In the first course about noise exposure that any audiologist takes, they are confronted with a pile high list of articles and research papers about the many studies concerning hearing loss and noise.
Animal studies are generally about creating a permanent hearing loss (or permanent threshold shift PTS) and human studies concentrate on creating temporary hearing losses (or temporary threshold shifts TTS). This, of course, is the ethical thing to do- I would doubt that any ethics review board would approve a study where someone was asked to give up their hearing for the sake of science. Animals, and research on animal models are quite different and over the years there have been many publications about creating PTS on lab animals in well-controlled environments.
This has not always been the case. Davis’s classic 1947 and 1948 studies on diplacusis involved American service men sacrificing their hearing on one side so that one normal hearing ear can be compared with one with a sensori-neural hearing loss. Thank goodness these experiments are a thing of the past.
Typical TTS studies involve creating a well-defined and controlled hearing loss using noise and measuring the resulting effect over time. This can be done with a range of parameters such as the application of other “pre-toughening noises” or certain medications.
But, what can studies on TTS in humans tell us about future permanent hearing loss? This is where many of our colleagues go off the rail. At most, one can say that prior to having a PTS, one must first have a TTS, but other than that, there really isn’t much of a relationship between the two.
A person who goes to a rock concert and suffers a 25 dB TTS after a three hour performance is not more susceptible to future PTS than one who suffers no TTS. TTS is simply not a predictor of PTS. And we really don’t have a good predictor of PTS. Some people are indeed more susceptible to hearing loss from noise or music, but we have no way of telling who is whom.
This should not be that surprising however. The underlying mechanisms for TTS and PTS are actually quite different. In the case of TTS, the concentration of Glutamate (a neurotransmitter substance found in the synapse of the inner hair cells) can reach ototoxic levels when a person is exposed to high levels of noise or music. After 16-18 hours, the Glutamate levels return to a normal level which is why it takes about 16-18 hours for hearing to return to a baseline level after exposure to loud noise or music. Mechanically the tectorial membrane also becomes disconnected from the tips of the outer hair cells during TTS and it takes some time for them to re-establish their normal mechanical relationship.
In contrast, PTS is related to cell death- necrosis or apoptosis. Apoptosis is a more common process where cells are gradually and passively disassembled over time. The loss of hair cells eventually results in a measureable hearing loss. Necrosis is a much more active and destructive process where the cells “explode” and their cytoplasmic contents are dumped into a region of neighboring cells. This typically results in cell death over a wide range of locations and associated frequencies.
Given the differing mechanisms of pathology in the cochlea for PTS and TTS, it is not really surprising that the two don’t have a predictive or one-to-one relationship.
Clinically if we see a client who is quite concerned that they experienced a large TTS, at least we can tell them that they shouldn’t worry too much. They should wear hearing protection, but I would say that to all of their friends regardless of whether they experienced TTS or not.
So…what does TTS tell us about PTS? …. not much.