Brown v Commissioner of Police

Judgment 1HIS HONOUR: The plaintiff, Mr Mark James Brown, is a former sergeant of police. The plaintiff was attested as a probationary constable of police on 10 December 1979, and thereupon became a contributor to the Police Superannuation fund established under the Police Regulation (Superannuation) Act 1906 ("the Act"). On 31 May 2012, the Police Superannuation Advisory Committee ("PSAC") determined that the plaintiff was incapacitated for police duty due to the infirmities of "chronic post traumatic stress disorder; chronic major depression with anxious mood; bilateral hearing loss and tinnitus". 2On 13 June 2012 the defendant, the Commissioner of Police, decided that the suffering by the plaintiff of chronic post traumatic stress disorder and chronic major depression with anxious mood were caused by his having been hurt on duty, and the Commissioner determined that the notional date of injury for the plaintiff's psychiatric illnesses was 28 May 2007, which I understand to be the date of the last significant psychiatric stressor that the plaintiff experienced. At the same time, the defendant decided that the suffering by the plaintiff of "bilateral hearing loss and tinnitus" were not caused by his having been hurt on duty. Aggrieved by the latter decision, the plaintiff has made an application to this Court to determine whether that last decision of the Commissioner of Police should be confirmed, or set aside and replaced with another decision that the Commissioner of Police might be entitled to make. The medical evidence before me indicates that the plaintiff's tinnitus runs hand-in-hand with his hearing loss. Either the tinnitus is the result of hearing loss or the tinnitus results from the same causal factors that caused the hearing loss. Therefore, the tinnitus is either directly or indirectly related to the same cause as the hearing loss. 3The extent of the plaintiff's hearing loss is not agreed. Dr Joseph Scoppa diagnoses a 6.8 per cent impairment with hearing, finding underlying deafness of 4.8 per cent but adding thereto a further 2 per cent to account for the plaintiff's tinnitus. Professor Paul Fagan diagnoses a 4.7 per cent loss of hearing, allowing an underlying hearing loss of 1.7 per cent and adding thereto 3 per cent to account for the plaintiff's tinnitus. Associate Professor Croxson, qualified by the defendant, found only a 0.8 per cent loss of hearing and was not asked to make any allowance for the plaintiff's tinnitus. 4Very much in issue between the parties is the question of the causation of the plaintiff's hearing loss or deafness. The plaintiff says, through Dr Joseph Scoppa, that the totality of the plaintiff's hearing loss is due to the condition known as boilermaker's deafness or deafness of like origin, often these days refer to as industrial deafness. Professor Fagan says that part of the plaintiff's hearing loss is due to boilermaker's deafness or deafness of like origin but makes no point about the causation of the other part of the plaintiff's hearing loss. Associate Professor Croxson, qualified by the defendant, diagnoses a heredito-degenerative hearing loss. 5Sensorineural deafness can be inherent or acquired. Some children are born deaf due to sensorineural deafness. There are a number of ways in which sensorineural deafness can be acquired. For many years, there has been in my library a book called Deafness, 2nd ed (1970) published in London by J & A Churchill, written by an eminent British otologist Dr John Ballantyne. Dr Ballantyne provides me with the following list of the causes of acquired sensorineural deafness: 1. Due to head injuries which might include fractures of the skull base and concussion of the labyrinth. 2. Due to pressure changes such as blast injuries of the inner ear and barotraumatic otitis interna. 3. Due to noise (acoustic trauma). 4. Due to infections. 5. Due to the toxic effects of certain drugs, the commonest of which are aspirin and quinine. 6. Due to acoustic tumours. 7. Due to Meniere's Disease. 8. Presbyacusis. 6The section of Dr Ballantyne's work concerning deafness due to noise is this: "In 1831 Fosbroke discovered deafness occurring in blacksmiths, and in 1890, Barr surveyed 100 boilermakers who had worked at their trade for more than three or four years. Not one of them had normal hearing, and for more than half a century 'boilermaker's deafness' remained a classical example of 'acoustic trauma'. Many other occupations have been added in the intervening years, and the mid-twentieth century has witnessed another addition in the form of the jet engine. Acoustic trauma is of two types - the acute and the chronic. The acute type can be caused by a wide variety of 'acoustic shocks', such as the nearby detonation of fireworks or small-arms fire, atmospheric and other disturbances and the receivers of telephones, or the high-pitched shriek of a whistle. The deafness of rifle shooting is more marked in the left ear in the right-shouldered shot, since the butt of the rifle is nearer to this ear, and the audiogram (Figure 77) shows the typical V-shaped 'dip' at 4,000 Hz so commonly associated with many forms of traumatic perceptive deafness. The chronic type of acoustic trauma follows prolonged exposure to high-intensity levels of noise and is usually occupational. It occurs in boilermakers, drop-forge workers, shippers and riveters, stampers, platers, headers, welders, wormers, turners and those who work with pneumatic drills; is also found in petrol or jet aircraft workers, whether in the cabin or on the ground. According to Lieut-Colonel J E Lett of the United States Army Air Force School of Aviation Medicine, the noise of a jet engine is now the loudest industrial noise measuring between 120 and 140 dB above threshold level. The effects of noise are always worse in enclosed spaces, and the degree of deafness with its intensity and the duration of exposure. A level above 90 dB is considered to be 'unsafe' and high-frequency noise is more harmful than low-frequency noise. There is also a marked individual susceptibility to noise and it is of the utmost importance that all personnel should be 'screened' before employment in noisy industries. More recently there have been reports of high-frequency nerve deafness caused by exposure (of dentists) to high-speed dental drills; and there is growing concern among otologists about the potentially harmful effects produced by the enormous power output of certain modern hearing aids, some reaching a level of 140 dB. It has also been suggested that 'pop' musicians are now suffering from acoustic trauma! With the exception of head injuries with fractures of the skull base (when the hearing loss tends to be severe and permanent), the characteristic feature of most cases of traumatic perceptive deafness is a high-tone hearing loss, often with a marked V-shaped 'dip', and greatest at a frequency of about 4,000 Hz. It is thought by some this 'dip' at 4,000 Hz is due to the fact that the part of the cochlea which receives and analyses these higher tones is situated near to the labyrinthine windows, at the base of the cochlea, and that it is this proximity of the basal turns of the cochlea to the windows which makes them more exposed (and therefore more vulnerable) to soundwaves of high intensity. The problem of industrial noise is a growing one, but much work is being done to minimise its worst effects." 7Since that work was written, there have been many additions to our knowledge of sensorineural deafness. In this country at least, what Dr Ballantyne referred to as acute acoustic trauma is mainly known as traumatic deafness, and that which Dr Ballantyne described as chronic acoustic trauma, is generally known as either boilermaker's deafness or industrial deafness. 8It is now accepted by both judge-made law and statute law that exposure to noises of 85 dB(A) LAeq carries a real risk of inducing boilermaker's deafness or deafness of like origin. I discussed at some length the requisite level of noise exposure to carry a real risk of a person's suffering from boilermaker's deafness in Callaby v State Transit Authority (NSW) (2000) 21 NSWCCR 216. At [23] I pointed out that I dealt with general principles relating to industrial noise in Galdemar v Asta Enterprises Pty Ltd (1998) 17 NSWCCR 155, in which case I accepted that anything over 85 dB(A) LAeq carried a risk of inducing boilermaker's deafness. 9A number of my colleagues in the Compensation Court came to a similar view and I canvassed that in the succeeding paragraphs in my judgment in Callaby. At [32] I said this: "The law is that the employment must carry a real risk of the applicant's suffering boilermaker's deafness. The real risk is the test adopted by Geraghty J in Wright v State Transit Authority of NSW. It has also been adopted by the Court of Appeal in the Ambulance Service of New South Wales v Daniel (2000) 19 NSWCCR 697 at 708 [45]. Hodgson CJ in Eq. said: 'Having regard to that line of authority, in my opinion it would not be an error to proceed on the basis that what the worker has to prove is, in substance, that the nature of his employment with the employer involved a real, as opposed to a theoretical, risk of hearing loss. In my opinion, this is to say much the same as to say that the type of injury is incidental to that class of employment, or that the nature of that employment is apt to produce the relevant injury.'" 10 Earlier, in Blayney Shire Council v Lobley (1995) 12 NSWCCR 52, Cole JA, with whom Kirby ACJ and Rolfe AJA concurred said at 65D: "In my view, it is sufficient for a claimant worker to establish that the employment in which he was engaged occurred in an environment which, were he unprotected, could cause injury of the type suffered by him. If evidence establishes that circumstance, the worker satisfies the onus of establishing that at the time of giving notice he was employed in an employment the nature of which the injury was due." 11Another further development is to note that, that which Dr Ballantyne referred to as the "marked V-shaped 'dip'" is now generally referred to as the notch or V-shaped notch. Figure 77 on p 210 of Dr Ballantyne's work clearly shows that V-shaped notch at 4,000 hertz. This work was shown to the two medical practitioners who gave oral evidence in this case, Dr Scoppa and Associate Professor Croxson, and both agreed in general with the principles stated in it. In the current matter, the plaintiff's various audiograms do not show the classic V-shaped notch. 12On 7 January 2000, the plaintiff complained to his general practitioner Dr McRae of "crackles" in his ears and Dr McRae thought that the plaintiff needed a hearing assessment. That was carried out by Ms Kay McIntosh, an audiologist at Orange, and that audiogram is before me. The audiogram appears to show a decline in hearing in a straight fall from 3,000 hertz to 8,000 hertz. On 28 February 2011, the plaintiff again requested Dr McRae to have his hearing checked and that led to Ms McIntosh carrying out a further audiogram on 3 March 2011. That audiogram again shows a straight fall or hearing loss falling in a straight line essentially from 3,000 hertz to 8,000 hertz, but the fall is more acute indicating a deterioration in the plaintiff's hearing between 14 January 2008 and 3 March 2011. 13Dr Scoppa's audiogram, annexed to his first report of 30 November 2011, shows a straight linear fall from 2,000 hertz to 8,000 hertz. Professor Paul Fagan saw the plaintiff for the SASTC, the statutory administrator of the Police Superannuation Fund, on 22 September 2011. Dr Fagan's audiogram appears to show a marked linear decrease between 3,000 hertz and 8,000 hertz. 14It appears that Associate Professor Croxson did not himself perform or have cause to have performed any audiogram. In his primary report of 10 November 2011, it refers to the audiograms carried out at Orange on 3 March 2011, and that performed by Professor Fagan dated 22 September 2011. Associate Professor Croxson sums up the results of audiometry in this fashion: "The audiogram reveals a sloping, bilateral sensorineural hearing loss involving 4,000, 6,000 and 8,000 hertz." Professor Croxson offered this opinion: "I believe that the hearing loss found on audiometry is consistent with heredito-degenerative hearing loss rather than work-related noise exposure." 15When Associate Professor Croxson came to give evidence, he brought with him audiograms published in a work made by an American otorhinolaringologist, Dr Robert Dobbie, called, "Medical Legal Evaluation of Hearing Loss." This essentially is epidemiological evidence upon which the Associate Professor relied. Copies of those audiograms published in Dr Dobbie's work were put into evidence. 16Figure 4-7 in Dr Dobbie's work provides a mean audiometric results for 450 ears with uncomplicated noise-induced hearing loss. That shows the characteristic V-shaped notch at 4,000 hertz. Figure 7-2 provides the median NIPTS for jute weavers with different duration pressures as a function of frequency. INPTS means noise-induced permanent threshold shift. A temporary deafness is referred to by the doctors as a temporary threshold shift. A permanent threshold shift represents permanent deafness. NIPTS accordingly means noise-induced deafness. Figure 7-2 shows the extent of deafness for a worker exposed between one and two years, for a worker exposed between five and nine years, for a worker exposed between 15 and 19 years, for a worker exposed between 25 and 29 years and for a worker exposed between 35 and 39 years. The audiogram for each group shows the characteristic V-shaped notch at 4,000 hertz. The V going upwards from 4,000 hertz upwards to reach the 8,000 hertz range. 17Here, it appears that the plaintiff last worked in conditions to which boilermaker's deafness might be induced in or before August 2009. In August 2009, he went on restricted duties referred to on p 25 of the transcript of 21 October 2013 as "temporary sick report", when he was given desk duties in the Highway Patrol office at Orange. He went onto permanent sick report, meaning a fulltime absence from work, in November 2009. Accordingly, the plaintiff was exposed to various noises as a member of the police force between his attestation on 10 December 1979 and August 2009, a period of some 30 years. Were the plaintiff a jute weaver in America, one would expect his audiogram to show the V-shaped notch at 4,000 hertz rising up when one reaches 8,000 hertz because that is the pattern for those who are exposed to industrial noise in the range between 25 and 39 years. However, the plaintiff's audiogram does not. 18Figure 7-3 from Dr Dobbie's work provides the median (50th percentile) and extreme (10th and 90th percentage) PTS after 40 years of workplace exposure at 90 and 100 dBA. Again, that shows the V-shaped notch at 4,000 hertz for workers in the tenth, 50th and 90th percentiles, whether they are exposed to noise levels of 90 dBA or 100 dBA. 19 One audiogram from Dr Dobbie's work shows a pattern of deafness consistent with the pattern of deafness shown on the plaintiff's audiogram. That is figure 6-2, which is the pattern for age-related permanent threshold shift for males aged 50 (the plaintiff was born on 7 January 1960 and turned 50 in January 2010). The audiogram drops from 2,000 hertz almost in a straight line to 6,000 hertz but the audiogram has not been carried on to 8,000 hertz. 20In his report of 17 September 2013, Associate Professor Croxson said this of the nature of noise-induced hearing loss: "There are two types of noise-induced hearing loss. The first is acoustic trauma which is associated with blast or explosive injuries related to sound pressure levels of greater than 140 dB. The second form of noise-induced hearing loss is chronic noise-induced hearing loss also known as 'boilermakers' deafness'. Boilermakers' deafness was described as early as the 17th century in people whose occupation included a hammering of metal objects. It is generally held that boilermakers' deafness can occur where there is continuous industrial noise of greater than 85 dB for eight hours a day, over many years. Boilermakers' deafness is a cumulative injury and it occurs mostly in the first ten to fifteen years of noise exposure. Boilermaker's deafness causes a predictable and repeatable hearing loss, with a notching in the audiogram typically occurring at 3,000 and 4,000 Hz, and less commonly at 6,000 Hz. 8,000 Hz is spared. As the noise injury worsens, the notching in the audiogram deepens and eventually will widen." 21Figure 7.2 in Dr Dobbie's work clearly confirms that opinion. In the same report, Associate Professor Croxson advanced these reasons for maintaining his diagnosis about heredito-degenerative deafness: "My reasons for this are: The audiogram shows no notching at 3,000, 4,000 or 6,000 Hz. There is no preservation of hearing thresholds at 8,000 Hz. There is evidence of progressive hearing loss in the audiograms obtained between 14th January 2008 and 3rd March 2011. During this period of time, Sergeant Brown was not fit for work between 22nd December 2009 and 3rd March 2011. Such progression in hearing loss despite the absence of noise related to his police duties, would suggest that the hearing loss is not noise related." 22One can add to the latter bullet point, the fact that the plaintiff was only performing clerical work from August of 2009 until completely stopping work in November 2009, and that his exposure to noise in the earlier days of his police career was obviously greater than it was in the later years of his career. I should advert to this later on. 23Further, in the same report the Associate Professor points out that the plaintiff's audiograms show a sloping sensorineural hearing loss worse at 8,000 kilohertz. Again, the Associate Professor makes the point that the shape of the audiogram is not supportive of noise-induced hearing loss. The audiograms produced from Dr Dobbie's work, clearly epidemiological, evidence support Professor Croxson's contention. SHORT ADJOURNMENT 24Professor Fagan was not called to give oral evidence. His report was tendered in the plaintiff's case. Initially the report was admitted conditionally but eventually Ms McFee withdrew her objection or conceded that the ruling that I made concerning the admissibility of Dr Scoppa's report could be applied to the report of Professor Fagan. 25Professor Fagan's report is interesting for what it does not say. After enclosing his audiogram, Professor Fagan said this: "There is a subtotal hearing loss of 1.7%. There is no allowance for noise-induced hearing loss but tinnitus allowance is 3.0. The total hearing loss therefore is 4.7% which equates to a whole person impairment of 0%." A "subtotal hearing loss" means that the total hearing loss was greater than 1.7 per cent. The quotation which I have just made is followed by a table. That gives a frequency in hertz, a reading for the right ear and a reading for the left ear and then a percentage. The frequencies are between 500 hertz and 4,000 hertz. There is a "percentage" of 0.24 at 3,000 hertz and a percentage of 1.5 at 4,000 hertz. Those two added together, of course, amount to 1.74 per cent and that, I infer, led to the Professor to believe that there was a 1.7 per cent hearing loss. In other words, it is clear that Professor Fagan disregarded hearing losses above 4,000 hertz. The implication must be that he did not accept that hearing losses above 4,000 hertz were caused by exposure to loud, or industrial noise. 26However, the only diagnosis given is of noise-induced hearing loss and the Professor makes no mention at all as to what is the cause of the hearing loss above 4,000 hertz. One would have to accept, therefore, that the Professor would not accept that the hearing loss above 4,000 hertz was caused by exposure to industrial noise. The inference is that the Doctor must be diagnosing what would otherwise be called a "mixed hearing loss" but does not tell me what might be the cause of the hearing loss above 4,000 hertz. One must ask, rhetorically, whether Professor Fagan would agree with the view of his learned colleague, Associate Professor Croxson, that the hearing loss above 4,000 hertz was due to a heredito-degenerative condition. 27This brings me to the opinion of Dr Scoppa. Dr Scoppa's evidence-in-chief was given on 22 October 2013 but he did not have sufficient time to be cross-examined on that day. He returned for cross-examination on 4 November 2013 to give evidence on the afternoon of the Monday on which I called through the Special Statutory Compensation List at 10 o'clock. In his evidence-in-chief, Dr Scoppa said this: "Q. What is it about that history when viewed in light of the audiogram that led you to come to that conclusion about the hearing loss being due to noise? A. In my opinion, when you have to come up with a diagnosis of a hearing loss in respect of - if someone comes in complaining of a hearing loss and you have an audiogram, if you just look at the audiogram you haven't got a clue what could have caused it. You have got to take a history to try and work out what caused it; so in addition to taking a history of any potential cause of hearing loss consistent with that audiogram, you have also got to exclude other things as well, and in my report under Personal History you will see that there are a lot of negatives. Q. Yes? A. There's no history of ear infection, there's no family history of deafness or any disease, there's no history of exposure to ototoxic drugs and so on, so when you take a history I have excluded other potential causes to make sure that they may in my mind not be contributing, or indeed causing, the hearing loss. So the only positive sort of thing they could get out of the history that is consistent with the hearing loss was a history of occupational noise exposure over perhaps a 30 year period as a police officer. ..." The Doctor went on to make comment about his having seen many other police in the course of his practice over the years as a medicolegal consultant. 28 With the utmost respect to Dr Scoppa, any worker presenting with an audiogram showing the V-shaped notch at 4,000 hertz would be immediately suspected of having noise-induced hearing loss because such an audiogram is typical of noise-induced hearing loss. It is quite incorrect for Dr Scoppa to have said, "If you just look at the audiogram you haven't got a clue what could have caused it". 29For many, many years I viewed audiograms as a judge of the Compensation Court and the typical V-shaped notch at 4,000 hertz was the typical presentation of somebody suffering from boilermaker's deafness. Here the Doctor relies purely on history to discount the fact that the current plaintiff's audiogram is not typical of a noise-induced hearing loss. He appears from the quotation I have just given to think that he has excluded other possible causes of hearing loss. 30 However, in that regard I must consider the evidence of Associate Professor Croxson. The Associate Professor told me that one cannot obtain a history of a heredito-degenerative condition because the gene which causes such hearing loss is recessive and therefore one does not obtain a history of it from the patient because it may not have been known to either his parents or his grandparents. In other words, "No family history of deafness" does not exclude the possibility of there being a heredito-degenerative condition. 31Later in his evidence-in-chief, Dr Scoppa agreed with the position of Associate Professor Croxson that it is the early exposure to noise which causes the greater amount of deafness. At p 48, Dr Scoppa said this: "Mostly hearing loss occurs within the first five to ten years, and then thereafter, even though the noise exposure may be even greater, because you have lost the essential part of your hearing, if you like, the resistant bit is left and therefore it's more resistant to progressive loss. This is why it's difficult to sometimes apportion loss over a period of employment of, say, 30 years and just to say, 'Well, we will deem that it happened one-third at a time' in order to apportion between different employments. It's unfair to do that, because we know that in the first five or ten years more of the damage is done and thereafter the ear becomes less resistant." I then queried what the Doctor meant by "less resistant" and the Doctor agreed that it meant more resistant to further loss. 32Of course, that proposition is inconsistent with the deterioration in the audiogram shown between 14 January 2008 and 3 March 2011 and indeed the audiogram performed by Dr Scoppa himself on 30 November 2011. In order to calculate the plaintiff's hearing loss, Dr Scoppa applied what is called the Extension Tables to the NAL report of January 1988, which are used to determine the percentage loss of hearing. The Extension Tables allow one to include in the determination of the percentage loss of hearing, losses above 4,000 hertz. At the foot of p 50 of the transcript of his evidence-in-chief, Dr Scoppa said this: "I applied the Extension Tables because in my opinion in this particular case, the loss of 6,000 and 8,000 was due to industrial deafness and it would have been unfair not to apply the Extension Tables in this particular case. Because I formed the opinion that all of the losses - and it would have been - this, in my opinion, was one of the examples it would have been unreasonable not to do so." In other words, Dr Scoppa took into account hearing losses above 4,000 hertz because he thought they were due to industrial deafness. Again, that appears to be postulated on his view that the only possible explanation was industrial noise. He is therefore excluding a condition such as that diagnosed by Associate Professor Croxson and in so doing, going against what was done by Professor Fagan. 33Commencing at p 56 the Doctor told me that it was not uncommon for industrial deafness to involve a hearing loss at 8,000 hertz. To do that he relied not upon any epidemiological evidence as such, but his experience as a full-time medico-legal consultant since 2000 and even before that time. Indeed, the Doctor went on to say that a loss of hearing at 8,000 hertz due to industrial deafness is "very commonplace", a proposition on which Associate Professor Croxson did not agree, which the textbooks referred to by Professor Croxson do not agree, and which, by inference, Professor Fagan does not agree. 34The Doctor then had shown to him Dr Ballantyne's work which I cited at the beginning of these reasons. He agreed that the typical V-shaped notch at 4,000 hertz was typical for noise-induced hearing loss but limited that to "early noise-induced hearing loss". He went on to say this: "I agree that there's usually recovery at eight [8,000] but the absence of recovery at eight doesn't exclude the assessment of the rest of the audiogram in relation to noise exposure because eight can just go up and down and you still have to take your history into account in sort of saying, 'Eight is not notching, therefore I'm not going to give any noise in this particular case.' " Again the Doctor appears to have been discarding the lack of any notch in the plaintiff's audiogram because of what appears to me to be an a priori view that the plaintiff's hearing loss was caused by exposure to loud noise. 35Further on, the Doctor, when discussing the question of deterioration between the audiograms of 2008 and 2011, pointed out that it was "well accepted that the variation is insignificant between audiograms and some people would push that to 10 dB." Clearly, Dr Scoppa was pushing that proposition himself to downplay what Associate Professor Croxson thought was a significant deterioration between the audiograms of 2008 and 2011. Associate Professor Croxson would not agree with Dr Scoppa that a variation of 10 dB was "insignificant" and indeed he pointed out that by definition any loss of 5 dB or more was significant. Clearly, the inference to be drawn from how Dr Scoppa expressed himself "some people would push that to 10 dB" is an implicit acknowledgement by Dr Scoppa of the general proposition advanced by Associate Professor Croxson. Again, later in his evidence, to downplay the alleged deterioration, Dr Scoppa again pointed out that there was only a 10 dB deterioration and he thought it might be due to "a little bit of presbyacusis". 36In cross-examination, Dr Scoppa said that the V-shaped notch at 4,000 hertz was very valuable in his view in diagnosing low levels of hearing loss but he thought it was not "as relevant" when determining long standing boilermaker's deafness. Later in cross-examination, the Doctor said that a hearing loss at 8,000 hertz was usually due to presbyacusis, having been asked whether it was usually due to ageing, and, of course presbyacusis is only the word used to describe loss of hearing due to ageing. 37Further when pressed in cross-examination, Dr Scoppa agreed that one of the significant things to take into account in diagnosis is the shape of the audiogram. He went on to agree that his diagnosis was based purely on a history of the plaintiff's noise exposure. The Doctor went on to say that "getting older knocks out the notch" in the typical boilermaker's deafness audiogram thereby suggesting that a large part of the current plaintiff's audiogram might be due to presbyacusis but the plaintiff was not of an age where that is usually relevant. The Doctor went on to concede that the loss of 8,000 hertz was due to both noise exposure and age and agreed that ageing affects higher frequency losses. 38I found there to be inherent tension in the evidence of Dr Scoppa. To completely disregard the audiogram, which is in effect what Dr Scoppa has done, and rely purely on history is not the methodology used by Associate Professor Croxson and clearly not the methodology used by Professor Fagan. Further it is not the methodology of which I have been hearing for over 19 years on the Bench. The plaintiff himself could not be aware of any recessive gene which might induce heredito-degenerative hearing loss. His evidence cannot assist. 39Having seen and heard both Dr Scoppa and Associate Professor Croxson giving evidence I prefer the evidence of Associate Professor Croxson to that of Dr Scoppa. I formed the view that Dr Scoppa's evidence was tainted with partiality and overlooked the generally accepted methodology used by otorhinolaryngologists in diagnosing boilermaker's deafness or deafness of like origin: the shape of the audiogram. Furthermore, the opinion of Professor Croxson is supported by the epidemiological evidence gleaned from the textbook to which he had referred and, indeed gleaned, from the old textbook which I cited at the commencement of these reasons, with the propositions of which Dr Scoppa himself in general agreed. 40I am therefore not persuaded on the balance of the probabilities that the plaintiff's deafness and tinnitus were caused by exposure to loud noise, that is, I am not persuaded that it is due to boilermaker's deafness or deafness of like origin. I prefer the opinion advanced by Professor Croxson that is due to the heredito-degenerative condition which he diagnosed, which explains the shape and progress of the plaintiff's hearing loss, as shown on the audiograms. 41The methodology advanced on behalf of the plaintiff in essence invited me along a path which, by inference, Professor Fagan may have proceeded, by believing the plaintiff's total hearing loss to be due to a number of causes. 42In the current matter, no noise level readings were put into evidence. There has been no noise level testing, or as it is called, dosimetry. There are statements by the plaintiff of various noises to which was exposed and statements made by him on some occasions as to how close he was to the noise and at other times statements by him which might permit one to ascertain the duration of the noise. One must take such parts of the plaintiff's evidence as there is and relying upon estimates given by both by Dr Scoppa and Associate Professor Croxson apply such information or assessments to the plaintiff's exposure and then come to a conclusion that a certain noise for certain time carried a real risk of inducing boilermaker's deafness or deafness or like origin. 43There is a validity in proceeding in that way in some cases where there is adequate evidence of both the loudness of the noise, the proximity of the plaintiff's ear to the noise and the duration of the noise. Both Dr Scoppa and Associate Professor Croxson agreed that those three things were of vital significance: the loudness of the noise, the proximity of the plaintiff's ear to the noise and the duration of the noise. For example, if one goes back to Callaby's case a noise of 85 dB(A) LAeq carries a real risk of a worker suffering from boilermaker's deafness or deafness of like origin. That is, if one is exposed to 85 decibels for eight hours in an employment, that employment carries a real risk to a worker's hearing. Both Dr Scoppa and Associate Professor Croxson agreed on the concept of "doubling". It is stated in Associate Professor Croxson's report on 17 September 2013 in these terms: "It is generally accepted in Australia and in the United States that continuous industrial noise of 85dB or less for eight hours a day will not cause noise-induced hearing loss. For each additional 3 decibel increase in sound intensity, the safe time to be exposed to such noise is halved. In other words, if the continuous industrial noise is 88dB, then the safe exposure time is only four hours. This occurs because the addition of three extra decibels in sound pressure levels essentially doubles the intensity. 44It is generally accepted that continuous industrial noise is more damaging than intermittent noise. 45It is also well accepted that the propensity of a noise to cause hearing injury is related to the intensity of the noise, the duration over which it is perceived, and the proximity of the worker to the noise. 46Finally, noise-induced hearing loss does not progress after the worker has been removed from the source of noise." 47The last two propositions within that quotation clearly go beyond the concept of doubling but are still germane in this case. 48Learned counsel for the plaintiff, Mr Ower, made a table which is MFI 4. However, it shows the safe duration for a noise at a certain decibel level and is consistent with the concept of doubling as described by both Dr Scoppa and Associate Professor Croxson. At 91dB the safe duration is two hours, at 94dB it is one hour, at 97dB it is 30 minutes and so on. When one gets to 140dB, the safe exposure level is 0.11 seconds: for practical purposes that might be said to be instantaneous. However, here another complication arises. As I stated much earlier, the specialists differentiate between traumatic deafness and boilermaker's deafness or deafness of like origin. 49Traumatic deafness occurs instantly due to exposure of a noise duly thought to be 140dB and above. Mr Ower submitted that there was no difference between traumatic deafness and boilermaker's deafness but I do not accept that to be the case. Indeed, Mr Ower submitted that traumatic deafness was a deafness of like origin to boilermaker's deafness and referred me to the provisions of section 17 of the Workers' Compensation Act 1987. Section 17 concerns special provisions for loss of hearing, subection (1) commences thus: "If an injury is a loss, or further loss, of hearing which is of such a nature as to be caused by a gradual process, the following provisions have effect:" Subsection (2) is in the following terms: "Without limiting the generality of subsection (1), the condition known as 'boilermaker's deafness', and any deafness of a similar origin shall, for the purposes of that section, be deemed to be losses of hearing which are of such a nature as to be caused by a gradual process." Subsection (2) has a predecessor in s 7(4B) of the Workers' Compensation Act 1926 which provided thus: "The condition known as 'boilermakers deafness', and any deafness of like origin, shall for the purpose of subsection (4) be deemed to be a disease and to be of such a nature as to be contracted by a gradual process." The former section of 7(4B) carried a sidenote referring to Milne v International Combustion Australia Ltd [1953] WCR80. In the second edition of his work "Workers' Compensation (New South Wales)" of the late Professor Mills said this about the former subsection: "The enactment of this subsection followed the decision in Milne v International Combustion Australia Limited [...] where Rainbow J held that a gradual loss of hearing resulting from long exposure to noise was not a disease, but was rather a succession of trauma each of which causes some minute amount of damage, the cumulative effect being the slow diminution of hearing ability. Hence it could not be classified as a disease of gradual onset within the meaning of sub-s (4)." This, of course, raises the persisting dichotomy between repeated microtraumata and disease, giving rise to that woolly concept "nature and conditions of employment" about which I have had much to say over the years. 50However, I cannot accept that traumatic deafness is of like origin to boilermaker's deafness. Indeed, the reason for doing that is because Associate Professor Croxson pointed out that evidence obtained post-mortem, that is, from autopsy, establishes that traumatic deafness causes structural destruction of the inner ear or parts of it, whereas, where there is only boilermaker's deafness or deafness of like origin, there is only found metabolic exhaustion of the outer hair cells of the cochlea. If such metabolic exhaustion is extensive there is morphological change in the cochlea. In other words, the effect of traumatic deafness is destruction of the inner ear or parts of, it whereas exposure to persistent industrial noise shows metabolic exhaustion of the outer hair cells of the cochlea. The difference can be visualised when the ear is cut open, something which, most fortunately, does not occur to live patients. 51However, the difference in pathology might explain why some people exposed to 140 dB or more, even for short periods, do not suffer from traumatic deafness but only suffer from some insult which could cause further industrial or boilermaker's deafness. That is, a noise of 140 dB could affect different people in different ways. In some people it might cause a destruction of structures within the inner ear but in others it might only affect the outer hair cells of the cochlea. Much would depend on the person's anatomy and resilience, and one thing is clear from all the literature: noise can affect people differently. 52The time available to me to continue to give these reasons is not great. Suffice it to say that, were I pressed to ascertain whether the plaintiff's employment carried a real risk of his suffering from boilermaker's deafness or deafness of like origin, I would so find. For example, in his address Mr Ower was kind enough to refer me to certain parts of the evidence which show such a real risk occurring. 53On 6 June 1982 while serving at Orange the plaintiff was transferred to the Highway Patrol. He went on to perform highway patrol duties for some ten years. On one occasion he was involved in the pursuit of an offender, obviously in a motorcar, from Orange to Dubbo. The plaintiff pointed out that he chased the offender around Orange for some period and then went from Orange all the way to Dubbo, which was an hour and a half away, and so the plaintiff estimated that he pursued the offender for anywhere between an hour and a half and two hours with the siren activated for "the majority of the time". A space of between 1.5 hours and two hours is an average of 1.75 hours and a "majority" of that time might be an hour. Associate Professor Croxson tells me that the noise to which the plaintiff might have been exposed when sitting in a police vehicle with a siren sounding in pursuit is 90 dB. If one is exposed to 91 dB for two hours the employment carries the risk of boilermaker's deafness or deafness of like origin. Of course there is difficulty relying upon estimates between "one and half and two hours" and then what does one mean by the "majority of the time", literally majority just means 51 per cent but of course the plaintiff could have been referring to 90 per cent. The evidence was not given in any great detail. 54Later in his evidence-in-chief the plaintiff referred to one job which he did on the Mitchell Highway. He was required to go to a point on the highway in order to direct traffic. When he arrived at the location, he had to leave his vehicle quickly and direct traffic down Millthorpe Road in order to get it off the highway. He was required to act so quickly that he did not have time to turn the siren off and he told me that he was standing about two steps from the driver's door of his vehicle directing traffic down Millthorpe Road and the siren was going until all that traffic had left and he was able to turn the siren off, after several minutes of exposure to the noise from some two steps away. According to Associate Professor Croxson's report that might have exposed the plaintiff to a noise level of between 115 and 120 dB. An exposure to 115 dB carries a risk of inducing deafness if the duration is 28 seconds. At 121 dB the duration need only be seven seconds. One could infer that the plaintiff may have been exposed to noise for more than a minute and that, therefore, carried a real risk of inducing boilermaker's defence or deafness of like origin. 55There is also evidence of the plaintiff's in his early years being required to euthanase animals who were, what we would now call, "road kill" using his Smith & Wesson .38 calibre revolver. He estimated that in his early years he carried out euthanasia about three to six times per annum and on one occasion on the Molong Road he needed to euthanase a steer and it took him four shots into the steer's head before he managed to kill the animal. Whether the plaintiff used his Smith & Wesson revolver or his Glock pistol, according to Dr Scoppa he was exposed to noises between 130 and 160 dB and according to Professor Croxson between 140 and 170 dB. As I have earlier mentioned at 140 dB the exposure need only be for 0.11 of a second. The discharging of four bullets one would think would take much more than 0.11 seconds. 56There is also evidence about the plaintiff's exposure to radio noises and the plaintiff in that regard relied upon what was said in-chief between pp 20 and 21 and on the estimates of noise given by both Dr Scoppa at p 63 of his evidence and by Associate Professor Croxson on pp 2 and 3 of his second report. I shall not cite those for the question of brevity. 57As I said, I would be prepared in this case to hold that the plaintiff had established that his employment as a police officer carried a risk of his suffering from boilermaker's deafness or deafness of like origin. However, merely because the employment carried that risk does not mean that the plaintiff actually suffered from boilermaker's deafness or deafness of like origin. I was asked by the learned counsel for the plaintiff to find that some part of the plaintiff's total deafness might be due to industrial deafness or deafness of like origin. However, there is no direct evidence of that, the evidence of Dr Scoppa says wholly one thing and the evidence of Associate Professor Croxson says wholly the other. One could infer that Professor Fagan went down the road of a mixed deafness but he did not give any evidence and he did not explain himself. 58According to Associate Professor Croxson, the whole of the plaintiff's hearing loss can be attributed to a heredito-degenerative condition and he, for example, did not tell me that the hearing losses at or below 4,000 hertz were due to boilermaker's deafness or deafness of similar origin and hearing losses above 4,000 hertz were not. I am afraid that Ockam's razor must be applied. 59There is no way that I know of, or that the evidence points me to, which could allow me to distinguish what might be due to industrial deafness and what might be due to the heredito-degenerative condition. This causes another problem, that is, the Commissioner of Police was required under s 10B(3)(a) of the Act to decide whether or not the infirmity to which the certificate of the PSAC related was caused by the plaintiff's having been hurt on duty. In essence, counsel invited me to find that part only of the condition certified by PSAC was caused by the plaintiff's having been hurt on duty. In that regard, counsel referred me to the decision of Commissioner of Police v Kennedy [2007] NSWCA 328; (2007) 5 DDC R380. However, that was a very different case. That case is authority for the proposition that it is up to the SASTC to decide the quantum of any case where there is an application for a gratuity pursuant to section 12D of the Act. There are dicta in the case which also refer to the question of causation being left to the SASTC but failing to differentiate between the injurious event and the pathology involved. Unfortunately the learned judges in Kennedy's case did not draw the distinction that "injury" within Workers' Compensation legislation can refer to both the injurious event and the pathology which is said to be the injury. 60However, in the present case there is no acceptable evidence that would enable me to say that part of the plaintiff's hearing loss is due to boilermaker's deafness or deafness of like origin and another part is due to a heredito-degenerative condition. 61I have enquired of the parties whether any further reasons for judgment are required but I am told none is so required. For those reasons I confirm the decision of the Commissioner of Police made on 13 June 2012.