INTRODUCTION Noise exposure, both occupational and non-occupational, is a leading factor affecting auditory health worldwide.1,2 Occupational noise, prevalent in industrial and construction settings, is a well-established cause of noise-induced hearing loss (NIHL).3 More recently, non-occupational noise from personal listening devices (PLDs), gaming, nightclubs, and concerts has emerged as a widespread but under-recognized threat, particularly among young adults.4,5Figure 1: (a) Mean and standard deviation of the pure-tone hearing thresholds of the right ears in the LNE and HNE groups. (b) Mean and standard deviation of SNRs in dB of the TEOAE.Figure 2: Mean MDT (dB) between HNE and LNE groups across modulation rates (2–128 Hz) for a broadband noise carrier stimulus.Unlike occupational noise, non-occupational exposure often occurs repetitively at dangerously high intensities, with no regulation or monitoring. Long-term noise exposure can also affect the body and mind, With prolonged exposure, it can increase blood pressure, affect sleep, cause stress, and tiredness.6–9 This exposure can damage inner hair cell structures, especially the basilar membrane and cochlear hair cells, leading to irreversible damage.10,11 Prolonged exposure may also impair synapses between inner hair cells and cochlear neurons, affecting neural transmission necessary for understanding speech in noise and processing temporal cues.12–14 These changes occur immediately and worsen over time, affecting ribbon synapses that transmit signals from inner hair cells to auditory nerves.15 Prolonged noise exposure preferentially damages LSR fibres, which are crucial for detecting timing and modulation cues.13 These nerve fibres are also responsible for listening in noise. Studies done on animals show that such damage may occur before hair cell loss or threshold shifts are evident. Individuals exposed to occupational noise who have normal hearing often report difficulty with speech in noise and poor temporal resolution.16,17 They also report tinnitus and increased listening effort.18 Evidence shows that individuals with occupational noise exposure have poorer speech perception in noise abilities than individuals without occupational noise exposure.19 A study done to evaluate amplitude modulation detection abilities reported that individuals with high recreational noise exposure had poorer modulation detection thresholds, especially at high modulation rates.20 While the effects of occupational noise exposure are well-documented, research on non-occupational noise exposure in normal hearing young adults is limited. This population frequently engages in high-risk listening behaviours using PLDs or attending loud recreational venues, often without awareness of the potential damage. Even in the absence of measurable hearing loss, synaptic damage from chronic non-occupational noise exposure may result in early auditory deficits, particularly in speech-in-noise understanding and temporal processing. As these subtle deficits are not typically detected by conventional audiometry, they remain underdiagnosed and unaddressed. Hence, there is a critical need to investigate the early auditory consequences of non-occupational noise exposure in young adults with normal hearing. This study aims to investigate speech in noise and amplitude modulation detection abilities in low and high annual non-occupational noise exposed young adults with normal hearing. METHODS Study setting and design The study was conducted in a sound-treated room at the Audiology Lab of Nitte Institute of Speech and Hearing in Mangalore, India. A between-group comparison design was employed, and participants were recruited through convenience sampling. Sample Size: The sample size was determined using the formula n = (2(z + z )²²)/d², where z = 1.96 at 95% confidence, z = 1.28 at 90% power, = 0.99, and d = 1. Based on this formula and referring to Vasudevamurthy however, the differences between the two groups were not significant. A previous study has reported similar results in individuals with occupational noise exposure.19 However, a study reported poorer amplitude modulation detection in individuals with occupational noise exposure than in individuals without a history of noise exposure.17 The elevated MDTs in noise-exposed individuals can be due to the reduced synchronization of neural response, particularly at higher modulation rates.31 The brain’s ability to synchronize neural firing with sound timing is stronger at low frequencies and declines as the frequency increases.27,32 This decline affects the rapid envelope fluctuations, leading to elevated modulation detection thresholds at higher modulation rates.33 As a result, individuals with noise exposure or early hearing loss may experience diminished sensitivity to amplitude modulation, especially at higher frequencies.11 The noise exposure may affect modulation detection, but the effect was not strong enough in this study to reach statistical significance, possibly due to variability within groups or a limited sample size. CONCLUSION These findings highlight the need for monitoring suprathreshold auditory functions, such as speech perception in noise, among young adults exposed to non-occupational noise. Although all participants exhibited normal hearing sensitivity, the observed differences in speech-in-noise performance suggest that prolonged exposure to recreational noise may lead to subtle auditory deficits not captured by conventional audiometry. This underscores the importance of early identification and prevention strategies aimed at preserving auditory health in populations at risk due to high levels of non-occupational noise exposure.
Goyal et al. (Sun,) studied this question.