Context: Noise-induced deafness (NID) contributes a significant disease burden internationally, and is a leading occupational disease in Singapore. Aims: This study profiles the epidemiological characteristics of advanced noise-induced deafness (NID(A)) cases and explores whether these have evolved with time. Settings and Design: A quantitative retrospective analysis of prior NID(A) cases was performed. National records of NID(A) cases from 2001 to 2010 were obtained, with permission from the Ministry of Manpower, consisting of worker audiograms, case records, and noise monitoring reports. Methods and Material: Comparison was made with data from a prior study (127 cases, 1985–1994) to identify shifts in NID(A) epidemiology; 71 out of 73 NID(A) case records (2001–2010) from the national data were reviewed. Statistical Analysis Used: Statistical Package for Social Sciences (IBM) was used for statistical analysis. Results: Mean noise exposure (24–29.6 years) and age at diagnosis (48–54.6 years) have risen. Total case numbers (127 to 73 cases), average hearing loss levels (61.5 to 56.0 A-weighted decibels), and delayed reporting of NID(A) cases (82.7% to 47.9%) have decreased. Metal manufacturing and marine industries remain top contributors (69.1%, from 68.5%); 31% were noncompliant with hearing protector (personal protective equipment, PPE) use and 38% did not use PPE properly. Conclusions: NID(A) case profiles have shifted over time, with reduced case numbers, lower hearing loss levels at diagnosis, and earlier case notification, possibly linked to improvements in legislative coverage and NID prevention programs. Changes in age and average duration of noise exposure may be related to these improvements. Early case notification, PPE compliance, and proper usage should be focus areas for NID prevention and hearing conservation programs.

The time course of apoptosis and the corresponding neuronal loss was previously shown in central auditory pathway of mice after a single noise exposure. However, repeated acoustic exposure is a major risk factor for noise-induced hearing loss. The present study investigated apoptosis by terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling (TUNEL) assay after a second noise trauma in the ventral and dorsal cochlear nucleus and central nucleus of the inferior colliculus. Mice [Naval Medical Research Institute (NMRI) strain] were noise exposed [115 dB sound pressure level, 5–20 kHz, 3 h) at day 0. A double group received the identical noise exposure a second time at day 7 post-exposure and apoptosis was either analyzed immediately (7-day group-double) or 1 week later (14-day group-double). Corresponding single exposure groups were chosen as controls. No differences in TUNEL were seen between 7-day or 14-day single and double-trauma groups. Interestingly, independent of the second noise exposure, apoptosis increased significantly in the 14-day groups compared to the 7-day groups in all investigated areas. It seems that the first noise trauma has a long-lasting effect on apoptotic mechanisms in the central auditory pathway that were not largely influenced by a second trauma. Homeostatic mechanisms induced by the first trauma might protect the central auditory pathway from further damage during a specific time slot. These results might help to understand the underlying mechanisms of different psychoacoustic phenomena in noise-induced hearing loss.

Objective: This study investigated effects of S-allylmercaptocysteine (SAMC), diallyl disulfide (DADS), and vitamin B₁₂ on inner ear functions and morphology after long-period high-level broadband noise exposure. Materials and Methods: Twenty-four healthy rats were randomly divided into four groups. First group was chosen as the control group. Vitamin B₁₂, SAMC, and DADS were applied to other groups for 4 weeks. On the 14th day, each group was exposed to broadband noise. Auditory brainstem response test was performed before and immediately after noise exposure and repeated on the 2nd and 14th day. Results: Permanent threshold shifts were significantly lower in groups treated with vitamin B₁₂, SAMC, and DADS. Histologically, cochleae of SAMC and DADS groups were found to be better preserved than the cochleae of vitamin B₁₂ and control groups. Conclusion: Physiologically and histologically, SAMC and DADS reduced the long-term effects of noise. However, physiological recovery was not consistent with the morphological findings in vitamin B₁₂ group.