DR RICE: Thank you very much, Eric. I think we have about 5 minutes for questions. Do we have any questions from the audience for either Narelle or Eric?

MR PETERSON: Thank you for that very enlightening presentation. You related the music industry and so on. As a matter of fact, I knew a band drummer who was deaf, but the thing that alarmed me and we were talking about doctors a while ago is the fact that antibiotics destruction of the cochlear cells was up to 1,000 times greater. Is there any research on this? I know my own GP said, “Can you give me a list of those drugs that do affect your hearing?” Part of my education program for my GP, by the way.

DR LE PAGE: We know about aminoglycosides, which have been isolated as the antibiotics of choice when your life is at stake. Streptomycin and such are drugs that tend to be used if your life is very much threatened. It is known that these drugs, at least certainly from animal studies, can wipe out the basal turn of outer cells in 10 days. If combined with certain diuretics, it can wipe them out in hours.

It may be that, with the sensitivity emission screening method we have evolved, other antibiotics which are not previously known to be a risk, may in fact be a risk, so we have some interest to conduct a study where we are looking at things that we believe are innocuous like the penicillins such as amoxycillin, or Septrin and Bactrim. It is possible that even these drugs are hazardous for hearing. As they are handed out very freely to young people in the first decade of life, it may contribute to the rapid rate of decline that we see in the first decade.

DR RICE: As a corollary to that, the aminoglycosides may be used in sick babies. As I understand it, the emissions are very high in young children. It may be that, if we could measure the otoacoustic emissions in these children, we would see their hearing going down when it is in fact being affected by the antibiotic at an earlier stage than we do at the moment where we monitor them by pure tone audiometry.

There is another question from the audience.

MR HOOVER: I would like to ask Eric whether his studies of young people have made any differentiation according to socioeconomic group).

DR LE PAGE: No, we have not done that yet.

DR DAVIS: That was very interesting. I would like to discuss some of that with you in detail at some other time. Perhaps there is another way of interpreting these data which you might care to look at. There is some data that exists which people are looking at around the world at the moment in terms of the development of the emission and how it flattens of from being very high when children are born and deteriorating in the first few years of life. A lot of people said that, rather than reflecting the ageing of the cochlea, in a way it reflects the maturation in that it may be the maturation of the efferent and the myelinisation – a function that is taking place here. It would be perhaps wrong to incorporate that in a purely ageing model.

I think the studies that have been done including some by our own group, Summerfield and others, shows that, whilst we may think that hearing is perfect when kids are born, in fact, it seems to mature to an optimum up to seven or eight years. Other work I did with Tony Rice and others in a European study shows precisely the same deterioration in the density of outer hair cell functionally decreasing, levelling out and then going down slightly, which contra indicates the hearing thresholds which seems to go quite straight and then accelerate off at 50 to 60. Do you have any comment in terms of that other interpretation, the efferent and the similarity with other phenomenon, such as the density of hair cells?

DR LE PAGE: I have spent a great deal of time agonising over this over the last several weeks, as Maureen can tell you. I wondered whether we were jumping the gun by modelling it in this way. Again, the efferent system has been the basis of my career. I have been working on cochlear mechanics for 20 years and certainly that may be a consideration. We have done other studies looking at the effect of efferent behaviour on cochlear emissions and we are amongst many groups who are not finding a very strong effect on cochlear emissions with efferent behaviour.

There are a couple of other factors, too. We have tried to normalise for differences in probe size and ear canal size with neonates, which we would expect to produce a higher emission strength in any case, so there are a few unresolved issues but we think that we are sufficiently normalising the results to take into account these factors.

Again, the dip from what would appear to bea simple decline – it comes back to the fact that we see an enormous number of young people with clearly damaged cochleas. I still think that the dip below a linear decline is a real phenomenon. I will talk to you some more about that.

Notes added in proof

If the rapid decline in the first decade was due either to maturation or measurement artifact, we would expect the rapid decline to appear in all the percentile curves particularly the curve defined by the maximum values in each age range. Instead we find that the maximum value curve declines monotonically and no faster than about 2 dB/decade.

Perhaps the reason that hearing loss is the most common form of human physical disability reported in western nations (Davis et al, 1994) has to do with the fact that the actual mechanisms which are degraded when hearing loss presents are still poorly understood by the public at large. While specific features of the mechanism are well described by hearing research scientists there is still a large gap between the basic science and the clinical application. Until recently, it has been virtually axiomatic, dictated by “common sense” that hearing levels within normal limits imply no permanent damage to the ear. Instead there is growing evidence that outer hair cell damage, which is primarily responsible for sensorineural hearing loss may accumulate before there is any sign of hearing loss (LePage and Murray, 1993). It is therefore important to further evaluate the relationship between such latent damage and hearing loss and why the onset of hearing loss is such an insidious process. The normal range for hearing threshold levels is 0 ± 20 dB HL. Typically difficulties are first reported when pure tone thresholds rise above 20 dB. Investigations of pure tone audiometric thresholds have failed to show why the relationship between temporary threshold shift and permanent threshold shift is so difficult to define (Macrae, 1971), and why extensive exposure monitored in a cohort study, over periods as long as ten years failed to produce any significant, detectable permanent shift (Carter et al., 1982; Carter et al., 1984).

Doubts about whether the shape of the pure ageing curve would or should be linear with age in a population not normally exposed to noise and ototoxic agents. There is no particular reason to think that it should decline linearly with age. However, the database contains two primary trends which leads us to believe a linear decline. We only have indications that makes us think that the dip between ages 15 and 25 is real because of the emission spectra; the patterns in young people appear very damaged on average. These spectra display what we locally call a “picket fence” effect, i.e. instead of the more or less smooth spectra which we see in newborn kids, they display pronounced notches considerably before any such notches appear in the pure tone audiogram.

Notion of ear age. If one projects the emission strength for any ear across to the intersection with the “pure presbycusis” curve one can come up with an estimate of the ear’s age dictated by the degree of damage, to be compared with the chronological age of the person. For example, in the case of one orchestral percussionist aged 28 had emission strengths of -3 dB SPL