Section of Occupational Medicine, Department of Public Health, University of Naples Federico II, Naples, Italy.
Noise Health. 2020 Oct-Dec;22(107):77-89. doi: 10.4103/nah.NAH_17_20.
Noise-induced hearing loss (NIHL) is one of the leading causes of acquired sensorineural hearing loss. However, molecular mechanisms responsible for its pathogenesis remain to be elucidated. Epigenetic changes, i.e. DNA methylation, histone and microRNA expression modifications may function as a link between noise exposure and hearing loss. Therefore, the aim of the present review was to assess whether epigenetic alterations may serve as biomarkers of noise exposure or early effect.
A systematic review of studies available in Pubmed, Scopus, and ISI Web of Science databases was performed.
Noise exposure was able to induce alterations in DNA methylation levels in workers and animal models, resulting in expression changes of genes related to hearing loss and also to extra-auditory effects. Differently expressed microRNAs were determined in NIHL workers compared to noise-exposed subjects with normal hearing, supporting their possible role as biomarkers of effect. Acoustic trauma affected histon acethylation and methylation levels in animals, suggesting their influence in the pathogenesis of acute noise-induced damage and their role as targets for potential therapeutic treatments.
Although preliminary data suggest a relationship between noise and epigenetic effects, the limited number of studies, their different methodologies and the lack of adequate characterization of acoustic insults prevent definite conclusions. In this context, further research aimed to define the epigenetic impact of workplace noise exposure and the role of such alterations in predicting hearing loss may be important for the adoption of correct risk assessment and management strategies in occupational settings.
噪声性听力损失（NIHL）是后天感音神经性听力损失的主要原因之一。然而，导致其发病的分子机制仍需阐明。表观遗传改变，即 DNA 甲基化、组蛋白和 microRNA 表达修饰，可能作为噪声暴露与听力损失之间的联系。因此，本综述旨在评估表观遗传改变是否可以作为噪声暴露或早期效应的生物标志物。
对 Pubmed、Scopus 和 ISI Web of Science 数据库中可获得的研究进行了系统评价。
噪声暴露能够诱导工人和动物模型中的 DNA 甲基化水平改变，导致与听力损失和非听觉效应相关的基因表达变化。与听力正常的噪声暴露者相比，NIHL 工人中确定了差异表达的 microRNAs，支持其作为效应生物标志物的可能作用。声创伤影响动物的组蛋白乙酰化和甲基化水平，表明它们在急性噪声诱导损伤的发病机制中的影响及其作为潜在治疗靶点的作用。
尽管初步数据表明噪声与表观遗传效应之间存在关系，但研究数量有限、方法不同以及对噪声暴露的充分特征描述缺乏，阻止了明确的结论。在这种情况下，进一步研究旨在确定工作场所噪声暴露的表观遗传影响以及这种改变在预测听力损失中的作用，对于在职业环境中采取正确的风险评估和管理策略可能很重要。
