In Reference to <i>Do Disinfectants Induce Ototoxicity and Cause Structural Damage to the Inner Ear?</i>

We read with great interest the article entitled “Do Disinfectants Induce Ototoxicity and Cause Structural Damage to the Inner Ear?” by Xi Wang et al. [1], which investigated the ototoxic effects of commonly used clinical disinfectants (indophor, alcohol, and chlorhexidine). This study not only corroborates prior research but also addresses a critical gap by systematically evaluating the impact of these disinfectants on cochlear hair cells and spiral ganglion neurons (SGNs). Although this work provides ground breaking insights into a previously underexplored area, several methodological aspects warrant further discussion [2-5]. First, the sole reliance on auditory brainstem response (ABR) for hearing loss detection may benefit from complementary techniques. Incorporating otoacoustic emissions (OAEs) would provide a more comprehensive evaluation, as the combined approach aligns with the physiological sound transmission pathway (external → middle → inner ear). Additionally, during unilateral ABR measurements (particularly at high intensities), contralateral masking should be implemented to minimize cross-hearing interference [2]. The absence of masking procedures—if indeed not performed—should be explicitly stated in the methodology. The observed right-ear damage, whereas speculated upon, lacks mechanistic clarification. To enhance experimental precision, unilateral application of disinfectants is recommended. This limitation, however, presents an opportunity for future studies to elucidate the underlying mechanisms. Secend, the authors reported alcohol-induced SGN demyelination showing partial recovery at 1 week; whereas chlorhexidine-induced damage persisted. Given this differential trajectory, extending the observation period (e.g., 4–8 weeks) could determine whether chlorhexidine's effects represent delayed recovery or permanent injury. Additionally, spiral ganglion neurons (SGNs) are known to have different subtypes (Type I and Type II). While this study presumably examined Type I SGNs, the specific subtype was not explicitly identified in the manuscript [6]. And then, the study did not specify the concentrations of the three disinfectants used. Standardization of this parameter is essential for experimental reproducibility and clinical extrapolation. In conclusion, we commend the authors for this clinically impactful work, which highlights the risks of disinfectant misuse and advances our understanding of ototoxic mechanisms. The study's limitations, as noted above, serve as a catalyst for deeper investigations into this critical field. All the authors thank Jining Medical University and its Affiliated Hospital for providing the learning platform and also express our gratitude to the corresponding author for the careful guidance on this report. The authors have nothing to report. The authors declare no conflicts of interest. The data that support the findings of this study are available from the corresponding author upon reasonable request.