

Introduction Tinnitus patients with apparently normal hearing represent a challenge to models of tinnitus generation which rely on compromised cochlear function. Although it is known that any cochlear changes even subclinical can cause tinnitus, our rational was to apply an objective measure that can aids in the quantification of these cochlear changes. Objective The of study was designed to evaluate possible hidden or subclinical cochlear dysfunction in idiopathic subjective tinnitus patients with normal hearing using extended high frequency audiometry and otoacoustic emissions. Methods Forty seven subjects enrolled in this study divided into control group (20 normal hearing adults without tinnitus) and a study group (27 normal hearing adult patients complaining of tinnitus). Extended high frequency (EHF) audiometry and otoacoustic emissions (OAEs) in addition to tinnitus matching study were done for all subjects. Study group further subdivided according to tinnitus pitch matching into low- and high-pitched tinnitus groups. Results The data of this study showed that patients with normal hearing sensitivity in the conventional frequency range (up to 8 kHz) and reporting tinnitus, present alterations of the auditory system in the affected side. This affection manifested as elevated EHF audiometry thresholds at 9000, 10,000, 11,200, 14,000 and 16,000 Hz. Most tinnitus patients had pitch matching frequency at high frequency range between (3000 and 8000 Hz). Transient evoked OAEs and distortion product OAEs amplitude was lower in tinnitus patients relative to controls. Conclusion The ultrahigh frequency hearing loss is not hidden – but – exists and awaits identification with appropriate testing.

Acute Recreational Noise-Induced Cochlear Synaptic Dysfunction in Humans With Normal Hearing: A Prospective Cohort Study

ObjectivesThe objective of the study was to identify the acute high-intensity recreational noise-induced effects on auditory function, especially the cochlear synaptopathy-related audiological metrics, in humans with normal hearing.MethodsThis prospective cohort study enrolled 32 young adults (14 males and 18 females); the mean age was 24.1 ± 2.4 years (ranging from 20 to 29). All participants with normal hearing (audiometric thresholds ≤25 dB HL at frequencies of 0.25, 0.5, 1, 2, 3, 4, 6, and 8 kHz for both ears) had already decided to participate in the outdoor music festival. Participants were asked to measure the noise exposure dose and complete auditory examinations, including the air-conduction pure-tone audiometry (PTA), distortion product otoacoustic emission (DPOAE), contralateral suppression (CS) on transient evoked otoacoustic emission (TEOAE), auditory brainstem response (ABR) test and Mandarin Hearing in Noise Test (MHINT), at baseline and 1 day and 14 days after music festival noise exposure.ResultsThe mean time of attending the music festival was 7.34 ± 0.63 h (ranging from 6.4 to 9.5), the mean time-weighted average (TWA) of noise exposure dose was 93.2 ± 2.39 dB(A) (ranging from 87.9 to 97.7). At neither 1 day nor 14 days post exposure, there were no statistically significant effects on PTA thresholds, DPOAE amplitudes, CS on TEOAEs, or MHINT signal-to-noise ratios (SNRs) of acute outdoor music festival noise exposure, regardless of sex. While the ABR wave I amplitudes significantly decreased at 1 day after exposure and recovered at 14 days after exposure, the exposed/unexposed ABR wave I amplitude ratio was significantly correlated with MHINT SNR change at 1 day after exposure, although it was not correlated with the noise exposure dose.ConclusionIn young adults with normal hearing, we found the self-compared decrement of ABR wave I amplitudes at 1 day post acute recreational noise exposure at high intensity, which also contributes to the change in speech perceptual ability in noisy backgrounds. This study indicated that auditory electrophysiological metric changes might be a more sensitive and efficient indicator of noise-induced cochlear synaptic dysfunction in humans. More attention should be paid to the recreational noise-induced cochlear synaptopathy and auditory perceptual disorder.

The influence of combined exposure to noise and whole-body vibration on hearing loss under simulated heavy equipment driving conditions

Noise-induced hearing loss (NIHL) is a serious problem in occupational environments; however, there is little information about hearing loss due to combined exposure to noise and vibration. This study aimed to investigate the combined effects of exposure to noise and whole-body vibration (WBV) on hearing responses under simulated heavy equipment driving conditions. A repeated measures study was designed to evaluate the changes in distortion product otoacoustic emissions (DPOAE) amplitudes as hearing responses to 40 min of noise and/or WBV exposure. Thirty healthy males with an average age of 30.17 (±3.94) years, exposed to noise level of 85 dB(A) and two WBV levels (0.87 and 1.3 m/s2) in six experimental scenarios. The findings revealed that there was a significant change in DPOAE amplitudes after single noise exposure and combined noise and WBV exposure (p < 0.05); however, there was no significant difference in WBV exposure alone (p > 0.05). The changes in DPOAE amplitudes were greater in combined exposure to noise and WBV (1.3 m/s2) in all sessions. The statistical analysis showed the effect sizes of the combined exposure to noise and WBV were more than the sum of the exposure to each one alone. It can be concluded that some synergic effects can occur in DPOAE amplitudes in the combined noise and WBV exposure under heavy equipment driving conditions. These findings can help the occupational health experts adapt the existing physical agents' exposure limits to the realistic conditions of the occupational settings.

Pure-Tone Hearing Thresholds and Otoacoustic Emissions in Students of Music Academies.

The objective of this study was to assess the hearing of music students in relation to their exposure to excessive sounds. A standard pure-tone audiometry, transient-evoked otoacoustic emissions (TEOAEs) and distortion-product otoacoustic emissions (DPOAEs) were determined in 163 students of music academies, aged 22.8 ± 2.6 years. A questionnaire survey and sound pressure level measurements during solo and group playing were also conducted. The control group comprised 67 subjects, mainly non-music students, aged 22.8 ± 3.3 years. Study subjects were exposed to sounds at the A-weighted weekly noise exposure level (LEX,w) from 75 to 106 dB. There were no significant differences in the hearing thresholds between groups in the frequency range of 4000–8000 Hz. However, music students compared to control group exhibited lower values of DPOAE amplitude (at 6000 and 7984 Hz) and signal-to-noise ratio (SNR) (at 984, 6000, and 7984 Hz) as well as SNR of TEOAE (in 1000 Hz band). A significant impact of noise exposure level, type of instrument, and gender on some parameters of measured otoacoustic emissions was observed. In particular, music students having LEX,w ≥ 84.9 dB, compared to those with LEX,w < 84.9 dB, achieved significantly lower DPOAE amplitude at 3984 Hz. Meanwhile, both TEOAE and DPOAE results indicated worse hearing in students playing percussion instruments vs. wind instruments, and wind instrument players vs. students playing stringed instruments.

RIP3-mediated necroptosis was essential for spiral ganglion neuron damage

To identify the role of RIP3 in ouabain-induced necroptosis and offer clinical implications to prevent spiral ganglion neurons (SGNs) from death, ouabain was applied in SGNs derived from fetal rats and injected into Sprague–Dawley rats to construct injury model in vitro and in vivo, respectively. The necroptosis rate of SGNs was determined by flow cytometry and MTT assays. The protein levels and phosphorylation of RIP3 were evaluated using western blotting and immunofluorescence. SGNs injury was observed using H&E staining and immunofluorescence. The hearing function of rats was evaluated by the auditory brainstem response (ABR) and Distortion Product Otoacoustic Emissions (DPOAE) methods. Ouabain caused dose-dependent necroptosis in SGNs and significant loss of SGNs of the cochlear axis in vivo. RIP3 and pRIP3 were upregulated with SGNs injury promoted, and RIP3 overexpression promoted ouabain-induced necroptosis in SGNs in vitro, which could be suppressed by necrostatin-1. RIP3 knockdown inhibited ouabain-induced necroptosis and reduced the phosphorylation of MLKL but no RIP3-dependent effect on the level of MLKL. RIP3 inhibition in vivo protected rats from ouabain-induced hearing damage with reducing ABR threshold shifts and promoting DPOAE amplitudes, while overexpression of RIP3 enhanced ouabain-induced injury that could be partially reversed by necrostatin-1. A decrease of SGNs density and an upregulation of pRIP3 were observed with RIP3 overexpression, which was in contrast when RIP3 was silenced. Therefore, RIP3 was essential for mediating necroptosis in ouabain-induced SGNs damage. Targeting RIP3 may prevent SGNs from death in clinical practice, and finally help the treatment of sensorineural hearing loss.

Otoacoustic emissions and contralateral suppression in tinnitus sufferers with normal hearing

BackgroundThe general consensus on the role of hearing loss in generating tinnitus is not relevant in tinnitus patients with normal hearing thresholds. One source of tinnitus may be related to damage to outer hair cells (OHC) of the cochlea. If the OHC of the human cochlea are to be involved in the generation of tinnitus, testing of Otoacoustic emissions (OAE) could provide a reliable means of recording OHC dysfunction. We investigated the role of OHC and cochlear efferent system in tinnitus development in normal hearing ears through studying of Distortion Product Otoacoustic Emissions (DPOAE) and Transient Evoked Otoacoustic Emissions (TEOAE) amplitudes, contralateral suppression amplitudes and suppression value in 15 normal hearing tinnitus patients and 15 control subjects.ResultsMean f2 DPOAE amplitudes and contralateral suppression were significantly lower in tinnitus group compared to controls for all frequencies from 1001 to 6348 Hz. Suppression values of DPOAEs revealed lower but not significant difference between tinnitus and control groups for all frequencies except 1587 and 6348 Hz. TEOAE amplitudes and contralateral suppression were significantly lower in tinnitus groups for all frequencies from 1000 to 4000 Hz compared to the control group. Suppression value of TEOAEs revealed no significant difference between the two groups for all frequencies except 3000 and 4000 Hz were significantly lower in the tinnitus group compared to the control group.ConclusionsNormal hearing manifested by pure tone audiometry in non-vascular tinnitus sufferers does not exclude OHC and/or cochlear efferent pathology.

A clinical comparison of DPOAE fine structure reduction methods

Objective To evaluate two real-time methods for reducing distortion product otoacoustic emission (DPOAE) fine structure in terms of DPOAE amplitude and fine structure depth. Design A prospective, repeated-measures design was used to assess DPOAE characteristics in response to a conventional stimulation method (Conv.), as well as for methods implementing either a generic suppressor tone (Supp.) or frequency modulation of the f2 primary tone (FM). Study sample Eighty-three young adults (58 females) between the ages of 20 and 34 years with normal hearing completed testing for this study. Results Use of the Conv. and FM methods resulted in consistently higher DPOAE levels relative to the Supp. method, with average advantages of 6 and 5 dB, respectively. For all methods, increased fine structure depth was observed for stimulation with lower level (25−45 dB SPL) and lower frequency (1000−3000 Hz) primary tones. Finally, use of the Supp. and FM methods resulted in significantly decreased fine structure depth relative to the Conv. method. Conclusion Through frequency modulation of the f2 primary tone, it was possible to reduce the depth of fine structure across a clinically meaningful range of stimulation levels and frequencies without concomitant reduction in DPOAE amplitude.

Pterostilbene protects cochlea from ototoxicity in streptozotocin-induced diabetic rats by inhibitingapoptosis.

Diabetes mellitus (DM) causes ototoxicity by inducing oxidative stress, microangiopathy, and apoptosis in the cochlear sensory hair cells. The natural anti-oxidant pterostilbene (PTS) (trans-3,5-dimethoxy-4-hydroxystylbene) has been reported to relieve oxidative stress and apoptosis in DM, but its role in diabetic-induced ototoxicity is unclear. This study aimed to investigate the effects of dose-dependent PTS on the cochlear cells of streptozotocin (STZ)-induced diabetic rats. The study included 30 albino male Wistar rats that were randomized into five groups: non-diabetic control (Control), diabetic control (DM), and diabetic rats treated with intraperitoneal PTS at 10, 20, or 40 mg/kg/day during the four-week experimental period (DM + PTS10, DM + PTS20, and DM + PTS40). Distortion product otoacoustic emission (DPOAE) tests were performed at the beginning and end of the study. At the end of the experimental period, apoptosis in the rat cochlea was investigated using caspase-8, cytochrome-c, and terminal deoxyribonucleotidyl transferase-mediated dUTP-biotin end labeling (TUNEL). Quantitative real-time polymerase chain reaction was used to assess the mRNA expression levels of the following genes: CASP-3, BCL-associated X protein (BAX), and BCL-2. Body weight, blood glucose, serum insulin, and malondialdehyde (MDA) levels in the rat groups were evaluated. The mean DPOAE amplitude in the DM group was significantly lower than the means of the other groups (0.9–8 kHz; P < 0.001 for all). A dose-dependent increase of the mean DPOAE amplitudes was observed with PTS treatment (P < 0.05 for all). The Caspase-8 and Cytochrome-c protein expressions and the number of TUNEL-positive cells in the hair cells of the Corti organs of the DM rat group were significantly higher than those of the PTS treatment and control groups (DM > DM + PTS10 > DM + PTS20 > DM + PTS40 > Control; P < 0.05 for all). PTS treatment also reduced cell apoptosis in a dose-dependent manner by increasing the mRNA expression of the anti-apoptosis BCL2 gene and by decreasing the mRNA expressions of both the pro-apoptosis BAX gene and its effector CASP-3 and the ratio of BAX/BCL-2 in a dose-dependent manner (P < 0.05 compared to DM for all). PTS treatment significantly improved the metabolic parameters of the diabetic rats, such as body weight, blood glucose, serum insulin, and MDA levels, consistent with our other findings (P < 0.05 compared to DM for all). PTS decreased the cochlear damage caused by diabetes, as confirmed by DPOAE, biochemical, histopathological, immunohistochemical, and molecular findings. This study reports the first in vivo findings to suggest that PTS may be a protective therapeutic agent against diabetes-induced ototoxicity.

Ginsenoside Rd Ameliorates Auditory Cortex Injury Associated With Military Aviation Noise-Induced Hearing Loss by Activating SIRT1/PGC-1α Signaling Pathway.

Free radicals and oxidative stress play an important role in the pathogenesis of noise-induced hearing loss (NIHL). Some ginseng monomers showed certain therapeutic effects in NIHL by scavenging free radicals. Therefore, we hypothesized that ginsenoside Rd (GSRd) may exert neuroprotective effects after noise-induced auditory system damage through a mechanism involving the SIRT1/PGC-1α signaling pathway. Forty-eight guinea pigs were randomly divided into four equal groups (normal control group, noise group, experimental group that received GSRd dissolved in glycerin through an intraperitoneal injection at a dose of 30 mg/kg body weight from 5 days before noise exposure until the end of the noise exposure period, and experimental control group). Hearing levels were examined by auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE). Hematoxylin–eosin and Nissl staining were used to examine neuron morphology. RT-qPCR and western blotting analysis were used to examine SIRT1/PGC-1α signaling and apoptosis-related genes, including Bax and Bcl-2, in the auditory cortex. Bax and Bcl-2 expression was assessed via immunohistochemistry analysis. Superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GSH-Px) levels were determined using a commercial testing kit. Noise exposure was found to up-regulate ABR threshold and down-regulate DPOAE amplitudes, with prominent morphologic changes and apoptosis of the auditory cortex neurons (p < 0.01). GSRd treatment restored hearing loss and remarkably alleviated morphological changes or apoptosis (p < 0.01), concomitantly increasing Bcl-2 expression and decreasing Bax expression (p < 0.05). Moreover, GSRd increased SOD and GSH-Px levels and decreased MDA levels, which alleviated oxidative stress damage and activated SIRT1/PGC-1α signaling pathway. Taken together, our findings suggest that GSRd ameliorates auditory cortex injury associated with military aviation NIHL by activating the SIRT1/PGC-1α signaling pathway, which can be an attractive pharmacological target for the development of novel drugs for NIHL treatment.

Search for Electrophysiological Indices of Hidden Hearing Loss in Humans: Click Auditory Brainstem Response Across Sound Levels and in Background Noise.

Recent studies in animals indicate that even moderate levels of exposure to noise can damage synaptic ribbons between the inner hair cells and auditory nerve fibers without affecting audiometric thresholds, giving rise to the use of the term "hidden hearing loss" (HHL). Despite evidence across several animal species, there is little consistent evidence for HHL in humans. The aim of the study is to evaluate potential electrophysiological changes specific to individuals at risk for HHL. Participants forming the high-risk experimental group consisted of 28 young normal-hearing adults who participated in marching band for at least 5 years. Twenty-eight age-matched normal-hearing adults who were not part of the marching band and had little or no history of recreational or occupational exposure to loud sounds formed the low-risk control group. Measurements included pure tone audiometry of conventional and high frequencies, distortion product otoacoustic emissions, and electrophysiological measures of auditory nerve and brainstem function as reflected in the click-evoked auditory brainstem response (ABR). In experiment 1, ABRs were recorded in a quiet background across stimulus levels (30-90 dB nHL) presented in 10 dB steps. In experiment 2, the ABR was elicited by a 70 dB nHL click stimulus presented in a quiet background, and in the presence of simultaneous ipsilateral continuous broadband noise presented at 50, 60, and 70 dB SPL using an insert earphone (Etymotic, ER2). There were no differences between the low- and high-risk groups in audiometric thresholds or distortion product otoacoustic emission amplitude. Experiment 1 demonstrated smaller wave-I amplitudes at moderate and high sound levels for high-risk compared to low-risk group with similar wave III and wave V amplitude. Enhanced amplitude ratio V/I, particularly at moderate sound level (60 dB nHL), suggesting central compensation for reduced input from the periphery for high-risk group. The results of experiment 2 show that the decrease in wave I amplitude with increasing background noise level was relatively smaller for the high-risk compared to the low-risk group. However, wave V amplitude reduction was essentially similar for both groups. These results suggest that masking induced wave I amplitude reduction is smaller in individuals at high risk for cochlear synaptopathy. Unlike previous studies, we did not observe a difference in the noise-induced wave V latency shift between low- and high-risk groups. Results of experiment 1 are consistent with findings in both animal studies (that suggest cochlear synaptopathy involving selective damage of low-spontaneous rate and medium-spontaneous rate fibers), and in several human studies that show changes in a range of ABR metrics that suggest the presence of cochlear synaptopathy. However, without postmortem examination by harvesting human temporal bone (the gold standard for identifying synaptopathy) with different noise exposure background, no direct inferences can be derived for the presence/extent of cochlear synaptopathy in high-risk group with high sound over-exposure history. Results of experiment 2 demonstrate that to the extent response amplitude reflects both the number of neural elements responding and the neural synchrony of the responding elements, the relatively smaller change in response amplitude for the high-risk group would suggest a reduced susceptibility to masking. One plausible mechanism would be that suppressive effects that kick in at moderate to high levels are different in these two groups, particularly at moderate levels of the masking noise. Altogether, a larger scale dataset with different noise exposure background, longitudinal measurements (changes due to recreational over-exposure by studying middle-school to high-school students enrolled in marching band) with an array of behavioral and electrophysiological tests are needed to understand the complex pathogenesis of sound over-exposure damage in normal-hearing individuals.

Detecting changes in distortion product otoacoustic emission maps using statistical parametric mapping and random field theory.

Distortion product otoacoustic emission (DPOAE) maps collect DPOAE emissions over a broad range of frequencies and ratios. One application of DPOAE mapping could be monitoring changes in intracranial pressure (ICP) in space, where non-invasive measures of ICP are an area of interest. Data were collected in two experiments to statistically assess changes in DPOAE maps. A repeatability study where four maps per subject were collected across four weeks to establish "normal" variability in DPOAE data, and a posture study where subjects were measured supine and prone with lower body negative pressure, lower body positive pressure (LBPP), and at atmospheric pressure. DPOAE amplitude maps were analyzed using statistical parametric mapping and random field theory. Postural changes produced regional changes in the maps, specifically in the range of 5-7.5 kHz and between primary tone ratios of 1.13-1.24. These regional changes were most pronounced in the prone LBPP condition, where amplitudes were lower from baseline for the Postural Cohort than the Repeatability Cohort. Statistical parametric mapping provided a sensitive measure of regional DPOAE map changes, which may be useful clinically to monitor ICP noninvasively in individuals or for research to identify differences within in cohorts of people.

Effect of Auditory Predictability on the Human Peripheral Auditory System.

Auditory perception is facilitated by prior knowledge about the statistics of the acoustic environment. Predictions about upcoming auditory stimuli are processed at various stages along the human auditory pathway, including the cortex and midbrain. Whether such auditory predictions are processed also at hierarchically lower stages—in the peripheral auditory system—is unclear. To address this question, we assessed outer hair cell (OHC) activity in response to isochronous tone sequences and varied the predictability and behavioral relevance of the individual tones (by manipulating tone-to-tone probabilities and the human participants’ task, respectively). We found that predictability alters the amplitude of distortion-product otoacoustic emissions (DPOAEs, a measure of OHC activity) in a manner that depends on the behavioral relevance of the tones. Simultaneously recorded cortical responses showed a significant effect of both predictability and behavioral relevance of the tones, indicating that their experimental manipulations were effective in central auditory processing stages. Our results provide evidence for a top-down effect on the processing of auditory predictability in the human peripheral auditory system, in line with previous studies showing peripheral effects of auditory attention.

Stroke risk in African Americans with subclinical auditory dysfuntion evidenced by Distortion Product Otoacoustic Emissions: the Jackson heart study

Objective: Distortion product otoacoustic emissions (DPOAEs) are sensitive to early indices of cochlear pathology. Pathology to the cochlea is in part mediated by ischaemic related mechanisms. We propose that DPOAEs may provide an objective measure of cardiovascular risk. Design: Cross-sectional. Study sample: The relationships between stroke risk and DPOAEs of 1,107 individuals from the Jackson Heart Study (JHS), an all-African-American cohort, were assessed. Linear regression models were used for analysis among all participants and delimited to normal hearing, defined as either a pure-tone threshold average of 500, 1000, 2000, and 4000 Hz (PTA4) ≤ 25 dBHL or pure-tone thresholds for all individual tested frequencies for each ear (500, 1000, 2000, 4000, and 8000 Hz) ≤ 25 dBHL. Results: We observed a significant inverse relationship between DPOAE amplitudes and stroke risk scores in the pooled cohort and in the subgroups with normal hearing defined by pure tone thresholds. Participants in the high-risk group had significantly lower DPOAE amplitudes than those in the low stroke risk group. Conclusions: Our results indicate that auditory dysfunction as measured by DPOAEs are related to stroke risk. Further prospective studies are needed to determine if DPOAEs could be used as a predictive tool for cardiovascular disease.

Cochlear dysfunction is associated with styrene exposure in humans.

AimOccupational exposure to styrene has been shown to be associated with an increased probability of developing hearing loss. However, the sites of lesions in the auditory system in humans remain unknown. The aim of this study was to investigate the possible adverse effects of styrene exposure on the cochlea of human subjects.DesignThe hearing function of 98 styrene-exposed male workers from the glass fibre-reinforced plastics industry (mean concentration of 55 mg/m3) was evaluated bilaterally using pure-tone audiometry (1000–16000 Hz), distortion product otoacoustic emissions (DPOAEs), and auditory brainstem response (ABR). The results were compared to a group of 111 male workers exposed to noise (above 85 dBA) and 70 male white-collar workers exposed to neither noise nor solvents. Age and noise exposure levels were accounted for as confounding variables in all statistical models.ResultsStyrene exposure was significantly associated with poorer pure-tone thresholds (1–8 kHz), lower DPOAE amplitudes (5–6 kHz), and shorter wave V latencies in both ears compared to control-group subjects. Similar results were found among noise-exposed subjects. A further analysis with wave V latency showed that styrene-exposed subjects showed significantly shorter latencies than expected according to normative data. These results suggest that occupational exposure to styrene at moderate concentrations is associated with cochlear dysfunction, at least at high frequencies. DPOAEs may be considered a valuable diagnostic tool in hearing conservation programs in workers exposed to styrene.

Effect of chronic suppurative otitis media on distortion product otoacoustic emission input-output functions in conventional and ultra-high frequencies.

Detection and valid measurements of distortion product otoacoustic emissions are not influenced by cochlear status alone, but also by middle-ear status. There is a need to understand the use of ultra-high frequency distortion product otoacoustic emissions in cases of abnormal distortion product otoacoustic emission findings for conventional frequencies related to the middle-ear condition. The present study investigated distortion product otoacoustic emission input-output functions in conventional and ultra-high frequencies in: 37 adults with chronic suppurative otitis media (clinical group) and 37 adults with normal hearing sensitivity (control group). There were significant reductions in distortion product otoacoustic emission amplitude and mean signal-to-noise ratio in the clinical group compared to the control group, especially for conventional frequencies. There was a significant reduction in the rate of ears with measurable distortion product otoacoustic emissions in the clinical group, especially for conventional frequencies. The effect of chronic suppurative otitis media was more pronounced in the conventional frequency range compared to the smaller effect seen in the ultra-high frequency range.

Behavioral Hearing Thresholds and Distortion Product Otoacoustic Emissions in Cannabis Smokers.

Purpose Cannabis is a widely used drug both medically and recreationally. The aim of this study was to determine if cannabis smoking is associated with changes in auditory function, as measured by behavioral hearing thresholds and/or distortion product otoacoustic emissions (DPOAEs). Method We investigated hearing thresholds and 2f1-f2 DPOAEs in 20 cannabis smokers and 20 nonsmokers between 18 and 28 years old. Behavioral thresholds were obtained from 0.25 to 16 kHz. DPOAEs were measured using discrete tones between f2 of 0.5 and 19.03 kHz using an f2/f1 ratio of 1.22 and L1/L2 = 65/55 dB SPL. Thresholds and DPOAE amplitudes were compared between groups using linear mixed-effects models with sex and frequency as predictors. Results Behavioral thresholds in smokers did not differ significantly between smokers and nonsmokers (all ps > .05). Although not significant, long-term smokers exhibited poorer thresholds than short-term smokers and nonsmokers. Smokers generally exhibited lower DPOAE amplitudes than nonsmokers, although the differences were not significant. Male smokers had significantly poorer DPOAE amplitudes than male nonsmokers in the low frequencies (f2 ≤ 2 kHz; p = .0245). Conclusion Results indicate that smoking cannabis may negatively alter the function of outer hair cells in young men. This subtle cochleopathology is evident in the absence of measurable differences in behavioral hearing thresholds between cannabis smokers and nonsmokers.

Otological aspects of Fabry disease in patients with normal hearing.

ABSTRACTWe investigated the otological aspects of Fabry disease (FD) in patients with normal hearing. Forty-one patients (21 men, 20 women) with bilaterally normal hearing were recruited, and their otological symptoms and hearing evaluations, which included pure tone audiometry (PTA) and distortion product otoacoustic emission (DPOAE), were investigated. Ten of the 21 male (47.6%) and eight of the 20 female (40.0%) patients had otological symptoms, of which tinnitus was the most frequent. Cardiac dysfunction was more frequently observed in female patients. The average thresholds on PTA were below 25 dB at all frequencies, but DPOAE amplitudes were significantly lower in female patients at some frequencies. Otological symptoms were frequently observed in patients with FD, despite their normal hearing levels on PTA. DPOAE might provide useful information regarding cochlear disturbances related to the disease..

Distributed sources as a cause of abrupt amplitude decrease in cubic distortion-product otoacoustic emissions at high stimulus intensities.

The amplitudes of distortion-product otoacoustic emissions (DPOAEs) may abruptly decrease even though the stimulus level is relatively high. These notches observed in the DPOAE input/output functions or distortion-product grams have been hypothesized to be due to destructive interference between wavelets generated by distributed sources of the nonlinear-distortion component of DPOAEs. In this paper, simulations with a smooth cochlear model and its analytical solution support the hypothesis that destructive interference between individual wavelets may lead to the amplitude notches and explain the cause for onset and offset amplitude overshoots in the DPOAE signal measured for intensity pairs in the notches.