HEARING HAZARD ASSOCIATED WITH INDUSTRIAL NOISE EXPOSURE

产业工人的听力损失是通过每天重复的方式积累的 (中断)长时间暴露在过量噪音中 就业。大多数旨在评估听力损失的策略要么依赖于 根据从短期急性脑出血获得的实验数据进行推断 暴露或不间断的长期噪声暴露或来自 跨受试者通常为70分贝或更高的流行病学数据 可变性。最近的发现表明，外周听觉系统 可以调制高达40分贝的噪音暴露的影响。这些 据信，这种影响部分是由外毛细胞马达介导的。 可由之前的低水平噪声暴露激活的系统 危险的噪音暴露，或通过中断日常噪音暴露 政权。外毛细胞双向转导系统也 负责产生耳蜗辐射，现在正在 深入研究，因为它们可能被用作非侵入性和 噪声致外毛细胞改变的客观诊断试验 功能。暴露在高强度冲击噪声中仍然是一个问题 在许多工业环境中都能听到声音。此外，还有 几乎没有关于听力损失累积的实验数据 中断的高级冲击噪声和相对较少的可用数据 噪声诱发的感觉细胞与耳蜗声发射的关系 病理学。同样，我们知道外界的低水平噪音是如何 工作场所对后天听力损失的影响在工作环境中非常严重 不够充分。拟议的研究旨在研究所提出的问题。 上图在动物模型(栗鼠)中使用刺激：(A)窄带 (400赫兹)中心频率在0.5到8.0千赫之间的撞击以进行探测 耳蜗的频率范围宽；(B)宽带影响；和(C) 复杂的高峰度连续噪声。曝光范例将 包括20天和5天中断和不中断曝光 分别是几天。暴露将在总能量中保持平衡，以便 基于能源的比较可以与现有数据进行比较。纯音 诱发反应测听法和立方体测听法测定听阈 失真产物诱发的耳蜗声发射测听图和输入/输出 功能将被收集并与感觉细胞病理相关联。 我们的目标是帮助：(L)了解听力是如何 反复的间断撞击和复杂的噪音会累积损失 曝光；(2)失真产物发射作为一种 客观的非侵入性诊断工具；(3)了解和 预测个体对噪声性听力损失的易感性。

Hearing loss in industrial workers accumulates from repeated daily (interrupted) exposures to excessive noise over a long period of employment. Most strategies designed to estimate hearing loss rely either upon extrapolations from experimental data acquired from short-term acute exposures or from noninterrupted long-term noise exposures or from epidemiological data with its typically 70 dB or more across-subject variability. Recent discoveries show that the peripheral auditory system can modulate the effects of noise exposure as much as 40 dB. These effects are believed to be partially mediated by the outer hair cell motor system which can be activated by a low-level noise exposure that precedes a hazardous noise exposure, or by interrupting a daily noise exposure regime. The outer hair cell bi-directional transduction system is also responsible for generating cochlear emissions which are now being intensively studied because of their potential use as a noninvasive and objective diagnostic test for noise-induced changes in outer hair cell function. Exposure to high-level impact noise continues to pose a problem to hearing in many industrial environments. Furthermore, there is virtually no experimental data on the accumulation of hearing loss from interrupted high-level impact noise and relatively little data available on the relation between cochlear emissions and noise-induced sensory cell pathology. Similarly, our knowledge of how low-level noise outside the work place affects hearing loss acquired in the work environment is very inadequate. The proposed research is designed to study the issues raised above in an animal model (chinchilla)by using as stimuli: (a) narrow band (400 Hz) impacts with center frequencies between 0.5 and 8.0 kHz to probe a wide frequency extent of the cochlea; (b) broad band impacts; and (c) complex high kurtosis continuous noise. The exposure paradigms will include both interrupted and noninterrupted exposures for 20 days and 5 days respectively. Exposures will be balanced for total energy so that comparisons based on energy can be made with existing data. Pure tone hearing threshold measured using evoked response audiometry and cubic distortion product evoked cochlear emission audiograms and input/output functions will be collected and correlated with sensory cell pathology. The objective is to contribute to: (l) an understanding of how hearing loss accumulates from repeated interrupted impact and complex noise exposures; (2) the development of the distortion product emission as an objective noninvasive diagnostic tool; and (3) an understanding and prediction of individual susceptibility to noise-induced hearing loss.