Deafness at the D.E.F.A.
Deafness at the D.E.F.A. — Le Médecin d'usine (1954)
Report of the address by Dr Tomatis, otorhinolaryngologist, to the May 1954 Congress of the Direction des Études et Fabrications d’Armement (D.E.F.A.), published in the journal Le Médecin d’usine (pp. 401-404). Tomatis here reports his observations on workers exposed to the most extreme noise environments of the arsenals: gun firers, machine-gun firers, and workers in the wind tunnels at Vernon and Meudon. He describes deafness through the loss of the physiological means of protection of the auditory nerve — a mechanism distinct from the simple, progressive occupational deafness of the boilermaker.
Deafness at the D.E.F.A.
by Doctor TOMATIS, otorhinolaryngologist
The Direction des Études et Fabrications d’Armement (D.E.F.A.) brings together each year, thanks to the happy initiative of Dr Lemoine, chief medical officer, the physicians of all the armament establishments in a symposium where certain questions of occupational medicine are discussed. The May 1954 Congress had placed several important questions on its agenda. One of them concerned deafness. The report was presented by Dr Tomatis, whose principal points we summarise in his own words.
I have examined the workers who are in ambient environments equivalent to 110-120 decibels. These individuals are of relatively secondary interest, since they merely confirm what we have seen in the arsenals. They have an occupational perception deafness that begins with a dip at 4,000 cycles. I shall show you the evolution of this type of deafness.
This diagram represents the frequencies; the loss in decibels evolves from 0 to 100 decibels.
A normal occupational deafness in a boilermaker will evolve through a loss at the level of 4,000 cycles, which will appear most often from the first days of work in a noisy environment, always of the order of minus 50 decibels — a very considerable loss from the outset, of the order of 50 decibels.
It then regresses a little for a period of one year, after which it begins, over a period extending between one year and ten years depending on the individual, depending on the individual capacity for resistance; up to ten years, sometimes, you will have a subject falling towards the low frequencies, and the individual will continue to hear but will no longer understand. This is the occupational perception deafness which likewise affects the individual, but which is of secondary interest.
Independently of these elements, which once again merely confirm what we have seen in the other environments, two groups have particularly interested us: those individuals working in the wind tunnels — about 4 to around 20% — who came chiefly, I believe, from Vernon.
There were two types of wind tunnels: pulsed tunnels and continuous tunnels. Both have produced identical lesions.
Contrary to what I expected — that is, to what we had seen in the Aeronautics wind tunnels — none of these subjects presented any very significant general disturbances.
From the haematological point of view, we examined them; they presented no leucocytic modification, contrary to what we had seen in the arsenals. By contrast, they presented, much more markedly than those of the arsenals, extremely interesting auditory lesions. These subjects are all hyperauditive.
We had noted from the outset that there were doubtless lesions of the auditory nerve — or at least the hypothesis was put forward about two years ago, for it was at that time that there came to our attention a sufficient number of individuals to make a report of them.
At present, we have them, as do you, since we have collected at the Meudon wind tunnels some fifty individuals; and it seems that there had been not stimulations provoked by noise, which would simply have come about through phenomena of pressure and of bursting air or otherwise, but rather a progressive destruction of the transmitting apparatus, such that the means of protection provided by the muscles of the malleus, the elements of protection for the tympanic cavity, are lost, and immediately a nerve laid bare, reaching the nerve without any protection.
On a normal audiogram, what we shall find must evolve in parallel over a distance of 4 to 20, 30 decibels, which seems to be, from the standpoint of the nerve, a protection. The individuals we have seen at Vernon, all without exception, no longer have this protection. The nerve is found to be practically laid bare, immediately, above the zone, which may be impaired by at least 10 decibels for most of them.
Those who work at Vernon have not been in the wind tunnels for too short a time for anything to be seen, but those who have worked for 5 to 6 years in the wind tunnels are very seriously affected.
It seems that the nerve no longer benefits from the protection provided by the tympanic cavity, and as a result, the whole protective mechanism — provided so promptly — being lost, the nerve will find itself, in the upper region, very rapidly affected within two or three months; one sees a progression that descends only the low-frequency line, and the individual becomes deaf very quickly, without anyone noticing.
Although they are deaf in the nerve, they present a hyperaudition. These subjects have greatly interested us, for not only do they not notice it, but very often they understand nothing. They are subjects who do not hear normally and yet feel they are in a very silent environment.
For these subjects, we carried out an audiogram in the following way: we produced an industrial noise of the order of 30 decibels at the same time as we performed their audiogram. Immediately, we found ourselves before individuals who were absolutely incapable of perceiving the sounds we sent them.
These individuals, although no longer hearing normally, are already partially deaf, for they are incapable of distinguishing two sounds of different pitches.
Another experiment was performed on them in the following manner: we took a sound starting at high frequencies at 2,000 cycles and descended towards the low frequencies, observing at what moment the individual felt a change of tonality. Most of them allowed us to descend from 12,000 cycles to 500, without the slightest change. This is extremely significant: with an individual reaching a stage of auditory amblyopia, it seems that the nerve is no longer used.
Furthermore, there are 3 or 4 individuals, also from Vernon, who present another finding: the right ear is far more affected than the left ear.
The audiogram demonstrated this clearly; these subjects have always presented phonatory disorders; they had extremely damaged voices.
Finally, a last element: among the subjects who have been examined, perhaps half — 50% — are firers. The firers examined are machine-gun firers, and then gun firers.
The gun firers are not entirely the same as the older ones; one cannot make a direct comparison. The firers we have seen are absolutely fearful: there remains absolutely nothing. What struck us, however, is that their transmitting apparatus was distinctly impaired well before the auditory lesions; there is an extraordinary collapse of the apparatus, of the muscles of the malleus and the stapes; and moreover the nerve is found to be impaired by at least 60 decibels — for most of them, they no longer hear anything.
Once again, this is relative, for these subjects had at least 10 or 15 years of service.
The most interesting cases are those of the firers; these firers we have seen present audiograms that we relate quite closely to those of the wind-tunnel workers.
They are also extremely hyperauditive in the young; however, up to 4,000 cycles, the nerve will be found to be impaired solely because it seems to be stripped of its means of protection. Until now, apart from Vernon, we had never encountered, except in certain wind tunnels, identical lesions.
We shall be able, in a few days, to carry out spectrum tests: we are awaiting an apparatus that will allow us to take recordings down to 4,000 cycles, in order to ascertain what is the element that disrupts the transmitting apparatus.
In other words, we are dealing with individuals who, very rapidly, find themselves stripped of the physiological possibilities of protecting their nerve.
In the firer, we are confronted with the same phenomenon as in an individual in whom one would prevent ocular accommodation: light will immediately reach the retina and go directly onto it.
At present, I think, the firer is not the most interesting case; the most interesting will be, at a later stage, the possibility of inducing machine-gun fire and, at the same time, performing the audiogram to see what happens.
I do not have experience of these individuals: are they in their normal environment, do they nevertheless hear? Yes, they hear.
We shall conduct tests to see whether their audiograms reveal them in their ambient environment; I have recorded noises, but what I do not have are machine-gun noises; one would have to be able to record them, and as long as one does not have an oscilloscope, this is of no use.
In any event, what is significant nonetheless — and this is the first time I have been able to examine it — is that some fifty individuals present a far more cyclical deafness which will appear in the individual at the middle ear at the outset, and then secondarily in a laid-bare nerve which will collapse very rapidly. You have seen deaf subjects whose deterioration is much more rapid than that of boilermaker’s deafness.
I have seen men who had barely two years of firing and were already partially deaf. From the human standpoint, from the social standpoint, this presents something of significance.
Source: Tomatis A., “La surdité à la D.E.F.A.”, Le Médecin d’usine, 1954, pp. 401-404. Report of the address to the May 1954 Congress of the Direction des Études et Fabrications d’Armement (D.E.F.A.). Digitised document from Alfred Tomatis’s personal archives.