Early Noise Exposure Research Articles

Safe Listening at Venues and Events with Amplified Music — United States, 2022

Nearly one in four (24.4%) U.S. adults aged 20-69 years show evidence of noise-induced hearing loss (1). Among those reporting exposure to noise outside of work, 19.9% showed possible noise-induced hearing loss. Exposure to non-job-related noise can be substantial (2). Loud music from personal listening devices and entertainment venues might place more than 1 billion teenagers and young adults at risk for hearing loss worldwide (3). Early noise exposure might increase the risk for age-related hearing loss later in life (4). CDC analyzed data from the 2022 FallStyles survey (conducted by Porter Novelli via the Ipsos' KnowledgePanel) on U.S. adult perceptions regarding preventing hearing loss from amplified music at venues or events. More than one half of U.S. adults agreed with one or more of the following protective actions: limiting sound levels, posting warning signs, and using hearing protection when music at such events reaches potentially hazardous levels. Hearing and other health professionals can make use of existing materials available from the World Health Organization (WHO), CDC, and other professional organizations to raise awareness about noise risks and promote protective behaviors.

Noise-induced auditory damage affects hippocampus causing memory deficits in a model of early age-related hearing loss

Several studies identified noise-induced hearing loss (NIHL) as a risk factor for sensory aging and cognitive decline processes, including neurodegenerative diseases, such as dementia and age-related hearing loss (ARHL). Although the association between noise- and age-induced hearing impairment has been widely documented by epidemiological and experimental studies, the molecular mechanisms underlying this association are not fully understood as it is not known how these risk factors (aging and noise) can interact, affecting memory processes. We recently found that early noise exposure in an established animal model of ARHL (C57BL/6 mice) accelerates the onset of age-related cochlear dysfunctions. Here, we extended our previous data by investigating what happens in central brain structures (auditory cortex and hippocampus), to assess the relationship between hearing and memory impairment and the possible combined effect of noise and sensory aging on the cognitive domain. To this aim, we exposed juvenile C57BL/6 mice of 2 months of age to repeated noise sessions (60 min/day, pure tone of 100 dB SPL, 10 kHz, 10 consecutive days) and we monitored auditory threshold by measuring auditory brainstem responses (ABR), spatial working memory, by using the Y-maze test, and basal synaptic transmission by using ex vivo electrophysiological recordings, at different time points (1, 4 and 7 months after the onset of noise exposure, corresponding to 3, 6 and 9 months of age). We found that hearing loss, along with accelerated presbycusis onset, can induce persistent synaptic alterations in the auditory cortex. This was associated with decreased memory performance and oxidative-inflammatory injury in the hippocampus, the extra-auditory structure involved in memory processes. Collectively, our data confirm the critical relationship between auditory and memory circuits, suggesting that the combined detrimental effect of noise and sensory aging on hearing function can be considered a high-risk factor for both sensory and cognitive degenerative processes, given that early noise exposure accelerates presbycusis phenotype and induces hippocampal-dependent memory dysfunctions.

Effects of early noise exposure on hippocampal-dependent behaviors during adolescence in male rats: influence of different housing conditions.

Central nervous system (CNS) development is a very complex process that can be altered by environmental stimuli such as noise, which can generate long-term auditory and/or extra-auditory impairments. We have previously reported that early noise exposure can induce hippocampus-related behavioral alterations in postnatal day (PND) 28 adolescent rats. Furthermore, we recently found biochemical modifications in the hippocampus (HC) of these animals that seemed to endure even in more mature animals (i.e. PND35) and that have not been studied along with behavioral correlates. Thus, the aim of this work was to reveal novel data about the effects of early noise exposure on hippocampal-dependent behaviors in more mature animals. Additionally, extended enriched environment (EE) housing was evaluated to determine its capacity to induce behavioral modifications, either by its neuroprotective ability or the greater stimulation that it generates. Male Wistar rats were exposed to different noise schemes at PND7 or PND15. Upon weaning, some animals were transferred to EE whereas others were kept in standard cages. At PND35, different hippocampal-dependent behavioral assessments were performed. Results showed noise-induced behavioral changes that differed according to the scheme and age of exposure used. In addition, housing in an EE was effective either in preventing some of these changes or in inducing the appearance of new behavioral modifications. These findings suggest that CNS development would be sensitive to the effects of different type of environmental stimuli such as noise or enriched housing, leading to maladaptive behavioral changes that last even until adolescence.

Hazardous sound outputs of white noise devices intended for infants

ObjectivesTo measure the sound intensity of popular infant white noise machines and Apple iPhone applications (apps) as they vary with volume setting and distance, and compare these output levels with current National Institute for Occupational Safety and Health (NIOSH) noise exposure threshold recommendations. MethodsA total of eight infant white noise machines and six iPhone applications were included in the study based on product rating, number of ratings, and cost. The NIOSH Sound Level Meter application through the Apple App Store was used to measure output levels in A-weighted decibels (dBA). Each device was tested at its lowest and highest volume setting and at speaker-to-microphone distances simulating placement within a crib (10 cm), just outside of a crib rail (30 cm), and on a nightstand across the room (100 cm). ResultsAt the minimum volume setting, no device exceeded the NIOSH recommended noise exposure threshold of 85 dBA at any distance tested. At maximum volume setting, nine out of fourteen (64.3%) devices exceeded output levels of 85 dBA at a speaker-to-microphone distance of 10 cm. No device exceeded the recommended threshold at its maximal volume when placed 30 cm or 100 cm away. ConclusionExcessive white noise exposure has the potential to lead to noise-induced hearing loss and other adverse health effects in the neonatal and infant population. We recommend conservative use of white noise machines and apps by avoiding maximal volume setting and placing any device well outside of the crib or at least 30 cm away from the child. To promote safe use of white noise devices, future studies are needed to fully understand the association between early noise exposure and hearing loss in infants.

Noise-induced hippocampal oxidative imbalance and aminoacidergic neurotransmitters alterations in developing male rats: Influence of enriched environment during adolescence.

Living in big cities might involuntarily expose people to high levels of noise causing auditory and/or extra-auditory impairments, including adverse effects on central nervous system (CNS) areas such as the hippocampus. In particular, CNS development is a very complex process that can be altered by environmental stimuli. We have previously shown that noise exposure of developing rats can induce hippocampal-related behavioral alterations. However, noise-induced biochemical alterations had not been studied yet. Thus, the aim of this work was to assess whether early noise exposure can affect rat hippocampal oxidative state and aminoacidergic neurotransmission tone. Additionally, the effectiveness of an enriched environment (EE) as a neuroprotective strategy was evaluated. Male Wistar rats were exposed to different noise schemes at 7 or 15days after birth. Upon weaning, some animals were transferred to an EE whereas others were kept in standard cages. Short- and long-term measurements were performed to evaluate reactive oxygen species, thioredoxins levels and catalase activity as indicators of hippocampal oxidative status as well as glutamic acid decarboxylase and a subtype of glutamate transporter to evaluate aminoacidergic neurotransmission tone. Results showed noise-induced changes in hippocampal oxidative state and aminoacidergic neurotransmission markers that lasted until adolescence and differed according to the scheme and the age of exposure. Finally, EE housing was effective in preventing some of these changes. These findings suggest that CNS development seems to be sensitive to the effects of stressors such as noise, as well as those of an environmental stimulation, favoring prompt and lasting molecular changes.

Occupational noise and age: A longitudinal study of hearing sensitivity as a function of noise exposure and age in South African gold mine workers.

BackgroundA relationship exists between occupational noise exposure and age, which remains poorly understood.ObjectivesThe aim of this study was to establish the relationship between hearing loss and age over time.MethodAudiological data from 2583 mine workers in South Africa were utilised. Data were received from a non-noise exposed group (NNEG) (n = 951) and a noise exposed group (NEG) (≥85 dBA) (n = 1632). Data comprised a low-frequency average (LFA512) (average of audiological thresholds for 0.5 kHz, 1 kHz and 2 kHz) and high-frequency average (HFA346) (average of audiological thresholds for 3 kHz, 4 kHz and 6 kHz). Data were compared by using mixed-effects regression analysis.ResultsBase threshold values were higher for the NEG than for the NNEG across frequencies. All year-to-year increases in mean hearing thresholds were statistically significant (p < 0.01). When correcting for age, increases in mean hearing thresholds were higher for the NEG than for the NNEG for HFA346 (3.5 dB vs. 2.9 dB decline over a 4-year period) but similar for LFA512 (0.6 dB vs. 0.7 dB decline). Uncorrected for age, increases in mean hearing thresholds were higher than when age was corrected for.ConclusionAge and occupational noise exposure influence hearing thresholds over time. The continued increase in hearing thresholds of the NEG above that of the NNEG can be related to ineffective noise management programmes and/or the fact that early noise exposure leads to a higher burden of hearing loss over time – even after noise exposure had stopped.

Auditory Cortical Plasticity Dependent on Environmental Noise Statistics

SUMMARYDuring critical periods, neural circuits develop to form receptive fields that adapt to the sensory environment and enable optimal performance of relevant tasks. We hypothesized that early exposure to background noise can improve signal-in-noise processing, and the resulting receptive field plasticity in the primary auditory cortex can reveal functional principles guiding that important task. We raised rat pups in different spectro-temporal noise statistics during their auditory critical period. As adults, they showed enhanced behavioral performance in detecting vocalizations in noise. Concomitantly, encoding of vocalizations in noise in the primary auditory cortex improves with noise-rearing. Significantly, spectro-temporal modulation plasticity shifts cortical preferences away from the exposed noise statistics, thus reducing noise interference with the foreground sound representation. Auditory cortical plasticity shapes receptive field preferences to optimally extract foreground information in noisy environments during noise-rearing. Early noise exposure induces cortical circuits to implement efficient coding in the joint spectral and temporal modulation domain.

Rearing immature rats in an enriched environment can prevent the behavioral alterations induced by early noise exposure

Rearing immature rats in an enriched environment can prevent the behavioral alterations induced by early noise exposure

Enriched environment is able to counteract some of the histological alterations induced by early noise exposure

Enriched environment is able to counteract some of the histological alterations induced by early noise exposure

Environmental enrichment rescues the degraded auditory temporal resolution of cortical neurons induced by early noise exposure.

The accurate processing of sound temporal information is crucial to human speech perception and other species-specific communication. During postnatal development, the auditory cortex shows environmental and experience-dependent plasticity. However, how the postnatal environment affects cortical processing of sound temporal information is not fully understood. The aim of the present study was to determine whether postnatal noise exposure impairs neural temporal resolution in the auditory cortex, and, if so, whether environmental enrichment can rescue this degraded neural temporal acuity. Using the neural gap detection threshold determined in anesthetized rats as an index of temporal acuity, we found that exposure of juvenile rats to moderate-level noise induced much higher neural gap detection thresholds in adulthood than exposure of adult rats to the same noise. Environmental enrichment did not affect cortical neural gap detection thresholds in normally developing rats. However, rearing of rats with early noise exposure in an enriched environment promoted recovery from the noise-induced degraded neural temporal resolution. In addition, the tonal stimuli in the enriched environment contributed to only a portion of the recovery. These results provide evidence for noise-induced developmental impairment in neural gap detection thresholds in the auditory cortex, and suggest a therapeutic potential for environmental enrichment as a non-invasive approach to rescue developmentally degraded auditory temporal processing.

Analysis of Factors Affecting Output Levels and Frequencies of MP3 Players.

Exposure to high levels of music that could lead to music induced hearing loss (MIHL) has been of recent interest especially for young adults, considering their excessive use of personal listening devices such as MP3 player. More attention should be drawn to MIHL for noting that early noise exposure leads to earlier onset of presbycusis. In search of appropriate and safe listening habits for young adults, this investigation was aimed to evaluate output levels and frequencies generated by the Samsung galaxy note MP3 player depending on two earphone types; ear-bud and over-the-ear earphones and three music genres; rock, hip-hop, ballade. A sound level meter was used to measure output level and frequency spectrum between 12.5 and 16000 Hz at all 1/3-octave bands. The following results can be summarized. 1) The earphone styles did not produce significant difference in output levels, but the music genres did. However, the results of music genres varied. 2) Neither earphone styles nor music genres produced significant difference in frequency response spectrum, except music genres at the volume settings we usually listen to. Additionally, volume levels should be lower than 50% for usual listening situation. Through this investigation, it was noted that the frequency range was substantial between 50 and 1000 Hz regardless of the styles of earphones and music genres, implying that we should be cautious of this frequency range when we listen to music. Researchers should give more attention to the effects of the mixture of output level and frequency spectrum, considering that the auditory system has frequency specificity from the periphery to the central to provide refined methods for protecting our ears from MIHL.

Noise-induced hearing loss: scientific advances

Noise-Induced Hearing Loss: Scope of the Problem: The Prevalence and Significance of Noise-Induced Hearing Loss.- .- Noise-Induced Hearing Loss and Tinnitus: Challenges for the Military.- Relation Between Noise Exposure and Resulting Anatomical, Physiological and Perceptual Changes in Hearing: Acoustic Parameters Influencing Noise-Induced Hearing Loss .- Anatomical Consequences of Noise Insult.- Changes in VIII Nerve Coding with NIHL.- Suprathreshold Changes in Auditory System Function after Noise Exposure.- Central Nervous System Plasticity: Noise-Induced Tinnitus.- Susceptibility and Factors Contributing to NIHL: Genes that Influence Susceptibility to Noise-Induced Hearing Loss .- Effects of Early Noise Exposure on Subsequent Age-Related Changes in Hearing.- Effects of Exposure to Industrial Chemicals on Noise-Induced Hearing Loss.- Protection and Repair: Conventional Hearing Protection: Improved Mechanical Devices.- Prevention of Noise-Induced Hearing Loss: Potential Therapeutic Agents.- Hearing at Frontiers of Biology.- Index.

Noise‐induced and age‐related hearing loss interactions

Noise‐induced hearing loss (NIHL) and age‐related hearing loss (AHL, or presbycusis) are widespread health problems that will continue to increase as our society ages. NIHL and AHL often coexist in the same ear; however, the conditions under which they interact and the mechanisms by which they do so remain poorly understood. Inspired by epidemiological studies suggesting that noise‐exposed ears age differently from nonexposed ears [Gates et al., ‘‘Logitudinal threshhold changes in people with audiometric notches,’’ Hear. Res. 141, 220–228 (2000)], we studied interactions between NIHL and AHL in mouse; an animal with a short life span, with intrastrain genetic homogeneity to minimize variability and with interstrain differences in vulnerability which can be exploited to probe mechanisms. Using such models, we have uncovered evidence that early noise exposure can have an ongoing influence on the nature and progression of an age‐related hearing loss. The nature of this age‐related hearing loss exacerbation is special; it can occur even in ears without permanent threshold shifts from the noise and leads to massive loss of spiral ganglion neurons despite intact hair cell populations. Findings have practical importance for investigations of NIHL in animal models, and may have implications for clinical practices allocating noise‐induced and age‐related components of hearing loss as strictly additive. [Work supported by NIH.]

Acceleration of Age-Related Hearing Loss by Early Noise Exposure: Evidence of a Misspent Youth

Age-related and noise-induced hearing losses in humans are multifactorial, with contributions from, and potential interactions among, numerous variables that can shape final outcome. A recent retrospective clinical study suggests an age-noise interaction that exacerbates age-related hearing loss in previously noise-damaged ears (Gates et al., 2000). Here, we address the issue in an animal model by comparing noise-induced and age-related hearing loss (NIHL; AHL) in groups of CBA/CaJ mice exposed identically (8-16 kHz noise band at 100 dB sound pressure level for 2 h) but at different ages (4-124 weeks) and held with unexposed cohorts for different postexposure times (2-96 weeks). When evaluated 2 weeks after exposure, maximum threshold shifts in young-exposed animals (4-8 weeks) were 40-50 dB; older-exposed animals (> or =16 weeks) showed essentially no shift at the same postexposure time. However, when held for long postexposure times, animals with previous exposure demonstrated AHL and histopathology fundamentally unlike unexposed, aging animals or old-exposed animals held for 2 weeks only. Specifically, they showed substantial, ongoing deterioration of cochlear neural responses, without additional change in preneural responses, and corresponding histologic evidence of primary neural degeneration throughout the cochlea. This was true particularly for young-exposed animals; however, delayed neuropathy was observed in all noise-exposed animals held 96 weeks after exposure, even those that showed no NIHL 2 weeks after exposure. Data suggest that pathologic but sublethal changes initiated by early noise exposure render the inner ears significantly more vulnerable to aging.

Enhanced reactivity to tone in inferior Colliculus following early noise exposure (priming)

Enhanced reactivity to tone in inferior Colliculus following early noise exposure (priming)