Thirty-six million Americans have hearing loss. Exposure to noise is the culprit in one of three of these people. Noise-induced hearing loss (NIHL) is the result of damage to the hair cells in the inner ear. These hair cells convert sounds that we hear into electrical signals that travel to the brain. If these cells receive damage, it is permanent, and hearing loss occurs. Your environment can significantly impact your risk for NIHL. Those of us who live and work around loud noise is more likely to damage our inner ear structures than others. Your inner ear is damaged slowly over time due to repeated exposure to these loud noises. Other environmental factors include smoking, taking certain medications, aging, head injury, certain illnesses, and diabetes.
In the inner ear, acoustic waves move along through the cochlear spiral. When these waves encounter the cochlear region that relates to their frequency, the outer hair cells amplify their energy. Excessive noise kills these outer hair cells. NIHL presents with a variety of symptoms. At times, loud noise exposure can lead to a temporary reduction in auditory thresholds. Chronic sounds can lead to permanent auditory threshold shifts. The symptoms of NIHL match the injury to specific structures in the ear.
There are over 140 gene variants that can cause hearing loss in the absence of other symptoms. These genes encode proteins that operate within the cochlea. All of these genes have particular functions, and the study of them is enhancing our understanding of cochlear function and hearing loss. The tasks include hair cell mechanotransduction and generating the endolymph.
Thirty-four genes associate with human NIHL. These variants are identifiable in populations that endure occupational noise such as workers in a loud factory. Roughly 38 percent of NIHL variants reside in genes with variants that associate with familial hearing loss. The healthy auditory function relies on energy-intensive activity that requires active mitochondria, which may compromise under oxidative stress. Identification of NIHL variants is possible in populations subject to occupational noise. The variants that do not cause hearing loss can still confer stress. These genes include proteins responsible for stereociliary function and maintenance of the endolymph potassium gradient. About 18 percent of NIHL are in genes that regulate other genes.
Susceptibility to NIHL varies according to our specific genes. The symptoms of NIHL may manifest in different ways, such as difficulty perceiving sounds in noise, tinnitus, or raised auditory thresholds that characterize hearing loss. The manifestations can be the result of cellular injuries from noise exposure. More investigation will focus on the genetic and cellular bases of NIHL and individual susceptibilities in the hope of preventing NIHL.
If you are experiencing a hearing loss from noise, please schedule a hearing evaluation with a hearing healthcare professional today. A hearing professional can diagnose your problem and prescribe treatment that can help you hear better while improving your quality of life.