Inflammatory Monocytes Infiltrate the Spiral Ligament and Migrate to the Basilar Membrane After Noise Exposure

A 41‐year‐old male firefighter arrived at a hospital emergency room 43 h post acute noise exposure (mechanical siren, 2.5 min total exposure time in an enclosed space) with complaints of tinnitus, decreased hearing, and vague balance problems. He was subsequently evaluated in an otolaryngology clinic and an audiology clinic. The presented complaints resolved during the next month. The subject did return for follow‐up. ENT findings were unremarkable at both visits. OSHA baseline audiometrics, audiometry at 47 h post noise insult, and audiometry at 30 days post noise exposure were reviewed. Extended high‐frequency audiometry (8 to 20 kHz) was obtained during the initial hospital audiometry (47 h post noise insult) and at the time of the follow‐up audiometry. Conventional audiometry and extended high‐frequency threshold data were explored and changes in threshold hearing acuity were examined for potential correlation with subjective complaints. Extended high‐tone andiometry did suggest a tenuous correlation with the presented complaints. Formal sound pressure readings during mechanical siren operation were taken at the site of noise exposure to delineate noise dosage. Implications of siren noise exposure on long‐term hearing sensitivity change were explored.

<sec><st>Introduction</st> Cortisol is a hormone produced by adrenal glands under the control of pituitary gland which helps the organism to cope with different types of stress. One of these possible stressors might be occupational noise exposure. Our research studied the possible influence of noise exposure on cortisol blood level (CBL) and if noise induced hearing loss (NIHL) may play a role in this relationship. </sec> <sec><st>Material and method</st> 118 workers from a silicon carbide facility were initially included of whom 67 completed the study. For each job site noise exposure was assessed and a cumulative exposure was calculated for every subject (number of years spent in the same job x noise level). A complete physical examination, a pre exposure audio-metric test and two blood samples taken at the same time one week interval (one pre noise exposure – afternoon shift; the other post noise exposure – morning shift) were performed. T Test was used to make statistical analysis. </sec> <sec><st>Results</st> Mean age = 42.2±6.29 years. Mean exposure time = 16.16±5.41 years. Mean noise level = 84.88±3.71 dB. Mean cumulative exposure = 1,377±470.9 dB-years. Normal hearing (NH) = 33 subjects (49.25%). NIHL = 34 subjects (50.75%). CBL pre exposure = 126.87 µg/l and post exposure = 114.92 µg/l (p = 0.204). CBL in NH subgroup: pre exposure = 110.04±63.35 µg/l, post exposure = 129.44±66.1 µg/l (p = 0.194). CBL in NIHL subgroup: pre exposure = 143.19±59.77 µg/l, post exposure = 100.82±47.24 µg/l (p = 0.000). CBL pre exposure: NH subjects = 110.04±63.35 µg/l, NIHL = 143.19±59.77 µg/l (p = 0.031). CBL post exposure: NH = 129.44±66.1 µg/l, NIHL = 100.82±47.24 µg/l (p = 0.045). </sec> <sec><st>Conclusions</st> There was no significant difference in CBL measured pre and post noise exposure in the entire group. However, we found a statistical significant difference in CBL in NIHL subgroup (lower level post exposure). This subgroup also had significant higher values pre exposure and lower post exposure compared to NH subgroup. These findings have to confirmed by more in depth research. </sec>

ObjectiveTo study the effects of D-methionine in a mouse model of noise-induced hearing loss (NIHL).MethodsWe investigated changes in auditory function and microscopic cochlear structure in a mouse model of NIHL, and carried out 4-hydroxynonenal (4-HNE) immunostaining and terminal deoxynucleotidyl transferase dUTP nick-end labeling, and examined expression levels of connexins 26 and 30 by western blot.ResultsThe auditory brainstem response threshold was significantly increased by noise exposure. Noise exposure also damaged the inner and particularly the outer hair cells in the cochlear basement membrane, while histochemistry demonstrated only scattered loss of hair cells in the basement membrane in mice treated with D-methionine before or after noise exposure. D-methionine inhibited apoptosis in the cochlear basement membrane, stria vascularis, and spiral ligament. 4-HNE expression in the basement membrane, stria vascularis, and spiral collateral ligament was increased by noise exposure, but this increase was attenuated by D-methionine. Connexin 26 and connexin 30 expression levels were reduced by noise exposure, and this effect was similarly attenuated by D-methionine administered either before or after noise exposure.ConclusionD-methionine administered before or after noise exposure could rescue NIHL by protecting cochlear morphology, inhibiting apoptosis, and maintaining connexin 26 and 30 expression.

Winch-assisted harvesting has expanded considerably in recent years as it enables ground-based machines to work safely on steep slopes. To analyze operator exposure to whole-body and hand–arm vibration (WBV, HAV) and noise exposure (LAeq, LCpeak) during winch-assisted harvesting (TW) and harvesting without winch assistance (NTW), a field study using a Ponsse Scorpion King harvester and an Ecoforst T-winch traction winch was conducted. Vibrations were measured at three locations inside the cabin (seat, seat base/floor, control lever), while noise exposure was recorded both inside and outside the cabin. WBV exposure during work time operations was highest in the Y-direction, both on the seat (0.49–0.87 m/s2) and on the floor (0.41–0.84 m/s2). The WBV and HAV exposure levels were highest while driving on the forest and skid road. Exposure during the main productive time was significantly influenced by the harvesting system, diameter at breast height (DBH), and tree species. Noise exposure was higher, while WBV and HAV exposures on the seat, floor and control lever were lower during non-work time than during work time. The daily vibration exposure on the seat exceeded the EU action value, while LCpeak noise exposure surpassed the limit value of 140 dB(C) on all measured days. Noise and vibration exposure were constantly higher during TW than NTW harvesting but differences were small. Compared to other studies, the results show that harvesting on steep terrain increases noise and vibration exposure, while non-work time has the opposite effect on vibration and noise exposure.

Manganese superoxide dismutase influences the extent of noise-induced hearing loss in mice

Effect of noise exposure on blood–labyrinth barrier in guinea pigs

Background Only few studies have investigated the association between environmental noise exposure and cardiovascular outcomes after an acute Myocardial Infarction (MI). Purpose We aimed to analyze the relationship between residential environmental noise exposure and one-year prognosis after a first MI. Methods Observational, longitudinal study from the French regional RICO registry including adult patients hospitalized for an inaugural MI in 2004 to 2009, residing in Dijon urban unit, and who survived > 28 days after the acute event. Major Adverse Cardiovascular Events (MACE) were collected at 1-year follow-up. Environmental noise and air pollutants exposure were derived from contamination prediction models and considered at each patient’s residence. Annual averaged noise exposure was assessed as daily (LAeq,24h) and at night (Lnight). Air pollution levels were evaluated as nitrogen dioxide (NO2) and particulate matter (PM10) exposure within the 30 days preceding a MACE. Results Among the subjects included (n=864), 19% underwent a MACE at follow-up. Both noise exposure during the night (Lnight) and daily exposure (LAeq.24h) were associated with prognosis in univariate analysis. The hazard ratio (HR) associated with a 10 dB (A) increase for Lnight and LAeq.24h were 1.25 (95% CI 1.09 to 1.43, P = .001) and 1.23 (95% CI 1.06 to 1.43, P = .007). In multivariable analysis, the associations between noise exposure and outcomes were only slightly modified and remained significant, even after adjustment for confounding including age, sex, CV risk factors, deprivation index, LVEF, GRACE risk score and air pollutants. Conclusion Our findings showed a strong association between residential noise exposure and prognosis one year after an acute MI. If confirmed by larger prospective studies, our study could help to identify original opportunities for environment-based secondary prevention strategies.

Received March 5, 2013 Revised April 9, 2013 Accepted April 10, 2013 Address for correspondence Yong Ho Park, MD Department of Otolaryngology-Head and Neck Surgery, Chungnam National University School of Medicine, 282 Munhwa-ro, Jung-gu, Daejeon 301-721, Korea Tel +82-42-280-7697 Fax +82-42-253-4059 E-mail parkyh@cnu.ac.kr Background and ObjectivesZZThere are several evidences of reduced cochlea blood flow after noise exposure in the cochlea. However, the pathophysiology of blood flow change is still obscure, and endothelins, proteins that constrict blood vessels and play a key role in vascular homeostasis using its receptors may have importance in this respect. In this study, we investigated the expression changes of endothelin-1 (ET-1), endothelin receptor A (ETAR) and B (ETBR) according to auditory threshold change after noise exposure. Materials and MethodZZMice were exposed to different noise to generate transient (group 2) and permanent threshold shift (group 3), respectively. Auditory threshold shifts were evaluated with auditory brainstem response and expression changes of ET-1, ETAR and ETBR after noise exposure were evaluated by immunohistochemistry and real time RT-PCR. ResultsZZAfter noise exposure, the increased ET-1, ETAR and ETBR immunoreactivities were observe in stria vascularis, spiral ligament and spiral ganglion neuron. ET-1 mRNA expressions increased after noise exposure in both group 2 and group 3 compared to those of the control group. At 2 weeks after noise exposure, however, the ET-1 mRNA expressions in group 3 increased compared to that of the control but decreased compared to that of group 2. On the other hand, ETAR mRNA expression increased at 2 weeks after noise exposure in both groups, just after noise exposure in group 2 and at 2 weeks after noise exposure in group 3. ConclusionZZThese results suggest that expression changes of ET-1, ETAR and ETBR might be associated with hearing threshold shift and recovery after noise exposure in the cochlea. Korean J Otorhinolaryngol-Head Neck Surg 2013;56:278-85

Stress response in rat brain after different durations of noise exposure

This is an assessment of occupational noise exposures in the construction industry based on (1) noise measurements observed during Occupational Safety and Health Administration (OSHA) inspections over the period from 1986 through early 1997 and (2) the observed incidence of noise exposures over 85 dB (A) in a national random sample of construction firms done as part of the NIOSH National Occupational Exposure Survey (NOES) in 1981-83. The OSHA inspection data are analyzed by both industry categories and a classification system of equipment and occupational types based on free form descriptions of “job title” by OSHA inspectors.Because construction workers' jobs and work tasks change frequently, the noise observations within each industry were treated as a distribution indicating the fraction of time that workers would be likely to spend at various noise levels projected to a common year (1995). The time at each noise level in OSHA measured dB(A) was summarized in terms of “90 dB(A) equivalents” using the “equal energy rule” which weights a day of exposure time at 100 dB(A), for example, as the equivalent of 10 days of exposure at 90 dB(A). Overall the 1995 projected exposures are slightly less than one “90 dB(A) equivalent” of continuous noise exposure per worker in the industry. This estimate is generally compatible with three other extensive sets of noise measurements for construction workers in the U.S. and Canada.In further work the exposure estimates developed here will be used to project the hearing losses likely to result from work in construction industries. Those results will be compared with extensive available data on the hearing loss experience of construction workers in British Columbia. The results will

Voluntary wheel exercise ameliorates cognitive impairment, hippocampal neurodegeneration and microglial abnormalities preceded by demyelination in a male mouse model of noise-induced hearing loss

LCCL peptide cleavage after noise exposure exacerbates hearing loss and is associated with the monocyte infiltration in the cochlea

Toxic levels of reactive oxygen species are key contributors to the lesion of dead outer hair cells (OHCs) seen in the cochlea after noise exposure. The current study follows previous work in which paraquat was used to demonstrate that NADPH oxidase is active in the cochlea and can contribute to cochlear reactive oxygen species formation and hair cell loss. The current study was undertaken to test whether pharmacological blockade of NADPH oxidase in the cochlea would lead to reduced noise-induced hearing loss and OHC death. A total of 18 chinchillas (36 ears) were assessed in the study. AEBSF (4-[2-aminoethyl]benzenesulfonyl fluoride), an inhibitor of NADPH oxidase activation, was dissolved in distilled water and delivered into the cochlea via diffusion across the round window membrane. The contralateral ears received distilled water as a vehicle control. Following treatment, chinchillas were exposed to one of two noises: a 4 kHz octave band noise at 106 dB SPL for 6 hr or an impulse noise that consisted of 75 pairs of 155 dB pSPL impulses. Pre- and post-noise exposure, thresholds of the auditory brainstem response at 2-8 kHz were measured. Postmortem OHC counts were conducted at the conclusion of the study. Two- and three-factor ANOVAs were used for statistical analysis of the OHC losses and ABR threshold shifts induced by the noise exposures. Permanent threshold shift from the impulse noise was reduced in the ears treated with the NADPH oxidase inhibitor, but no differences were found in the groups exposed to the continuous noise. OHC losses were not statistically different between the treated and untreated ears for either noise exposure. The results suggest that NADPH oxidase-mediated superoxide has a role in cochlear damage from impulse noise, and pharmacologic inhibition of NADPH oxidase can reduce cochlear susceptibility to noise damage. The lack of protection from the longer-duration continuous noise can be attributed to a number of possibilities related to dose level and delivery schedule.

In 2017, the Centers for Disease Control and Prevention (CDC) reported that almost 25% of American adults age 20-69 had noise-induced hearing loss (NIHL), with 53% of them reporting no significant noise exposure. 1 If we were in the movie business, our recent paper in Proceedings of Meetings on Acoustics2 might be called a prequel to the CDC report because it explains why so many Americans are losing hearing without occupational noise exposure: They are exposed to too much noise.Shutterstock/ivectorTable 1: Common Nonoccupational Noise Exposures.Occupational hearing loss has been known from stonemasons in the Middle Ages to factory workers in the industrial era, but nonoccupational noise exposure was not recognized as a problem until the 1960s. 3 Before World War II, noise exposure outside the workplace was rare. That changed in postwar America. Convenient electric appliances, home stereo systems boasting about their wattage outputs, the advent of rock and roll music, and the use of amplified sound at parties and life cycle celebrations such as weddings became common. By the end of the 20th century, personal audio systems (PAS), also called personal music players or personal listening devices, were common, with their use accelerating dramatically after PAS became available on MP3 players and then smartphones. Young people especially use PAS to listen to loud music and audio content for hours a day. Often, users must turn up the volume to overcome high ambient noise, especially while commuting. Flamme, et al., found that although people spend most of their time in relatively quiet environments when not at work, total noise exposure is dominated by a small number of high-level exposures. 4 Occupational and nonoccupational noise and auditory risk relationships are based on the time-weighted average (TWA) of regular and intermittent sound levels, commonly measured in A-weighted decibels (dBA), over a specified exposure duration, typically 8-h daily for occupational noise and 24-h for non-occupational noise. 5,6 In the United States, 85 dBA is the recommended occupational noise exposure limit, not a safe noise exposure level for the public. 6 In adult workers, the risk of hearing impairment is 1% at 80 dBA, 8% at 85 dBA, and 25% at 90 dB TWA. 5 Although other etiologies can’t be ruled out on the basis of an audiogram, NIHL typically first develops in the 3-6 kHz speech frequency range. Risk estimates don’t consider additional auditory impairments characteristic of noise damage, including tinnitus, hyperacusis or decreased sound tolerance, speech-in-noise performance deficits, impaired otoacoustic emissions, and extended high-frequency hearing loss. 7,8 CALCULATING SAFE NOISE LEVELS What is the safe noise level for the public? As calculated by the Environmental Protection Agency (EPA), the only evidence-based safe noise exposure level to prevent NIHL is a 24-h daily average of 70 dBA, 6 and even that may be too high. One thing is known for sure: The oft-cited 85 dB threshold is not the sound pressure level at which hearing loss begins. The auditory injury threshold is only 75-78 dBA regardless of listening time. 4 Auditory systems process total sound intensity instantaneously in real-time, not as a TWA. Nonoccupational noise sources are ubiquitous, and most Americans are now exposed to sufficient noise in everyday life to cause NIHL. Flamme, et al., 4 found that 70% of research subjects in Grand Rapids, MI, exceeded the EPA safe noise level. Neitzel, et al., reported that 90% of New York City transit users and 87% of nonusers exceeded the EPA 70 dB safe daily noise limit, 9 as did about 88% of subjects in Sweden, 84% of people studied in Spain, and 85% in China. 10 Smith, et al., analyzing data collected by the Apple Hearing Study, found average daily noise exposure in the United States to be 73 dBA before COVID-19-related lockdowns began in March 2020. 11 These noise exposures, not ear infections, ototoxic drugs, or aging alone, are most likely the cause of the high prevalence of hearing loss reported in industrialized countries. In our paper, we summarized published sound levels from six categories of nonoccupational noise sources common in everyday life. All research was done meeting ethical requirements, using standard equipment (e.g., OSHA Type II noise dosimeters), following accepted audiometric protocols (e.g., ISO 8253-1:2010), with study designs appropriate to the specific question being investigated. Each study cited used different methods in different populations in different settings, but even allowing for variations in instrumentation, possible errors in calibration, observer error, and lack of standardization of measurement, the sound levels were generally consistent among reports from different authors and with our own unpublished measurements. The consistency of the numbers provides great confidence in the generalizability of this research. As shown in Table 1, common nonoccupational noise exposures range from 70 dBA on average at the low end to as much as 111 dBA. The cumulative daily noise dose from all these activities is clearly sufficient to cause NIHL. NIHL is entirely preventable but once acquired is permanent and irreversible. Hearing loss is an invisible disability with major social, health, and economic consequences for individuals and society, costing the global economy $980 billion annually. 12 Early hearing loss is associated with lower educational attainment and decreased lifetime income. Untreated hearing loss in older adults is correlated with increased hospital use and greater total health care costs. Among the elderly, hearing loss is strongly correlated with social isolation, depression, dementia, falls, and accidents, all in turn associated with increased mortality. ROLE OF HEARING CARE PROFESSIONALS Audiologists and physicians, particularly otolaryngologists, have a responsibility to educate the public about nonoccupational noise risk from daily average exposures >70 dBA. Especially in this era of concern about the accuracy of public health -advice, it is no longer acceptable for audiologists to post inaccurate information on their practice websites or to make inaccurate statements in media reports. Misleading statements such as, “Sounds at 85 dBA can lead to hearing loss if you listen to them for more than 8 hours at a time” are still available on the American Speech-Language Hearing Association website, but the National Institute on Deafness and Other Communication Disorders recently removed the factually incorrect statement, “Know which noises can cause damage (those at or above 85 dBA),” from its webpage about NIHL. An 85-dBA noise exposure that doesn’t prevent hearing loss in working adults is far too high for a child’s delicate ears that have to last an entire lifetime. Society should no longer accept common nonoccupational noise exposures. Prevention of NIHL is both better and less expensive than the long-term health care and socioeconomic costs of hearing loss. Smoking was once seen as something normal, a harmless habit. Cigarette smoke was everywhere—in buses, trains, airplanes, offices, even hospitals, and doctors’ waiting rooms. Then science showed that smoking caused cancer, that secondhand smoke was a Class A carcinogen with no safe lower level of exposure, and the air became smoke free. Similarly, excessive noise is now just part of everyday life. We hope that awareness of the dangers of noise will lead to a quieter world. Depending on the source, required noise control includes mandatory noise emission limits and venue noise policies, including hearing protection requirements. Editor’s note: This article is adapted from Fink, D., Mayes, J. Too loud: non-occupational noise exposure is causing hearing loss. Proc. Mtgs. Acoust. 43, 004002 (2021) https://doi.org/10.1121/2.0001436, with the permission of the Acoustical Society of America.

Several studies have shown that type IV fibrocytes, located in the spiral ligament, degenerate first after noise exposure. Interestingly, this is the region where Coch expression is most abundant. As it is suggested that cochlin plays a role in our innate immune system, our goal is to investigate hearing thresholds and inner ear inflammation after noise exposure in Coch knockout (Coch−/−) mice compared to Coch wildtype (Coch+/+) mice. Animals were randomly allocated to a noise exposure group and a control group. Vestibular and auditory testing was performed at 48 h and one week after noise exposure. Whole mount staining and cryosectioning of the cochlea was performed in order to investigate hair cells, spiral ganglion neurons, inner ear inflammation, Coch expression and fibrocyte degeneration. Hearing assessment revealed that Coch+/+ mice had significantly larger threshold shifts than Coch−/− mice after noise exposure. We were unable to identify any differences in hair cells, neurons, fibrocytes and influx of macrophages in the inner ear between both groups. Interestingly, Coch expression was significantly lower in the group exposed to noise. Our results indicate that the absence of Coch has a protective influence on hearing thresholds after noise exposure, but this is not related to reduced inner ear inflammation in the knockout.