Judd v Amaca Pty Ltd [2003] NSWDDT 12

Dust Diseases Tribunal of New South Wales

CITATION : Judd v Amaca Pty Ltd [2003] NSWDDT 12 PARTIES : David Clarence Judd Amaca Pty Ltd MATTER NUMBER(S) : 341of 2002 JUDGMENT OF: Curtis J at 1 CATCHWORDS: Damages :- Causation LEGISLATION CITED: CASES CITED: DATES OF HEARING: 13,14,15,16,17 January 2003; 2,3,4,5,6,10,11,12,13 June 2003 DATE OF JUDGMENT: 07/04/2003

FOR PLAINTIFF: Mr JL Sharpe instructed by Turner Freeman LEGAL REPRESENTATIVES: FOR DEFENDANT Mr GM Watson SC with Mr AJ Abadee instructed by Phillips Fox

JUDGMENT: Introduction 1. The plaintiff, David Clarence Judd, has contracted lung cancer. He asserts that, although he was a heavy smoker over many years, asbestos fibres inhaled by him in his work as a carpenter materially contributed to the development of his disease. He sues Amaca Pty Limited (formerly known as James Hardie and Coy Pty Limited) as the manufacturer and distributor of asbestos cement building products with which he worked. 2. Lung cancer has a high incidence in the general population. The disease is nevertheless more prevalent in those groups who have inhaled cigarette smoke or asbestos fibre. The mechanisms by which healthy cells mutate into cancerous cells, either endogenously or through the agency of cigarette smoke or asbestos fibre, or some other agent, are unknown (see PX 87). Further, "All 4 major histological types (squamous, adeno-, large-cell and small-cell carcinoma) can be related to asbestos. The histological type of a lung cancer and its anatomic location (central or peripheral, upper lobe versus lower lobe) are of no significant value in deciding whether or not an individual lung cancer is attributable to asbestos. Clinical signs and symptoms of asbestos-related cancer do not differ from those of lung cancer of other causes." (PX13). 3. Mr Judd belongs to no known sub-group particularly vulnerable to the carcinogenic effects of asbestos by reason of family history, diet, genetic make-up, or other factor peculiar to him. He does not suffer from clinically detectable asbestosis and his lung fibre burden is unknown. He is 63 years old and was a heavy smoker for over 42 years. His contentions are: (1) his cancer is more likely to have been induced by asbestos, or asbestos in combination with smoking, than either the background risk to which the whole population was exposed, or to smoking alone, or (2) all lung cancers which develop after exposure to both cigarette smoke and asbestos fibre are caused by the agency of both toxins operating in combination and his asbestos exposure has contributed to that pathological process which resulted in his cancer. Causation By Increase in Risk 4. The plaintiff's first submission recognizes that his case may be similar to that of the plaintiff in Wilsher v Essex Area Health Authority [1987] 2 QB 730 at 771 to 772 where Mustill LJ said this: Instead of a single risk factor known to have caused the injury there is a list of factors, which cannot be fully enumerated in the current state of medical science, any one of which might have caused the injury. What the defendant did was not to enhance the risk that the known factor would lead to injury, but add to the list of factors which might do so. 5. In this regard "The law does not equate the situation where the defendant has materially increased the risk of injury with one where he had materially contributed to the injury." (Mr Andrew Grubb in a case note in [1988] CAM LJ 350 as cited with approval by Mason P in Bendix v Barnes ((1997) 42 NSWLR 307 at 316). 6. Such a case may be made out upon epidemiological evidence which establishes that a plaintiff falls into a class of persons who are more likely to have contracted the disease because of the designated risk rather than from any other cause; that is, not only that there was an additional risk, but upon the probabilities it was that risk which came home (see Seltsam Pty Ltd v McGuinness and anor (2000) 49 NSWLR 262). 7. Relative risk is a measure of the incidence of a disease in a population exposed to a particular agent expressed in multiples of one where one is the background incidence of the disease in the non exposed population. A relative risk of 1.5 indicates that statistically one in three cases of the disease may be attributed to the agent in question. A relative risk of 2 indicates statistically that the background risk is doubled and that one of every two cases of the disease may be attributed to the agent. A relative risk of 3 indicates that two in every three cases of the disease may be attributed to the agent and that any case taken at random is more probably caused by the agent rather than the background risk. 8. Statistically then, a relative risk of 2 indicates that it is no more probable that in an individual case a disease was caused by the agent in question than that it was caused by a factor or factors independent of that agent. However, "the law never gives judgment in favour of a plaintiff when the only finding is equally consistent with liability and non-liability". (Moriarty v Evans Medical Supplies Limited [1958] 1 WLR 66 at 91 per Lord Denning). 9. Unless a plaintiff can rely upon other circumstances that operate to weigh the probabilities in his favour, proof of causation which relies upon epidemiological evidence generally requires proof that his relative risk was greater than 2. Causation and Common Sense 10. It is of course the case that the process by which a court reaches actual persuasion in the instant case ". . . does not involve a mechanical application of the probabilities" per Spigelman CJ (Seltsam Pty Limited v McGuiness [2000] NSWLR 262 at 285). 11. For instance the circumstances bearing upon the probabilities of the plaintiff's risk may approximate more closely a cohort in one particular epidemiological study rather than fall to be determined by a scientific average of many studies; he may suffer from some concurrent illness, itself a marker of either vulnerability or heavy exposure; he may have a family history or genetic make-up giving rise to an inference of peculiar susceptibility. 12. A finding of causation in law is not to be equated with scientific proof. Nevertheless, where the plaintiff can establish no circumstance beyond his exposure to a toxic substance, and the mechanism of injury is unknown, the court has no basis other than broad statistical probability on which it may rely. 13. Even where the relative risk does not reach two, a court may infer causation as a matter of common sense; for instance, if one or more postulates or criteria by which epidemiologists assess the strength of epidemiological data appeals more strongly to the judge than the expert. Such considerations as strength of association, dose response effect, time sequence, consistency, and biological plausibility are referred to in the judgment of Spigelman CJ in Seltsam Pty Ltd v McGuinness. It is for the court to assess the weight of any such criteria in drawing conclusions and in this regard it may infer causation even where an epidemiologist may not. 14. In the present matter however I am unable to rely confidently upon any fact or consideration other than the numerical conclusions of epidemiological studies in the terms of which the experts called by the plaintiff, Professor Henderson and Dr Leigh express their opinions. 15. Professor Henderson in attributing Mr Judd's cancer to asbestos specifically relies on " exposure sufficient to increase the relative risk of lung cancer to 2.0 or more, with an attributable fraction of at least (2-1)/2 = 0.5, equating to a probability of causation of 50 per cent or more, i.e. "on the balance of probabilities"" (PX 10, pp5 and 8). 16. Although Dr Wright and Dr Rosalion attributed Mr Judd's cancer to asbestos, each did so upon the assumption that the exposure was "heavy" or "extensive" and relatively continuous over more than 10 years (PX 7 p 1; PX 8, p 14). These assumptions are false. The opinion of Dr Jersman (PX 101) appears to be that any asbestos exposure contributes to a lung cancer which develops in a smoker. This opinion cannot stand with that of other experts called in the plaintiff's case. 17. Mr Judd took up smoking in 1955 when he was 15 years old. Forty three years passed between 1955 and 1998 upon almost every day of which Mr Judd smoked cigarettes. He averaged more than 10 cigarettes a day from 1955 to 1962 and thereafter until the age of 58 smoked an average of 35 cigarettes each day (PX35 p 3). During this time he was, other than minimally, exposed to asbestos fibre upon no more than about 350 days. His risk from smoking was so much greater than that from asbestos exposure that, as a matter of common sense, and uninstructed by experts, I would conclude that his disease was caused by smoking rather than asbestos exposure. Because scientific reality may be counter-intuitive it is necessary to test this common sense conclusion against the weight of expert opinion in this case. What Level of Exposure to Asbestos Fibre is Necessary to Double the Risk of Contracting Lung Cancer? 18. Because there was then no widespread agreement in the medical and scientific community as to an appropriate criterion by which lung diseases may be attributed to asbestos exposure, in January 1997 under the chairmanship of Professor Henderson, a group of like minded pathologists, radiologists, occupational and pulmonary physicians, epidemiologists, toxicologists, industrial hygienists, and clinical and laboratory scientists met in Helsinki and agreed upon a consensus report subsequently published in the Scandinavian Journal of Work and Environmental Health (1997) (PX 13). 19. This report was prepared for the guidance of occupational health authorities and tribunals in compensating persons suffering from diseases which may have been caused by asbestos. In relation to the attribution of lung cancer the report said this: Because of the high incidence of lung cancer in the general population it is not possible to prove in precise deterministic terms that asbestos is the causative factor for an individual patient, even when asbestosis is present. However attribution of causation requires reasonable medical certainty on a probability basis that the agent (asbestos) has caused or contributed materially to the disease. The likelihood that asbestos exposure has made a substantial contribution increases when the exposure increases. Cumulative exposure on a probability basis should thus be considered the main criterion for the attribution of a substantial contribution by asbestos to lung cancer risk. For example relative risk is roughly doubled for cohorts exposed to asbestos fibres at a cumulative exposure of 25 fibre years or with an equivalent occupational history at which level asbestosis may or may not be present or detectable. Heavy exposure, in the absence of radiologically diagnosed asbestosis, is sufficient to increase the risk of lung cancer. Cumulative exposures below 25 fibre years are also associated with an increased risk of lung cancer but to a lesser extent. 20. Having previously observed that "the relative risk of lung cancer is estimated to increase 0.5 to 4 per cent for each fibre per cubic centimetre per year (fibre-years) of cumulative exposure", (this range may not even have included the totality of the studies considered by the participants (T 188.1)), the authors of the document adopt without explanation the upper boundary of this range (4 per cent) and conclude that a cumulative exposure of 25 fibre years increases the risk of lung cancer twofold. Had the lower boundary been selected a cumulative exposure of 200 years would be required. 21. Professor Henderson has acknowledged that good science may justify the selection of the middle of the range (T 184, McDonald 225) and conceded that he does not know why the figure of 25 fibre ml years was adopted (McDonald page 252). He did not know the cohort upon which the figure was based (McDonald 249) and does not profess great epidemiological expertise (McDonald 223, 258, 223, 258, T 184). He says that the figure of 25 fibre ml years was "thrown up by one of the discussants" (T 188) in a "broad ranging discussion" (T 189) and a "broad multidisciplinary assessment based on different methodologies" (T 190) following "multivariable analysis of prevailing scientific literature" (McDonald 253). The figure was "arrived at by a multivariable crutch taking into account different pieces of information" (McDonald 253) as "a result of a variety of opinions from a variety of studies using a variety of methodologies" (McDonald 255). 22. These observations do not satisfy the requirement that an expert's "assumed " or "accepted" facts be identified. (Makita (Australia) Pty Ltd v Sprowles [2001] 52 NSWLR 705). As Heydon JA observed at 744, "an attempt to make the basis of the opinion explicit may reveal that it is not based on specialised expert knowledge, but, to use Gleeson CJ's characterisation of the evidence in HG v The Queen (at 428), on "a combination of speculation, inference, personal and second-hand views as to the credibility of the complainant, and a process of reasoning which went well beyond the field of expertise". 23. The Helsinki report should be seen for what it is: "A position statement from an expert group" (Prof Henderson T 188.47), not a document which reveals and draws together pursuant to any scientific protocol, identified sources upon which it relies. In consequence, as a persuasive authority upon the discrete question of when, upon the most reliable epidemiological evidence, the relative risk doubles, the figure advanced by the Helsinki group becomes no more than the bare "Because I say so" of a group of like-minded scientists. It cannot be tested or appraised independently as logically flowing from identified sources. 24. One reason suggested by Professor Henderson as possibly leading to the adoption of the figure of 25 fibre ml years as a threshold for the attribution of asbestos related lung cancer was that a British researcher, Kevin Brown, suggested many years ago that asbestosis was required for the attribution of lung cancer to asbestos, (McDonald 253). There is thought to be a threshold below which asbestos does not cause asbestosis (PX13 450, McDonald 253), and this threshold has for some years been seen as 25 fibre ml years, at which cumulative exposure cases of asbestosis begin to appear clinically (McDonald 253, 255.5). However, the Helsinki document conceded that "it is not possible to prove in precise deterministic terms that asbestos is the causative factor for an individual patient even when asbestosis is present" and Professor Henderson thought it merely coincidental that the Helsinki group fixed upon that threshold figure for asbestosis (T 168) as the figure at which the relative risk of lung cancer doubled. 25. Opinions inconsistent with the Helsinki accord are held by both Professor R M Fox, a very highly qualified oncologist, and Dr Julian Lee, an eminent physician. 26. Epidemiological studies have confirmed a correlation between the presence of histological asbestosis and an increased incidence of lung cancer. Because no mechanism by which the asbestosis itself causes the cancer has been established, Professor Fox and Dr Lee believe that the presence of asbestosis may be no more than an index or marker of the intensity of exposure sufficient to cause lung cancer. Given sufficient exposure to cause asbestosis each doctor would attribute a lung cancer to asbestos even in the absence of clinically detectable asbestosis. Dr Lee is of the opinion that because exposure in the order of 100-200 fibre ml years is likely to cause asbestosis, it is also likely to cause lung cancer. 27. Dr Lee's estimates may be conservative. The UK Health and Safety Commission in 1979 determined that a cumulative exposure of 100 fibre ml years was likely to produce an annual incidence of certified asbestosis of 0.5 per cent and an increased lung cancer risk across asbestos industries of around one per cent (Simpson, Asbestos: Final Report of the Advisory Committee, HMSO, 1979. AMACA 22 p10). 28. Both doctors are of the opinion that the Helsinki criteria of 25 fibre ml years is flawed because although it recognises that the risk of developing lung cancer is relative to the intensity of exposure, and recognises that the presence or absence of asbestosis is irrelevant, it attributes individual lung cancers to asbestos at a cumulative level at which the risk of contracting some degree of asbestosis is a mere possibility rather than a probability. 29. If only one per cent of workers exposed to 25 fibre ml years will develop asbestosis (T 168.44), and not all of those will develop lung cancer, this density of exposure may seem to constitute a very low threshold at which to attribute a lung cancer to asbestos in the presence of other independent and possibly compelling causes such as smoking. The reliance by Professor Henderson and the Helsinki group upon Mr Brown's supposition emphasises the need to test the Helsinki criteria of 25 fibre ml years against reliable epidemiological data. 30. The Helsinki conference took place in January 1977. In 2000, a paper "The Quantitative Risks of Mesothelioma and Lung Cancer in relation to Asbestos Exposure" by Hodgson and Darnton was published in Volume 44 of the Annals of Occupational Hygiene. The authors drew together the data from 17 epidemiological studies and, weighting their findings in accordance with the power and reliability of the study, drew up a table summarising lung cancer mortality and exposure specific data. (Table 2 PX26). This table indicates that the risk of contracting lung cancer increased by 4.8 per cent for each fibre ml year of amphibole exposure, and 0.062 for each fibre ml year of pure chrysotile exposure. The risk was in consequence doubled at about 20 fibre ml years for amphibole and at about 1600 fibre ml years for pure chrysotile fibres. In the light of this study, the epidemiologist Dr James Leigh called in the plaintiff's case, and Professor Geoffrey Berry a consultant bio-statistician and epidemiologist, called in the defendant's case, agreed the Helsinki criteria ought be modified so as to take account of the different carcinogenicity of different fibre types. 31. The matter was reconsidered by some of the Helsinki participants at the Adelaide Workshop on Asbestos Related Diseases and a resulting paper published in the Australian and New Zealand Journal of Occupational Health and Safety in 2002 (PX 13). At page 448 the following appears: For exposures to a mixture of amphibole and chrysotile asbestos, the cumulative exposure leading to a doubling of risk will be dependent on the proportions of the types in the mixture. 32. It is common ground that asbestos cement products manufactured by James Hardie and Coy in Australia in the years after 1955 contained approximately 15 per cent asbestos fibre made up of 10 per cent chrysotile and 5 per cent amphibole fibres. It is also common ground that amphibole fibres are more easily released, Professor Berry expressing the opinion that the airborne concentration of fibre released from these products would be constituted as to 40 per cent by amphibole fibres and 10 per cent chrysotile fibres. In order to calculate the risks associated with asbestos cement products, Professor Berry adopted the lowest end of the Helsinki range of 0.5 per cent increase in relative risk of lung cancer for each fibre year of exposure as appropriate for pure chrysotile exposure. This corresponds to a doubling of the risk in 200 fibre ml years. He further adopted the highest end of the Helsinki range being a 4 per cent increase in the relative risk of lung cancer for each fibre year as appropriate to doubling the risk for predominantly amphibole exposures. This corresponds to a doubling of the risk in 50 fibre ml years. Accepting a relative concentration of 40 per cent amphibole and 60 per cent chrysotile, Professor Berry concluded that the relative risk doubled at 50 fibre ml years of exposure to the asbestos cement building products. Dr James Leigh, having read the report of Professor Berry, agrees with his method and his conclusion. 33. Professor Henderson, agreeing that in general the risk is dependent on the proportion of fibre types, adheres to his opinion that the relative risk is doubled at 25 fibre ml years. 34. The professor harbours some reservations concerning the Hodgson and Darnton paper. The studies analysed by Hodgson and Darnton included asbestos miners, millers and insulation workers. Professor Henderson contends that because miners consistently show less risk than end users such as insulators, probably "because fibre size and degradation to fibrils is less advanced in mining and refining and more advanced in manufacturing application" (T 190.35) and because cutting asbestos cement building products releases disproportionately more amphibole fibres into the atmosphere. 35. It does seem reasonable to infer that application grinders to asbestos cement products will break up fibres into shorter lengths. The question of differential toxicity depending on fibre size was addressed by Hodgson and Darnton who at p 574 of the published study wrote that "the notion that the longest fibres used in textile processes do represent a higher risk, is consistent with experimental evidence that longer fibres are more carcinogenic." 36. That same conclusion was reached by Green et al (Journal of Occupational and Environmental Medicine 1997, PX 77) who wrote that the longer airborne fibres in asbestos textiles manufacture "provide the most plausible explanation for the high mortality from lung cancer and asbestosis in this population." Jaurand, in a study of the mechanism of fibre induced genotoxicity published in the Journal of Environmental Health Perspectives, Vol 105 Supplement 5, September 1997 (PX 78), found that longer asbestos fibres increased genotoxicity by frustrating phagocytosis and by producing a greater number of oxidants. 37. What is not clear to me is whether the grinding process affects the diameter of the fibres. It may be that the beneficial effect of an atmosphere contaminated with shorter fibres is cancelled out by a greater proportion of finer fibres. I am not persuaded that the circumstance of end use requires substantial alteration to the table of relative risk contained within the Hodgson and Darnton meta-analysis. It may be accepted that cutting asbestos cement products with a grinder liberates disproportionately more amphibole fibres but this circumstance may be taken into account in determining the relative toxicity of a known concentration of mixed fibres. 38. Professor Henderson relies upon two more recent studies. Gustavssen et al (2000) analysed low dose occupational exposure among men in Stockholm from end use of asbestos, mainly chrysotile (PX24). They found a relative risk of contracting lung cancer of 1.90 at a cumulative exposure of 4.0 fibre ml years. Pohlabeln et al (2002), studying the effects of various occupational carcinogens in a German cohort (PX25), found a relative risk of contracting lung cancer from asbestos of 1.94 for exposures exceeding 10 fibre ml years and concluded that the results were consistent with a doubling of risk at 25 fibre ml years. 39. The wide discrepancy in estimates of fibre ml years relevant to the incidence of lung cancer appears to be related to the imprecision of measurement when the industrial exposure took place at a known site and the necessary imprecision of estimates made upon an assumed historical exposure when there is long latency between exposure and contraction of the disease. As an example, in the present case, estimates vary between 3.24 (AMACA 22) and 60 fibre ml years (PX 61). 40. Professor Berry considered both the Gustavssen and Pohlabeln studies before concluding that the relative risk of end users of asbestos cement products doubled at 50 fibre ml years. He said in evidence that the studies should not stand either together or alone as appropriate guides because the mere fact that they were recently published does not indicate they are superior to earlier studies (T 319.27). They may be subject to bias in the way the exposures were measured or assessed. Nevertheless the studies merit consideration and if a meta-analysis were to be done today Professor Berry would include these studies. He does say however that because of the wide confidence intervals, (1.32 to 2.74 and 1.1 to 3.4 respectively, see AMACA 11 p4) even if they were included in the Hodgson and Darnton calculations they would not shift the estimates very much (T 319.22). 41. Although the Adelaide document states in terms that "for exposure to a mixture of amphibole and chrysotile asbestos the cumulative exposure leading to a doubling of the risk will be dependent on the proportions of fibres in the mix", it goes on to assert "the requirement of 25 fibre ml years of cumulative exposure which is set out in the Helsinki criteria represents a fair and reasonable approach for the attribution of lung cancer to asbestos for amphibole exposures . . . [and] mixed exposures". I cannot reconcile those two statements nor understand how it is that Dr Leigh, who attended the conference, joined the consensus pursuant to which the paper was published. 42. Throughout this case experts have used such words as "material contribution" when the context indicated that "material increase in risk" was a more appropriate phrase. It may be that the participants in Helsinki and Adelaide intended that "other circumstances" beyond an epidemiologically determined relative risk of 2.0 invite a common sense conclusion that at 25 fibre ml years lung cancer should be attributed to asbestos. Unfortunately the generalities offered by Professor Henderson in possible support of such an inference do not satisfy the test of admissibility mandated by Makita Pty Ltd v Sprowles. The Adelaide paper cites no references. No "other circumstance" has been advanced relevant to Mr Judd's exposure or risk. 43. In a paper published in the Annals of Occupational Hygiene (vol 43 No 1 1999), (PX 89), Burgdorf and Swuste observed that in the documentation of several [European] compensation schemes, claims were made that exposure at a level of 25 fibre ml years was associated with a twofold increase in risk "although references to supporting scientific evidence are lacking (Ahrens et al 1993; Anonymous 1997; Tossavainen, 1997)." 44. Upon the evidence of Dr Leigh and Professor Berry in this case I am of the opinion that the relative risk of contracting lung cancer in consequence of working with asbestos cement building materials in Australia between 1955 and 1980 doubled at 50 fibre ml years of cumulative exposure. Operation of Section 25B 45. In McDonald v State Rail Authority of NSW (16 NSWCCR 695), His Honour the President said at 720: the issue resolved in the plaintiff's favour specifically stated is: carcinoma of the lung may be attributed to asbestos exposure in the absence of asbestosis where the exposure was sufficient to have caused asbestosis. 46. In the present case the plaintiff filed a notice pursuant to s 25B contending that the issue the subject of determination in this passage of His Honour's judgment may not be relitigated or re-argued in these proceedings. On 24 December 2002 his Honour refused an application to relitigate the issue brought by the defendant. In his reasons His Honour said at par 24: It is appropriate to observe that in McDonald there was a concession that 25 fibre ml years was the exposure necessary to cause asbestosis. What exposure is sufficient to cause asbestosis was not an issue decided. It will therefore be necessary for the plaintiff to prove at the hearing what exposure is capable of causing asbestosis. 47. The parties in McDonald may have inadvertently misled His Honour by what may now be seen as an ambiguous concession. Although the plaintiff there submitted that the Helsinki criteria should be adopted by the Tribunal for the attribution of lung cancer in the absence of asbestosis, "exposure sufficient to have caused asbestosis" was as irrelevant to the minds of the participants at Helsinki as was the presence or absence of asbestosis itself. It is convenient to again quote from the consensus report: cumulative exposure on a probability basis should thus be considered the main criterion for the attribution of a substantial contribution by asbestos to lung cancer risk. For example, relative risk is roughly doubled for cohorts exposed to asbestos fibres at a cumulative exposure of 25 fibre ml years. 48. In his report upon Mr Judd's circumstance dated 20 August 2002 (PX 11), Professor Henderson said: For the individual case, The Helsinki Criteria set exposure estimates or correlates sufficient to increase the relative risk of lung cancer to 2.0 or more, with an attributable fraction of at least (2-1)/2 = 0.5, equating to a probability of causation of 50% or more - i.e. "on the balance of probabilities". As Professor Henderson said in evidence, the fact that cases of asbestosis begin to appear clinically at a particular exposure is interesting but irrelevant to the question of what degree of exposure doubles the risk (T 167.17). 49. There are problems with the formulation of the general issue in McDonald generated by the ambiguous terms in which the parties there framed the question for His Honour's determination. 50. If a causal connection may be drawn where the exposure was merely "sufficient" to cause asbestosis in some persons then the threshold may be too low. 51. At 25 fibre ml years, when asbestosis becomes clinically detectable in a small percentage of the exposed population, the relative risk is 1.5 and only 33 per cent of cancers are attributable to asbestos. Histological asbestosis may be present with exposures in the range 10 to 20 fibre ml years (Prof Henderson PX10 p 6). Ten fibre ml years imports a relative risk of 1.2. In a population exposed to a relative risk of 1.2, only 2 of every 12 lung cancers (around 17 per cent) will be attributable to asbestos rather than the background risk (smoking risks excepted). 52. If, on the other hand, a lung cancer is to be attributed to asbestos exposure at a level where asbestosis in a member of the exposed population was sufficient probably to cause asbestosis (following the common law test of proof as to facts relevant to facts in issue), then the threshold may be too high. 53. Dr Lee has said that 100 - 200 fibre ml years are required. This estimate requires a relative risk of between three and four, when statistically only 25 to 33 per cent of cancers in the exposed population are not attributable to asbestos (smoking risks excepted). 54. However, the question addressed by the Helsinki participants was never "what exposure is necessary to cause asbestosis?", it was "what is the cumulative exposure on a probability basis necessary to double the risk?" 55. An appropriate formulation may be "In the absence of any causal circumstance peculiar to the plaintiff, carcinoma of the lung may be attributed to asbestos exposure in the absence of asbestosis when the exposure was sufficient to more than double the risk of contracting lung cancer in an individual." Such a formulation admits of the possibility that in an individual case a lung cancer may be attributed to asbestos where the relative risk at large is less than two, but circumstances peculiar to the plaintiff permit a finding of causation. It also permits evidence to be led to prove that a doubling of the risk of lung cancer occurs at a cumulative exposure higher or lower than 50 fibre ml years. 56. Because the formulation in McDonald did not qualify the word "sufficient" with either "possibly" or "probably" a reformulation in these terms is not necessarily inconsistent with that in McDonald and may serve as a guide to future cases; as would my finding that upon the present state of medical knowledge the relative risk inherent in asbestos cement building materials doubles at 50 fibre ml years. I observe however that this finding cannot constitute an essential part of my reasoning because the plaintiff in this case does not reach the 25 fibre ml years threshold adopted in McDonald and in various judgments in the Compensation Court on appeal from the Dust Diseases Board. (Cavanough v DDB 16 NSWCCR 626; DDB v Kelly 20NSWCCR; Pizzini v DDB unreported Duck J 23/12/1994; Proudman v DDB unreported Geraghty J 20/5/99, Pizzini v DDB unreported Geraghty J). Measures of Cumulative Exposure to Asbestos Fibre 57. One fibre ml is a measure of concentration in the breathing atmosphere of one respirable fibre of asbestos in each cubic centimetre of air. A daily time weighted average (TWA) of fibre mls is the daily sum of sub-totals, each a product of fibre ml concentration in the breathing zone of a worker engaged upon a particular task, multiplied by the percentage of an eight hour day occupied upon that task. A fibre ml year is the average of the daily TWA's over a 48 week year, each week of five days and each day of eight hours. The cumulative fibre ml years of a worker is the sum total of all the fibre ml years of his exposure. 58. It is apparent that the concentration of fibres inhaled during cutting asbestos cement building products will exceed that concentration inhaled during other activities. Various tests have been attempted to measure the likely concentration in the breathing zone of persons cutting asbestos cement sheet with an angle grinder. A test conducted by James Hardie in an Industrial Hygiene study on 16 September 1971 cutting Super-Six corrugated roofing sheet measured 52.4 fibres per millilitre. A later test on 14 April 1976 measured 53.1 upon a sheet "at least six months old" (PX 63). 59. Mr D J Hamilton, a scientific officer with the South Australian Health Commission in October 1979 reported that he had measured dust concentrations "in excess of 50 fibres per millilitre when using a grinding wheel" (PX 63). 60. A test conducted by Wunderlich on 17 November 1976 measured 90 fibres per millilitre in a 25 millimetre breathing zone (PX63). A cutting tool study for James Hardie was conducted by Mr P A King in February 1980, using a bench grinder on Super-Six corrugated sheet. This test resulted in the overloading of the filters in the dust counter and a conclusion that the concentration was approximately 20 fibres per millilitre. However, Mr King concluded that this number could be a gross underestimate of the fibres collected (PX 57). On the face of these results a tentative conclusion may be reached that possible exposure in the breathing zone of an operator cutting asbestos cement sheeting with a grinder is in the order of 50 to 100 fibres per millilitre. 61. In May 1981 Mr Papworth, the manager of the occupational hygiene services of the Australian Mineral Development Laboratories (AMDEL) carried out tests of airborne asbestos fibre generated by application of an impregnated power disk cutter upon asbestos sheeting. The filter used became grossly overloaded with dust, however by application of mathematics to a sampling of the filter a conclusion was reached that the airborne fibre was in concentration of 210 fibres per millilitre. 62. Some caution must, however, be exercised in relating the laboratory tests to site conditions. Mr King in the introduction to his report observed large variations between the work rates of operators in the laboratory and those rates measured in field studies. He found that the work rate in the tool room was often as high as 10 times that occurring on building sites. Further, there is a proven increase in the amount of asbestos containing dust with an increase in the age of the asbestos cement products. Some of the material in Mr King's tool room study was over 18 months old. The materials the subject of the AMDEL study were 10 to 20 years old. Old dry friable asbestos is quite unlike green asbestos. Mr Stewart the expert called for the plaintiff agreed that the age of the material tested may double the number of fibres released into the atmosphere (T 553.21). The 1996 United Kingdom Health and Safety Executive Notes on Working with Asbestos state that asbestos cement sheeting becomes dry and more brittle with age. Further, concentrations outdoors may be dispersed by local atmospheric conditions. 63. For these reasons a better guide to the concentration of asbestos fibre in the breathing zone of a worker cutting asbestos cement with an abrasive wheel is to be found in field studies of workers installing recently manufactured asbestos sheet. Rodelsperger et al measured fibres generated by workers installing asbestos cement roofs while cutting with an angle grinder upon 40 building sites in Germany (Estimation of Exposure to Asbestos-Cement Dust on Building Sites, K Rodelsperger et al, IARC Scientific Publication 30, AMACA 12). He found concentrations of more than 100 fibres per millilitre when the sample was taken within the dust cloud caused by the grinder, and as a mean value of nine measurements, 20 fibres per millilitre within the breathing zone of the operators, the highest reading within that zone being 41 fibres per millilitre. Rodelsperger found that the average cutting time of the workers so engaged was 5.7 per cent of working hours (about 30 minutes) and concluded that the TWA of cutting over one day was 1.2 fibre mls. He found background exposure to be 0.6 and a daily TWA of 1.6 fibre mls as an average of 61 roofers. 64. Two Australian field studies are consistent with peak concentrations of 22 and 53 fibre mls and TWA's of 0.7 and 1.3 respectively. 65. J Winter, an industrial hygiene engineer employed by James Hardie, in about May 1977 (AMACA 25) conducted a study of roofing workers on a factory complex of five separate small factories at Blacktown. The work was performed by a two-man roofing team over nine days installing Super-Six corrugated sheet. Full dust samples were taken of each man on each day he worked. Calculations from the samples (not themselves in evidence) revealed that the man who did most of the cutting generated a TWA over the period of 0.7 fibre mls ranging from dust free to 2.5 fibre mls. His assistant was exposed to a TWA of 0.3 fibre mls. The mean daily cutting time was nine minutes, with a range of 0 to 15 minutes. These observations imply a fibre concentration of 22 fibre mls during the nine minutes of cutting time. 66. Mr P A King, in February 1980 performed two field studies to test the relevance of his cutting room studies (PX 57). In one study he monitored the fibre burden of two men cutting and fixing Super-Six roofing panels upon a factory site at Blacktown over a five hour period. During that time one operator performed all the cutting with an angle grinder, placing each sheet in an elevator for lifting to the roof line, and installation by the other. The atmospheric conditions were described as "very hot and still with no perceptible breeze". The actual time spent cutting was 10 minutes and 32 linear metres were cut. (A concurrent study by Mr King at Silverwater is not useful as the ambient weather conditions adversely affected the fibre count). The TWA of the man cutting was found to be 1.3 fibre mls and that of the man fixing the sheets 0.2 fibre mls. These findings are consistent with a peak concentration of about 50 fibre mls while cutting. 67. Confidence in the reliability of these field studies is increased by their general accord. A worker while cutting Super-Six asbestos cement roof sheeting in the open air is probably exposed to a peak concentration of up to about 50 fibre mls depending on weather conditions and a TWA of somewhere between one and two fibre mls. 68. There are no comparable field studies relating to asbestos flat sheet. However, it would seem probable that the exposure would be similar and my conclusions are consistent with other published material. 69. A summary of German data (Hauptverband HVBG 1977), referred to in AMACA 22 page 5, indicates that for exposure in asbestos cement user industries, the upper range of peak exposure (the 90th percentile) during cutting asbestos cement with power saws and disks, is 60 to 100 fibre mls, and for long term daily exposure when handling, cutting, drilling and fixing, a TWA of 0.4 to 6.4 fibre mls. The probable mean may be recalculated (as by Mr Rogers PX 22) as 30 to 50 fibres per ml peak exposure and a TWA of 0.2 to 3 fibres per ml depending on the time cutting and air movement. A mid-point is 1.6 fibre per ml which figure I propose to apply to the outside cutting and fixing work performed by Mr Judd. 70. It is difficult to estimate the daily TWA for cutting within partially completed buildings. Assuming 5 metres of cutting at the rate of 32 metres in 10 minutes (consistent with the P A King study Blacktown) the time of cutting for cladding a bathroom or laundry is about two minutes. If the peak exposure during this time was 50 fibres per ml, the daily TWA for this activity is only 0.2 fibre mls. Some allowance must be made for the concentration of fibres during the slower decay of this concentration indoors and for those fibres produced by other activities such as handling, nailing, rasping and such. I have no formula by which I may calculate this rate of decay. Estimates of the 1996 UK Health and Safety Executive report are 15 to 25 fibre mls without exhaust ventilation throughout the cutting process. A partly constructed house has some ventilation through windows and door openings but again a concentration of 15-25 fibre mls is generated only during the repeated cutting processes. 71. In the circumstances and in the absence of better evidence I believe it reasonable to apply the upper limit of the Hauptsberger study, a TWA of 6.4 fibre mls generally for work with asbestos cement sheet indoors. Mr Judd's Exposure to Asbestos Apprenticeship 722 Mr Judd was born on 18 May 1940. He left school at the age of 14 and in about April 1955 became indentured to his father as an apprentice carpenter. Thereafter, until approximately November 1959, with the exception of three months' national service, he worked upon the construction, extension and renovation of cottages in the suburbs of Melbourne. Counsel for the plaintiff has submitted that during his apprenticeship the plaintiff worked cutting and fixing asbestos cement sheeting upon between 57.5 and 83.83 days. I find that upon the probabilities he was so engaged for 70 days, the mean of these figures, 40 days of which he worked in the open air and 30 days inside the partially completed shell of a house. I believe the plaintiff is given to exaggeration, however, I find that 40 per cent of this work involved the plaintiff using a power grinder to cut the asbestos cement sheeting. For present purposes the asbestos fibre generated by the use of fibro cutters on the other days is so slight as to be immaterial. Conclusion: 28 days outside cutting and fixing and 12 days inside cutting and fixing. Burwood Timbers 73. After his father's business became insolvent in about November 1959 Mr Judd found employment with Burwood Timber Mills, a joinery division of A V Jennings Pty Limited where he worked for nine to 12 months manufacturing prefabricated windows. For about one and a half hours each week he was engaged upon a task of cutting, rasping and fitting asbestos flat sheet to a particular window designed for laundries and bathrooms. Accepting that the asbestos concentration disperses less rapidly in an enclosed room than outdoors, I assign each day upon which such work was performed the same average concentration of fibre as would be appropriate to one whole day working outdoors with asbestos fibre. Conclusion: 48 days of exposure at a concentration equivalent to outside cutting and fixing. Hansen and Yuncken 74. Upon leaving Burwood Timbers Mr Judd worked as a music salesman for three to four months and then commenced work in 1961 as a carpenter with a firm known as Hansen and Yuncken. He remained with this firm for two years carrying out construction work on commercial premises. Mr Judd's first work in this employment was upon a factory for a printing firm at Moorabin. He worked on that site for three to six months. The first three weeks of this exposed him to the possibility of asbestos dust from the activities of roofers, cutting and fixing the corrugated sheets. In cross-examination he conceded that the cutting of the sheets was performed upon the top of that part of the roof already in place and that he was not permitted to work immediately below where the roofers work. I discount the relevance of this exposure. 75. Other work of Mr Judd at the Moorabin site involved installing internal door jambs and cladding various areas with Masonite. Flat asbestos sheets were used to line the canteen. Mr Judd used a power saw to cut the sheets and the work lining the canteen took one week. The remaining work for Hansen and Yuncken was construction of the Age building in Collins Street, Melbourne. This was a building of nine or 10 storeys constructed on an area of perhaps the size of three to four tennis courts. In this work Mr Judd was engaged in carpentry formwork for six to eight months. Asbestos cement sheets were used by him to line the edges of stairwells. The time spent on this task is unstated but it cannot have been significant and I have assumed one half of a day each week on each of 10 storeys, a total of five days. Conclusion: Five days indoor cutting and fixing, five days outdoor cutting and fixing. Ullin Engineering Pty Limited 76. Mr Judd's next job was with Ullin Engineering Pty Limited, an engineering firm that made aluminium windows. Mr Judd contended that his job was measuring and installing aluminium windows but that he spent the majority of his time on site working closely with carpenters as they fitted asbestos cement flat sheets. He says that he gave the carpenters a hand while they fitted the sheets. I discount this evidence as an improbable source of asbestos fibre inhalation in any great degree. Mr Gordon Stewart, an industrial hygienist qualified to support the claim regarded this standby exposure as insignificant. I agree. H N Keast and Son 77. The next employment of Mr Judd was with the builder H N Keast and Son with whom he spent three to four months upon the construction of the number three tile plant at the Whitelaw Monier factory at Springvale. Discounting the background exposure from the activities of others Mr Judd spent two days cutting and fixing the asbestos sheets as eaves to the factory. Further exposure occurred when he removed and replaced the asbestos cement sheets on the old plant washroom which work occupied five days. Conclusion: Two days outside cutting, five days inside cutting. Tom Whitelaw 78. Mr Judd was next employed by Mr Tom Whitelaw upon a contract installing eaves in multistorey units that had been built in the Heidelberg area for the Olympics. In his affidavit the plaintiff described this exposure thus, PX1 paragraph 39: For the first six months I cut and rasped asbestos cement flat sheets day in, day out, for five days a week, eight hours a day. I cut the sheets using a power saw. The bird boards had already been installed on the rafters. This meant that the sheets on the eaves did not sit in between but rather on top of the rafters and that as a result the sheets do not have to fit accurately. I cut the sheets down the centre, three to four at a time. The sheets were placed on two carpenter's stools. Alan or myself cut the sheets whilst the other one held them at the other end. Clouds of dust were released when the sheets were cut. The dust got into my mouth, in my hair and on my clothes. I breathed in the dust, whether I cut the sheets or held them at the other end. I cut holes in the sheets for stink pipes that came from the toilets. I punched out the holes, then rasped the edges clean. This created dust which I inhaled. After the sheets were cut I nailed down battens onto the sheets. I then fixed them to a rope and the tilers pulled them onto the roof and installed them. All I did all day was cut, punch and nail battens onto the sheets or hold sheets down whilst Alan cut them. By the end of the day I was covered in dust. It got in my mouth leaving a gritty taste. The dust got in my hair, on my clothes, on my hands and on my body. I often worked overtime to finish the eaves on a unit block. The material was stored in a large furniture van, which was towed to the different unit blocks. At the end of each day I placed all of the asbestos sheets and equipment on the furniture van to make sure it was secure. In the mornings I took out the sheets and equipment. The sheets had dust on them. The dust was released onto me when I handled and moved the sheets. This account was not challenged in cross-examination and I accept it in general, however I do not accept that the cutting was continuous. Conclusion: 130 days of intense exposure. Whitelaw Monier 79. At the conclusion of the work upon the eaves Mr Judd took up work running the carpentry shop at the Springvale Whitelaw Monier plant. The first eight weeks of this employment were occupied in the construction of an engineering workshop lined externally and internally with asbestos cement sheeting and roofed with corrugated asbestos cement sheeting. Assuming that the framing, flooring and joinery work occupied one half of the total time Mr Judd was exposed to 20 days of asbestos cement work, one-third of which was indoors. Conclusion: 13 days exposure outdoors, seven days indoors. 80. Thereafter Mr Judd was employed in maintenance for some 18 months during which he was exposed to asbestos cement dust during periods of a few hours to one day each week. Although thereafter Mr Judd remembered the term of this work as three years that recollection is inconsistent with other evidence. He was unable to continue in the employment beyond May 1966 when he was hospitalised for six weeks following serious injuries while playing football. Conclusion: 35 days outside cumulative exposure. Whitelaw Monier, Sales Representative 81. Upon his convalescence in 1966 Mr Judd took up work as a sales representative for Whitelaw Monier. I regard his evidence that he often spent an hour to an hour and a half helping carpenters install asbestos cement sheets as implausible and I reject it. No mention of this exposure was made in the first history given by Mr Judd to his attorneys nor to Dr Rosalion to whom he was referred by the attorneys and who questioned him in relation to his exposure. J C and E D Jensen 82. In 1971 Mr Judd left Monier and worked for J C and E D Jensen, builders, of Wangaratta as a carpenter upon the construction of new villas. He did this work for nine months. In his first instructions to his solicitors confirmed to Dr Rosalion, Mr Judd stated that "There was some exposure to asbestos sheeting but only for approximately one to two months". In cross-examination Mr Judd said that it would take four to five months to build a brick veneer home and that the cutting and fixing of the eaves would have occupied perhaps two-thirds of a day to a day and a half, the gable ends a bit longer. The sheeting in the laundry and bathroom would occupy perhaps two days. Allowing two houses in the nine month period, outside cutting and fixing would occupy perhaps six days, and inside cutting four days, that is two working weeks. I propose to allow one month of four weeks. Conclusion: 12 days outside cutting, eight days inside cutting. Subsequent Exposure 83. After leaving Jensen until 1985 Mr Judd worked as a sales representative in the building trades. I reject his evidence that he assisted carpenters with their work other than upon trivial occasions such as passing a tool or holding a flat sheet for a moment. 84. In 1985 Mr Judd resigned from his sales job with Stegbar Windows and moved to Mansfield in country Victoria. From this time his exposure to asbestos cement sheeting appears to have been minimal. Probable Fibre Burdens 85. Applying the probable concentrations of fibre to Mr Judd's activities his cumulative burden of asbestos fibre may be calculated as follows. Apprenticeship: 16 days at 1.2 fibres per ml ......................................................................…….. 0.08 12 days at 6.4 fibres per ml ......................................................................…….. 0.32 Burwood Timbers: 48 days at 1.2 fibres per ml ........................................................................……. 0.24 Hansen and Yuncken: 10 days at 1.2 fibres per ml ...........................................................................….. 0.05 H M Keast: 2 days at 1.2 fibres per ml ..............................................................................… 0.01 5 days at 2.4 fibres per ml .............................................................................…. 0.05 (I have allowed increased concentration because part of this work involved demolition of old fibro) Tom Whitelaw: 130 days at 6.4 fibres per ml ............................................................................ 3.46 (Because of the intensity described I have applied the ninetieth percentile of the Hauptverband study. The plaintiff's expert Mr Stewart applies 5 to 8 fibre mls.) Whitelaw Monier Construction 13 days at 1.2 fibres per ml……………………………………………………… 0.06 7 days at 6.4 fibres per ml……………………………………………………… 0.19 Whitelaw Monier, Maintenance: 46 days at 1.2 fibres per ml ........................................................................…. 0.23 H D Jensen 12 days at 1.2 fibres per ml .............................................................................. 0.06 8 days at 6.4 fibres per ml ............................................................................... 0.22 Total..............................................................................................4.97 fibre ml years. The Expert Evidence as to Cumulative Exposure 86. I have found the experts called in this case of little assistance in assessing Mr Judd's probable cumulative exposure to asbestos fibre. Mr Kottek 87. Mr Kottek prepared a report in which he concluded that Mr Judd's cumulative exposure was 38 fibre ml years. It is instructive to consider some of the steps by which he reached that conclusion. 88. Mr Kottek opined that upon those days on which the plaintiff installed Super-Six roofing he was exposed to a TWA of 10 to 20 fibre mls. It appears that he was probably aware of the field studies of Mr King and he was certainly aware of the studies by Rodelsperger. Neither study could justify a TWA greater than 1.6. 89. He was not taken in cross-examination to Mr King's study. Mr Kottek said he rejected the Rodelsperger study because it did not factor in the additional background exposure after cutting. This assertion is false. At p 851 of the published study Rodelsperger writes From the standardised histories of the first 61 roofers, the frequency of handling asbestos products and of using the grinding machine was estimated for present as well as for prior working places. From the results of dust measurements and histories, cumulative doses of 0.3 years mg/cc asbestos fine dust and 1.6 years(sic) fibres/ml were calculated. I find Mr Kottek's reasons for rejecting the Rodelsperger study unconvincing.. 90. Mr Kottek asserted that in forming his opinion he relied upon a 1974 publication from the United Kingdom Health and Safety Executive (AMACA14). This publication recorded that machine sawing of asbestos cement sheet without effective ventilation indoors created a concentration of 10 to 20 fibres per ml. That measure is obviously relevant to levels in and around the cutting operation carried out indoors. Mr Kottek said in evidence that the atmospheric concentration of asbestos fibres falls to zero within five minutes of cutting outdoors. His selection of the range 10 to 20 fibre mls as the TWA for the whole of the time spent by Mr Judd installing Super-Six roofing, even if he did all the cutting, is indefensible. It represents a multiple of between 7 and 15 of the TWA's found in studies with which he was familiar but which he ignored and substitutes a figure which he must have known was wholly inappropriate. 91. A similar bias is apparent in Mr Kottek's opinion concerning asbestos cutting indoors. Mr Kottek estimates the intensity of that exposure to be between 10 and 100 fibre mls as a daily TWA although active cutting operations occupied a fraction of the day. The disparity between his upper limit of 100 fibre mls as a TWA for a whole day and the figure of 25 fibre mls, the upper limit in the United Kingdom document with which he was familiar, may have suggested caution to a wholly independent expert. 92. The plaintiff's counsel place much emphasis upon Mr Kottek's assertion that because 12 per cent of paid asbestos claims recorded by the New South Wales Dust Diseases Board are for carpenters it is most improbable that the long term exposure for carpenters working solely on asbestos sheeting is around 1 fibre ml per year. PX27 is a report of the Dust Diseases Board published in October 2000. It records that of 76 persons compensated for asbestosis in the year 1999 12 were carpenters. Records of the histories of the 14 men currently receiving payments from the Dust Diseases Board for asbestosis who are categorised as carpenters are in evidence (PX104). Discounting those cases of carpenters who also worked as shipwrights, as labourers in the asbestos works of James Hardie or Wunderlich, in the company of laggers, or with other atypical exposure (in one case three years only), six cases remain with an average of 31 years of exposure. 93. Between 1945 and 1954 more than 70,000 houses were built using asbestos cement cladding in New South Wales (PX27). Exposure to 25 fibre ml years of asbestos equates with a 1 per cent chance of contracting asbestosis. The risk of contracting asbestosis has been assessed in one study as between 7 per cent and 26 per cent after 50 years at 2 fibre mls, that is, with a cumulative exposure of 100 fibre ml years (G Berry et al, British Journal of Industrial Medicine 1979 36, 98-112 referred to by Mr Hamilton in PX63). The TWA exposures calculated by field studies of Rodelsperger (1.6 ml) and Winter (0.7), King (1.3) and Hauptverband (1.6) are entirely consistent with a very small number of carpenters contracting asbestosis after a lifetime in the industry. 94. The Dust Diseases Board's statistics give further cause to reject Mr Kottek's opinion. If roofers and persons cladding houses with asbestos cement sheeting were exposed to a daily TWA of 15 fibres per ml as Mr Kottek suggests then 1 per cent of men so employed would contract asbestosis within two years of entering the trade and after seven years between 6 and 26 per cent would be asbestotics. The experience of the Dust Diseases Board runs counter to such a suggestion. 95. I accept that Mr Kottek himself performed test chamber experiments in 1998 or 1999. However, the results are not useful because no attempt was made to correlate the test results with outdoor field conditions. Such a task was undertaken by Mr King who found the correlation between his test chamber results and actual field results was poor. 96. Assignment of TWA's requires some measurement or informed assessment of the periods during the working day in which peak exposures occur. Because Mr Kottek has no experience either in the building trade or in field measurement, he was unable to make any useful contribution to the question at hand. Mr Gordon Stewart 97. Mr Gordon Stewart in a report of 3 September 2002 concluded that the plaintiff had a cumulative exposure of between 30 and 60 fibre ml years and in a further report of 21 November 2002 (PX61), a cumulative exposure of between 25 and 49 fibre ml years. Again it is useful to examine some of the steps by which his calculations reached these figures. 98. Mr Stewart in his report of 21 November 2002 included a cumulative exposure of 0.15 to 0.3 fibre ml years in respect of that 1 per cent of Mr Judd's work time during his apprenticeship while rasping asbestos cement sheets. He assumed an exposure of 4 to 8 fibre mls as a TWA over 8.4 complete days and added this to other exposures in his calculations. When asked to justify the explanation of 4 to 8 fibre ml years in respect of this activity Mr Stewart asserted that "It's not guesswork, it's estimations based on my knowledge of these processes" (T 520.5). Mr Stewart had already spoken of his reliance upon the United Kingdom Department of Employment document estimating hand sawing to generate 2 to 4 fibre mls, and said that "hand sawing and rasping" would generate a peak concentration in the atmosphere "in the range of 2 fibres per millilitre" (T 519.11). Mr Stewart agreed that the correct measure of fibre exposure is a time weighted average across the peak concentrations (T 518.34). In the light of this evidence, his attempt to justify 4 to 8 fibre mls as a TWA upon his "experience" can only be seen as unconvincing. 99. Further, when closely questioned it became apparent that Mr Stewart had already allowed for the time spent rasping in his estimate of 0.7 to 1.7 fibre ml years for all other activities excluding power cutting (PX61 page 2, T 519.22). He included the fibre burden from rasping yet again in his cumulative exposure in work fixing eaves (PX61 page 2). 100. Mr Stewart has conducted no field study in which he has measured the time spent by carpenters upon various activities. He is unqualified by measurements or experience in the industry to make any assessment. His single occasion of measuring asbestos in an atmosphere occurred 28 years ago. He has exaggerated the time spent by the plaintiff upon various tasks by up to tenfold. He has applied daily TWA's higher than the peak range of emissions from a given task. His assumptions as to the peak loadings of fibre and the daily averages of persons engaged upon cutting asbestos fibres are informed only by the one AMDEL study commissioned by him, and carried out on material 10 to 20 years old. I was not assisted by his calculations. Mr Alan Rogers 101. Mr Rogers was called for the defendant. I was assisted by his review of published literature but not by his estimation of the plaintiff's cumulative exposure. Mr Rogers is of the opinion that the daily TWA of workers cutting, handling and fixing asbestos cement products is around 1.2 fibre ml years or less. He assumed that the plaintiff was employed as a carpenter for 27 years and that he was exposed to asbestos dust for 10 per cent of each working day. He then made the following calculations: 1.2 fibre mls x 27 years x 10/100 = 3.24 fibre ml years. 102. This method is objectionable for several reasons. Mr Rogers makes no attempt to apply his expertise as to dust counts generally to the plaintiff's particular and individual industrial history. He offers no basis upon which he may conclude that the plaintiff, when he worked with asbestos, did so for only 10 per cent of the working day. Mr Rogers discounts by 90 per cent a TWA appropriate to a whole day, upon which some time only is spent in cutting. He makes no attempt to asses the mean concentration for the time spent working with asbestos and then average that mean over a whole day. For instance, if the plaintiff spent 10 per cent of his time cutting (48 minutes) when employed by Tom Whitelaw at a peak exposure of 50 fibre mls, his TWA on that account alone would amount to 5 fibre mls, not 1.2 following Mr Rogers' method. 103. At p3 of his report of 27 October 2002 Mr Rogers says this: Other short term peak exposure values of 20 fibres/ml are reported from German studies (Rodelsperger et al, Estimation of Exposure to asbestos -cement dust on Building sites, Biological Effects of Mineral Fibres, IARC Scientific Publication 30, 845-853, 1980). Australian studies indicate short term peak levels whilst using dry power disc cutting of around 20+ fibres/ml (James Hardie, Asbestos Cement Cutting Tool Study, February 1980). These assertions are misleading. Rodelsperger reported fibre concentrations of more than 100 fibre mls within the dust cloud caused by the grinding wheel and up to 41 fibre mls close to the head of the operator with a mean value of 9 measurements as 20 fibre mls. Mr King in the James Hardie Cutting Tool Study reported that " The estimates of the fibre counts for the test . . .could be grossly underestimating the fibres collected in the filters ." 104. I do not accept that Mr Rogers fairly summarises the findings of these two studies nor do I have any confidence in his conclusion that Mr Judd's cumulative exposure was "3.24 fibre ml years or less". The Plaintiff's Cumulative Risks Smoking 105. Mr Judd was a heavy smoker between 1956 to 1998. In consequence his relative risk of contracting lung cancer, compared to a life-long non-smoker, was at least RR20 (Prof Berry, AMACA 11, Dr Leigh, PX14). Professor Henderson in a report of 3 December 2002 relying upon a paper by Simonato et al (PX 69), has argued that the relative risk of Mr Judd contracting lung cancer as a result of his smoking history was in the range of 5.5 - 8.0 because the relative risk of smoking found in Simonato's study was substantially greater for squamous and small cell carcinoma than for adenocarcinoma which is that which afflicts Mr Judd. 106. Because Simonato's conclusions did not fit with the Italian data and because no similar study has been conducted in Australia, I am presently unpersuaded that I should apply to the plaintiff's smoking a relative risk other than 20. This was a figure agreed by Dr Leigh and Professor Berry. It is a figure lower than the estimate of 25 assigned by Professor Henderson in his earlier report of 20 August 2002. Asbestos 107. The plaintiff's cumulative exposure to asbestos may be rounded up to 5 fibre ml years. Accepting that that relative risk of contracting lung cancer doubles at 50 fibre ml years then the relative risk due to Mr Judd's exposure may be assessed as: 1 + 5/50 = RR1.1 (following Professor Berry AMACA 11). 108. The combined effect of asbestos exposure and smoking on the lung cancer risk has been observed as approximately multiplicative, that is there is an effect additional to the sum of the several risks due to the combination of the risks. The overall relative risk of Mr Judd contracting lung cancer is then: RR20 x RR1.1 = RR22. If the risks were additive his overall risk would be RR20 + RR1.1 = RR21.1. Upon relatively low risks the multiplicative effect of synergy is not great. 109. This information is most easily understood when reduced to tabular form. (following modification of part AMACA 11, formerly MFI 4). Thus if the background incidence of unattributable lung cancers is 100 in a given population, then in a given period: Cause of cancer Number of cancers Percentage Background (unattributable) 100 4.5% Additional cancers attributable to asbestos alone (RR1.1) 10 0.5% Additional cancers attributable to smoking alone (RR20) 1900 86.4%