Promising New Strategies

The discovery of free radical scavengers in the inner ear opens the way for new treatments of noise induced hearing loss.

BY now it is well understood by industrial workers that unprotected exposure to loud noises can lead to permanent hearing loss. In fact, it could be said that most people living in the modern age have at least some sense of the potentially harmful effects of loud noise on hearing.

At some point in life, every person likely will experience the immediate effects of loud noise exposure: a reduction in hearing sensitivity, called temporary threshold shift (TTS); intense ringing in the ears, called tinnitus; and eventual recovery after several hours have passed. Today, more and more people are reporting the experience of these sensations after leaving movie theatres and music concerts, where sound levels can far exceed 90 dB (A), the exposure considered "safe" by OSHA for workers in a 40-hour work week. This means the sensation of hearing loss, whether temporary or permanent, in response to some exposure to noise, is becoming a shared experience of the whole population.

The troubling part of this reality is that temporary shifts in hearing threshold are indicators of actual physical damage to the sensory cells of the inner ear. Multiple exposures to loud noises that result in temporary losses of hearing can eventually lead to a permanent, irreversible, noise induced hearing loss (NIHL). This is easily recognized by a trained audiologist as a significant impairment in the high frequency range of hearing (i.e., around 4000 Hz, called a "noise notch") for mild cases and across more frequencies in severe cases.

Hearing loss of this type often leaves an individual with a disabling communicative disorder that can have a dramatic bad effect on the quality of life and, possibly, a worker's ability to remain gainfully employed. Once the damage is done, rehabilitation for this kind of disability can come only in the form of hearing aids, which are often very costly and therapy intensive.

Therefore, it can be said that prevention is the best policy. Though this may seem obvious, improvements in the prevention of hearing loss still depend on new advancements in science. On the forefront today is a new way of looking at the biological effects of noise on hearing.

New Insights into the Mechanism of NIHL
Until somewhat recently, it was assumed by the audiological community that the damaging effects of noise on the sensory cells of the inner ear were mostly, if not exclusively, mechanical in nature. Simply, it was thought that loud noise, once conducted to the inner ear, directly damages sensory cells with force and that all of the harm is done immediately, in one single incident.

There are new investigations, however, currently under way that are examining the metabolic changes that continue to occur in cells after exposure to loud noise. Investigators now suspect an additional level of injury occurs long after exposure. This new level of damage results in the eventual compromise of cells and leads to permanent shifts in hearing threshold. This long-term effect has been linked to the metabolic breakdown of cells in the inner ear by small extremely reactive molecules known as free radicals. These molecules have already been recognized to be involved with cardiac disease and cancer. A new, harmful role of free radicals in damaging the inner ear has thus been implicated, and they are now known to be unnaturally generated when cells are damaged by loud noise.

Normally, free radicals are eliminated from the cellular space by naturally occurring anti-oxidants, also known as free radical "scavengers." An example of a naturally occurring anti-oxidant in the inner ear is called "glutathione," which has been artistically represented in the accompanying figure. This molecule is normally released from surrounding membranes and aids in maintaining a healthy environment for the inner ear. In the case of extremely high noise exposures, however, free radical scavengers, such as glutathione, are insufficient to fully remove free radicals. The result is a somewhat continuous breakdown of cells, leading to increased susceptibility to the effects of noise and, eventually, a permanent hearing loss.

Our growing awareness of the metabolic breakdown of sensory cells after exposure to loud noise has resulted in a couple of interesting and useful recommendations from the scientific community. For example, audiologists and physicians alike agree that if the release of the free radical scavengers can be increased, then the metabolic damage to cells after exposure to noise would be reduced. This, they hope, would leave the ear less susceptible to future permanent shifts in hearing threshold as a result of loud noise exposure. Although the increased release of free radical scavengers would not reverse the mechanical damage of the noise, it likely would reduce any subsequent degradation of sensory cells. This concept has lead to several new strategies designed to enhance the release of anti-oxidants in the inner ear.

Pre-Exposure Conditioning to Noise as One Method of Protection
One new method of protecting the inner ear from the damaging effects of loud noise is known as "sound conditioning." This is simply the conditioning of ears to loud noises by pre-exposure to loud, but not harmful, sound. This is not a newly recognized phenomenon. In fact, sound conditioning has been observed in animal laboratories for the past 20 years.

Only recently, however, has enough research evolved to support the notion that this may actually be a method that may someday be used by workers to protect themselves from the damaging effects of loud noise. Though the actual mechanism of how the ear can be conditioned by certain "safe" noises is still relatively unclear, it is suggested by some of the more currently published studies that the natural release of anti-oxidant free radical scavengers is involved. This suggests that continuous pre-exposure to a loud, but safe, level of noise may influence the increased release of anti-oxidants that have a function of repairing damaged cells.

The idea of sound conditioning is similar to the pressure conditioning of divers before going on deep-sea dives. If divers are immediately plunged into extremely deep water, they may experience a series of harmful physiological effects or even death. This can be alleviated, in most cases, by putting the diver into a pressure tank that increases pressure slowly, allowing the body to naturally adjust. Even on fairly shallow dives, it is necessary for a diver to increase her depth slowly, in order to allow for the pressure inside the body to equalize with the surrounding environment. Though the inner ear can be a much more difficult system to understand, this analogy works in that it highlights the body's natural ability to adjust to fairly extreme circumstances as long as a period of adjustment is allowed.

Despite the fact that the research has shown that a person can be conditioned to the effects of damaging loud noises, it is thought this may represent a difficult method to implement in the workplace. The complications are many. For instance, a conditioning noise that is effective and safe for one person may actually be damaging to another. Also, one of the fastest-growing concerns among industrial hygienists and audiologists is the incidence of impact noises. Often, when exposed to this sudden and very often damaging type of noise, a worker is taken off guard and not prepared with hearing protection. Also, there are many instances when a person may be exposed to sudden loud noises at home or during leisure activities, and again be taken off guard without any kind of hearing protection. In these instances, sound conditioning would not be an adequate form of protection simply because these kinds of exposures are unanticipated.

A New Class of Drugs to Reduce the Effects of Noise on Hearing
A growing area of research in the prevention and treatment of noise trauma is in the development of drugs that can effectively eliminate free radicals from the cochlea and aid in the repair of damaged sensory cells. Already in development are such drugs that either act as anti-oxidant free radical scavengers (like glutathione) or affect the release of other naturally occurring substances that have the same action.

One example of this type of drug is called R-PIA (R-N6-phenylisopropyladenosine), which has been found to increase the activity of glutathione in the cochlea, thus providing enhanced protection from free radical damage that can result from exposure to loud noise.

To test the effect of R-PIA on hearing loss, a group of researchers applied the drug topically to the round window (a membrane of the inner ear) of one group of animals and applied a saline solution as a control in a second group. The animals then were exposed to mid-frequency noise for four hours at levels high enough to cause temporary deafness. The loss of hearing was verified by monitoring brain waves to the hearing center in the cortex. The lack of brain activity in response to normal sound indicated complete hearing loss. Brain wave activity was measured again at one day, four days, and 20 days following noise exposure. Results showed the animals treated with R-PIA recovered their hearing faster and more completely than those treated with saline.

R-PIA is only one of several drugs that are the focus of current research in the treatment of noise induced hearing loss. In fact, it has been shown in some laboratories that these types of drugs can possibly reduce the effects of other known causes of hearing loss that may result from free radical damage to the inner ear. For example, N-acetylcysteine and lactated Ringer's solution have been shown to reverse the ototoxic effects of cisplatin, a cancer drug that is known to cause permanent hearing loss. Also, drugs that increase the production of glutathione in the inner ear have been found to reverse the damaging effects on hearing of certain myacin antibiotics.

Of late, there seems to be a scurry of activity in science to develop new strategies that will enhance our protection against several well-known causes of permanent hearing loss. Many of these strategies (i.e., noise conditioning and ingestion of specific anti-oxidant drugs) are still in the research phase and are not readily available to the open market at this time. Nonetheless, we should all be on the lookout for the release of new ways we can reduce the effects of noise and other harmful agents on our hearing. In the meantime, however, we all should continue to protect ourselves by keeping our eyes covered and our ears . . . well . . . plugged.

This article appeared in the September 2005 issue of Occupational Health & Safety.

This article originally appeared in the September 2005 issue of Occupational Health & Safety.

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