The primary aim of this study was to investigate whether auditory brainstem response (ABR) and speech perception in noise (SPiN) were associated with occupational noise exposure in normal hearing young factory workers. Forty young adults occupationally exposed to noise and 40 non-exposed young adults (control group) from Zhejiang province in China were selected. All participants presented with normal hearing thresholds and distortion product otoacoustic emissions. Participants were evaluated with the Mandarin Bamford-Kowal-Bench (BKB) test and ABR. The latter was obtained for click stimulus at 50, 60, 70, 80, and 90 dBnHL. Peak-to-trough amplitudes and latencies for waves I and V were obtained. The ABR wave I amplitude, the wave I/V amplitude ratio, the slope of the wave I amplitude growth as a function of stimulus intensity (AMP-I_Slope), and the wave V latency shift with ipsilateral noise (LAT-V_Slope) were used as ABR outcomes. Finally, equivalent continuous average sound pressure level normalized to 8 h (L_Aeq.8h) and cumulative noise exposure (CNE) were obtained for noise-exposed participants. No significant differences between groups were found for any ABR outcomes. Noise-exposed participants exhibited worse BKB scores than control group participants. A multivariate regression model showed that 23.3% of the variance in BKB scores was explained by group category (exposed vs. non-exposed) and hearing thresholds. However, since none of the ABR outcomes exploring cochlear synaptopathy were associated with noise exposure, we cannot conclude that cochlear synaptopathy was the contributing factor for the differences between groups for BKB scores. Factors that go beyond sensory processing may explain such results, especially given socio-economic differences between the noise-exposed and control groups. We conclude that in this sample of participants, occupational noise exposure was not associated with signs of cochlear synaptopathy as measured by ABR and BKB.

Noise-induced hearing loss (NIHL), caused by direct damage to the cochlea, reduces the flow of auditory information to the central nervous system, depriving higher order structures, such as the hippocampus with vital sensory information needed to carry out complex, higher order functions. Although the hippocampus lies outside the classical auditory pathway, it nevertheless receives acoustic information that influence its activity. Here we review recent results that illustrate how NIHL and other types of cochlear hearing loss disrupt hippocampal function. The hippocampus, which continues to generate new neurons (neurogenesis) in adulthood, plays an important role in spatial navigation, memory, and emotion. The hippocampus, which contains place cells that respond when a subject enters a specific location in the environment, integrates information from multiple sensory systems, including the auditory system, to develop cognitive spatial maps to aid in navigation. Acute exposure to intense noise disrupts the place-specific firing patterns of hippocampal neurons, “spatially disorienting” the cells for days. More traumatic sound exposures that result in permanent NIHL chronically suppresses cell proliferation and neurogenesis in the hippocampus; these structural changes are associated with long-term spatial memory deficits. Hippocampal neurons, which contain numerous glucocorticoid hormone receptors, are part of a complex feedback network connected to the hypothalamic-pituitary (HPA) axis. Chronic exposure to intense intermittent noise results in prolonged stress which can cause a persistent increase in corticosterone, a rodent stress hormone known to suppress neurogenesis. In contrast, a single intense noise exposure sufficient to cause permanent hearing loss produces only a transient increase in corticosterone hormone. Although basal corticosterone levels return to normal after the noise exposure, glucocorticoid receptors (GRs) in the hippocampus remain chronically elevated. Thus, NIHL disrupts negative feedback from the hippocampus to the HPA axis which regulates the release of corticosterone. Preclinical studies suggest that the noise-induced changes in hippocampal place cells, neurogenesis, spatial memory, and glucocorticoid receptors may be ameliorated by therapeutic interventions that reduce oxidative stress and inflammation. These experimental results may provide new insights on why hearing loss is a risk factor for cognitive decline and suggest methods for preventing this decline.