Ellis, Executor of the Estate of Paul Steven Cotton (Dec) v The State of South Australia & Ors [2006] WASC 270

Ellis, Executor of the Estate of Paul Steven Cotton (Dec) v The State of South Australia & Ors [2006] WASC 270 - WASC 2006 case summary — Zoe

[187]

"He told me that a routine chest X-ray taken because of his work at Millennium Chemicals in Bunbury on the 28th April was abnormal, showing a mass in the right upper lobe. He was referred by Dr Minchin to the Sir Charles Gairdner Hospital for investigation. CT of his chest on 12 May 2000 confirmed a mass with extensive mediastinal lymphadenopathy in addition to extensive abdominal lymphadenopathy. Fine needle aspiration of the right upper lobe mass on the 16th May 2000 under CT guidance revealed non small cell carcinoma with features of squamous cell carcinoma. A bone scan on the 11th May showed no evidence of metastases. He has commenced on chemotherapy with Gemcitabine and Cisplatinum for Stage 4 non small cell bronchiogenic carcinoma on 22nd May 2000.

In the past he has been found to be suffering from hepatic cirrhosis due to hepatitis C on liver biopsy in November 1999. This was attributed to a blood transfusion given to his mother before he was born. He has also suffered from arthritis in his right wrist since a fracture of his scaphoid at the age of 17. He had a lipoma removed from his thigh in January 2000.

He said that he smoked about 15 cigarettes a day from the age of 16 to 43 years, stopping two months ago when he became unwell.

His mother died at the age of 68 from cirrhosis and hepato-cellular carcinoma. His father died at the age of 51 from bowel cancer. He has a sister and a brother in their early fifties who are well. He has daughters aged 15, 13, 11 and 4 who are all well ... He says he can still keep up with others of his own age when walking and still plays basketball with his children. His weight has been steady. He usually has a cough productive of about a quarter of a cup of white sputum. There has been no haemoptysis. He had some pains across the front of his chest prior to commencing on chemotherapy here recently but these have improved.

On examination he appeared heavily built. His pulse was 80 per minute and regular and blood pressure 120/70 mm Hg. His heart sounded normal. There was no lymphadenopathy or clubbing. His chest sounded clear.

His FEV1/FVC today was 3.9/5.3 litres (predicted 4.1/5.0).

... His prognosis for survival is about three to six months."

[215]

72 The evidence of Mr M H Kottek (t/s 733) was to the effect that, from his studies and experience, asbestos cement water pipes from the 1970's era almost always contained a mixture of Amosite and Chrysotile. The report of Dr de Klerk (Exhibit 74(1)) in par 5 stated that the type of asbestos in the pipes is likely to have been a mixed type and, at t/s 758, Dr de Klerk explained that the pipes probably contained Amosite and Chrysotile and probably a little bit of Crocidolite as well. Mrs Sowden, in cross-examination at t/s 1110, said that to the best of her knowledge Hardie's asbestos cement types of that era always contained Amosite and Chrysotile and said further, at t/s 1112, that she had assumed that the asbestos content would have been about 15 per cent and that this was typical - 10 - 15 per cent asbestos was a typical concentration of the asbestos in AC types and that she knew that James Hardie pipes in the late 1970's contained Amosite and Chrysotile. Again, at t/s 1121, Mrs Sowden said that she did not think that it was possible that the James Hardie pipes contained only Chrysotile and that she thought they always contained amphibole as well. Exhibit 157 indicates that the asbestos fibre content of these pipes is in the range of between 13.42 per cent and 14.92 per cent pure asbestos but the origins and original purpose of that document were never clearly established. At t/s 1287, in the course of cross-examination of Mr G Pickford, the witness said that the asbestos cement content of the water pipes consisted of between 8 per cent and 15 per cent of asbestos fibres. Mr Pickford doubted that any of the asbestos pipes contained Crocidolite which was known to be about five or ten times dustier in terms of airborne asbestos fibre generation than plain Chrysotile - t/s 1293. Finally, in Exhibit 94, a safety memorandum issued by the first defendant on 7 August 1979, stated that the asbestos cement types which the first defendant produced contained less than 20 per cent asbestos fibre.

[217]

74 As early as 1968 Dr McCullagh, the medical officer for James Hardie & Coy Pty Ltd, wrote to the manager of the second defendant in Adelaide enclosing a copy of the report which he had prepared following a visit to Canada, the United Kingdom and Germany to study the biological effects of asbestos (Exhibit 120). That report recognised the possibility that Chrysotile was causative of mesothelioma which was then under investigation and that lung cancer attributable to asbestos exposure may occur in the absence of asbestosis. It also recorded demonstrations that cigarette smoking greatly increased the likelihood of lung cancer in the asbestos exposed. In a report written in 1965 the same Dr McCullagh summarised the biological effects of asbestosis, following an examination of the annals of the New York Academy of Sciences of 1965. In that document he recorded that asbestos fibres produced in Australia were Crocidolites from Western Australia and a little Chrysotile from New South Wales. Chrysotile was used in asbestos cement and other products and Crocidolite was also used to make asbestos cement (page 1). At par 25 he noted that Amosite and Crocidolite were then held to be the most dangerous asbestos forms of carcinogens but it was doubtful whether Chrysotile alone was a carcinogen but that, in combination with smoking, Chrysotile may more readily cause cancer. Furthermore, in a confidential inter-house memorandum of James Hardie of 24 January 1968, Dr McCullagh drew attention to then recently published figures suggesting a greatly increased risk of fatal lung cancer from the combination of exposure to asbestos dust and cigarette smoking - a combination said to increase the risk of dying from lung cancer by a factor of some 90 times (Exhibit 139). As stated, Chrysotile is sometimes referred to as white asbestos, Amosite is brown or grey asbestos and Crocidolite is blue asbestos. This is the nomenclature adopted by Matprolabs in its survey for the third defendant of the presence of asbestos in the BDR shed at the SCM Bunbury plant in March 1990 (Exhibit 44).

[241]

"[64] Asbestos related diseases may be divided between the malignant and the non-malignant. Non-malignant conditions, such as asbestosis and pleural thickening, are the result of a cumulative exposure to asbestos. Where a claimant with such a condition has been exposed to asbestos by more than one employer, liability is divided between each employer and the employee has a separate claim against each employer for its share of the loss. In respect of these divisible diseases, no claims for contribution between employers can arise.

[65] In contrast, malignant diseases, such as mesothelioma and lung cancer, may result from a single exposure to asbestos. In the present state of scientific knowledge, it is impossible for a claimant to establish which of a number of employers is responsible for the exposure which caused the disease. In these circumstances, the House of Lords held in Fairchild v Glenhaven Funeral Service Ltd [2002] UKHL 22; [2003] 1 AC 32 that, rather than the claim failing due to an inability to prove causation against any particular employer, the claimant was entitled to claim damages against all or any of the employers who had exposed him to asbestos, and had materially increased the risk of contracting the disease. Until the decision of the House of Lords in Barker v Corus (UK) Ltd [2006] UKHL 20; [2006] 2 WLR 1027, it was widely thought, and the Court of Appeal in that case held, that the employee could obtain judgment for the full amount of his damages against any of the employers, who would then be entitled to make contribution claims against the other employers. The House of Lords reversed the decision of the Court of Appeal and held that the liability to pay damages to the claimant must be apportioned among the employers. There will not accordingly be contribution claims between employers where each employer has exposed an employee to asbestos if the exposure occurred on different occasions or over different periods of time. There remain circumstances in which contribution claims may be made, for example where T & N and another person are liable in respect of the same period or incident of exposure to asbestos. An example would be the case in which T & N failed to provide adequate safety equipment to an employee who was working on the premises of another person who in turn failed to provide a safe work place or who was liable as occupier of a premises ... "

[243]

92 Having regard to the evidence which is later examined in these reasons, I have reached the view that considerable care and reserve should be exercised before identifying a particular case of lung cancer, alleged to be due to asbestos exposure as being within the category of indivisible disease, despite the prevalence of the application of that distinction in the authorities. The principal reason for my view in this regard is the incomplete state of medical scientific knowledge about the details of the process of carcinogenesis in many types of asbestos related cancer. If the expert scientists and researchers are unable to explain how a particular cancer, or a particular type of cancer, resulted from asbestos exposure or from exposure to other carcinogens occurring simultaneously, it is very difficult to see how it can be established satisfactorily that that particular cancer had a single indivisible cause. However, so much depends upon the nature and circumstances of the individual disease and its presentation by the particular patient. In the case of mesothelioma where the tumour can be linked unequivocally solely to the effect of asbestos it may well be possible to establish that the disease was caused by one identifiable episode or period of exposure and, in such a case, the attribution of the description of indivisible disease would be justified. However, in other cases where the probable cause of the tumour is the cumulative effect of asbestos exposure, whether alone or in combination with other carcinogens, over time and where the preponderance of medical opinion is that it is the combined effect of those carcinogens working together over time which has initiated the incompletely understood mechanism of carcinogenesis, then it does not seem to me that that disease can properly be described as indivisible and that any breaches of duty by employers or others which constitute or contribute to the noxious effects of that exposure over the periods when it is probable that the cumulative process was occurring are each liable for the damages which result from the development of that disease. Quite possibly there may be complicated questions of contribution as between the parties whose conduct has led to the exposure of the claimant to such carcinogens during the formative process of the tumour but no claims for contribution are being made in the present proceedings and it is therefore unnecessary, and perhaps undesirable, to attempt to address such issues in the abstract. It is enough, in the present case, to conclude that I am satisfied that Mr Cotton's fatal lung tumour should not be categorised as an indivisible disease and that whether it resulted from the effects of exposure to asbestos alone, to his tobacco use alone, or to a combination of the effects of both those carcinogens it is almost certainly the result of the cumulative effect of one or more of those carcinogens operating over an extended period of exposure.

[247]

95 Generally speaking, the pipes would be laid in trenches which had been cut in the ground and this would require the lengths of pipe to be fitted, one to another and on occasions cut to fit in appropriate lengths, to follow the route of the pipeline and also to be cut where joins or turns in the line were required - whether involving "T" joins, angle turns or more complicated joins or turns. When the pipe had to be cut for any of these purposes it would usually be cut by a special chain disc cutter which would be fitted over the pipe and progressively tightened until it cut into the pipe sufficiently for the application of force, by a mallet or hammer, to break the pipe at the cutting (see illustrations on p 7 of Exhibit 41). Occasionally the pipe would be cut by other methods such as by a power-driven saw (Exhibit 41, illustration p 5) or by a hacksaw or bushman's saw (Exhibit 41, illustration p 6). Once cut by any of these methods it would be necessary for the newly cut end of the pipe to be bevelled off for later fitting and this was usually done by a manual rasp or file (see Exhibit 41, illustration p 9). Cutting the pipe to create a hole for connection to another pipe could be done by either using a mechanical hole saw or by hole cutting with drilling and rasping (Exhibit 41, illustrations at pp 10 and 11). To varying degrees, these processes involved the release of fragments, fibres and/or dust from the pipe which was being worked upon. On the evidence it was suggested, and I have inferred, that these processes not only released visible fragments and dust which found their way onto the workmen's clothes, hands and arms but also gave rise to smaller airborne particles which were likely to be inspired by the workmen performing these tasks, or working nearby through the ordinary processes of respiration. Just how much and how often inspiration of airborne particles of cement asbestos pipe would occur from these processes was controversial in the case, but I am satisfied that, inevitably, it occurred to some degree.

[323]

145 In his answer (response 10) to interrogatories delivered by the second defendant (Exhibit 3(D)), Mr Cotton described his duties at Millennium Inorganic Chemicals from 1990 onwards, distinguishing between the period before 1993 when he worked as a full-time casual employee and the following period when he worked as a permanent process operator or shift worker, but stating the work which he did under each classification was the same; namely, to bag the TiO2 pigment, sweep the floor, drive forklifts, make up the chemicals and clean up in the BDR, including cleaning the band drier machine inside and out. He said that in the BDR his job involved sweeping, removing debris from the floor and cleaning trays on the band drier conveyor belt, to access which he had to move the doors or hatches which were lagged with asbestos in bad state of repair. He explained that when he was required to sweep up the BDR floor there were fragments of the lagging from the hatch doors and also from insulation on the pipes. He asserted that the lagging on the band drier and associated pipe work remained until it was removed in about 1995 and that his exposure to asbestos occurred from his regular work in the BDR. He added that he believed that in about the early 1990's he was also exposed to asbestos when contractors were engaged to remove asbestos cement roof sheeting from the building in which he worked and he recalled visible dust from the roof sheeting removal. Next, in response 11 to the same interrogatories, he said that he believed that most of his exposure occurred in the BDR, an area in which he worked regularly throughout his employment and that this regular and frequent exposure in the BDR continued until the asbestos had been removed, according to his recollection not before 1995. He asserted that he had spent four to five hours pulling trays from the band drier or doing BDR work some three times per week, although on other occasions he may only have been engaged in the BDR once a month. He also asserted that his exposure to asbestos from the removal of asbestos roof sheeting took place some time in the early 1990's.

[430]

217 Further descriptions of the presence of asbestos at the Australind worksite was provided by Mr Paul Galen Foley in two statements - Exhibits 238(1) and (2). Mr Foley is an occupational hygienist, with qualifications in physics from WAIT (now Curtin University) and from Sydney University. He was employed with Matprolabs since 1988 and has a long experience in advising governments in relation to occupational health and safety with particular reference to the control of chemical, physical and biological hazards in the workplace. He examined the Matprolab's reports of March and August 1990 (Exhibits 44/45 and 113) and also attended at the SMC works at Australind on several occasions to observe the air monitoring work then being conducted. He explained how air monitoring was conducted at SCM Australind on roughly a monthly basis from about September 1989 until about July 1991, collecting about 20 samples across the site per month. Air sampling devices (utilising the membrane filter method) were positioned around the site, their contents later collected and processed by Matprolabs by a properly certified analyst. That led to Matprolabs being commissioned to identify areas which were found and identified as containing asbestos. Mr Ligman was made aware that there were concerns about asbestos in the BDR. There were various pipes in that area. He visited the BDR and examined the situation and found that the lagging was made either of pre-cast plaster or fibreglass, covered with a non-asbestos calico wrap and then sealed with paint. The pre-cast plaster lagging was found to contain asbestos and this was also known as calcium silicate block. He confirmed that the presence of asbestos in the pre-cast plaster lagging was quite extensive. Mr Foley said that on the occasion of his four or five visits to the BDR between 1990 and 1997 he did not see chunks of lagging on the floor and his recollection is that the damage to the cloth surrounding the lagging in the BDR was isolated and not extensive.

[435]

222 The Matprolab's reports, Exhibit 44 - 45 and Exhibit 113 (in its abbreviated form), tend to concentrate on the BDR and the packing areas where Mr Cotton was known to have worked from time to time, but it is clear that the extent of asbestos within the plant and the programme for its removal were, respectively, much more extensive and longer than these documents alone, the testimony of Mr Turk and many of the submissions for the third defendant, suggest. The only episode of complete sealing off and isolation of all employees during the asbestos removal programme appears to have been during the removal of the asbestos cladding from the pipes in the BDR. The evidence as to when this occurred is not precise but it seems to have been carried out in at least two stages, the first in about November 1991 and the second in about March 1992 on each occasion for several days at a time. During those two episodes the BDR was completely sealed off, isolated and protected by a process of depressurisation while only KBE Contractors wearing special protective clothing carried out the operations inside. The work was done according to then prevailing standards and the material was gathered up inside the BDR, put into containers which were later sealed and taken away under supervised conditions. No employees of the third defendant, nor in particular Mr Cotton, were within the building during these operations. Nevertheless, these necessary and extensive precautions were only in force during the actual removal of the asbestos lagging from the pipes. The operation was preceded by a process of sweeping clean the floors and fittings within the BDR and this was done by the third defendant's personnel before the precautions which I have described were in operation. It must follow, and I find indeed it is probable that, during this period any asbestos dust or fragments which had been deposited on the floor or other surfaces within the BDR, along with large quantities of TiO2 powder would have been swept up in a very dusty atmosphere and would have been circulating in the air that the men breathed.

[668]

Mr Cotton's occupational exposure to asbestos in Adelaide and at Australind is capable of causing his lung cancer but it is more likely that he inhaled more Amosite asbestos in the BDR room in the third defendant's employment than from sawing asbestos cement pipes in South Australia.
Amosite has a higher carcinogenic potential than Chrysotile which is more often used in asbestos cement pipes. As exposure is a combination of this potential, intensity and duration, his exposure in the BDR at Australind was to Amosite which is likely to have been a greater and longer exposure than in South Australia.
All the asbestos minerals (Chrysotile and the amphiboles) may cause asbestosis, lung cancer and benign pleural diseases but only the amphiboles appear to be related to the production of malignant mesothelioma ... All types of asbestos appear capable of causing lung cancer and all histological types of lung cancer are increased in incidence in asbestos-exposed individuals.
The amount of airborne asbestos fibre inhaled and the duration of exposure make independent contributions to the risk of development of lung cancer. Smoking greatly increases that risk. If the relative risk of developing cancer for members of the general population is expressed as 1, then that of smokers is up to 10 times as great. Exposure to asbestos alone over many years in the absence of smoking might marginally increase the relative risk, but where such asbestos exposure is combined with cigarette smoking, the risk could be extraordinarily changed so that the relative risk of the combined exposure may approach 100 times that in the general population. The exact relationship is uncertain but is certainly far greater than merely an additive risk.
Although a level of exposure below which an increased risk of lung cancer would not occur is not known, it is known that exposure sufficient to cause asbestosis increases the risk of lung cancer. According to the Helsinki Criteria established by the International Expert Meeting on Asbestos, Asbestosis and Cancer in 1997, four histological types (squamous, adeno, large cell and small cell carcinoma) can be related to asbestos. The histological type of 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. In some circumstances of extremely high asbestos exposure, a 2 fold risk of lung cancer can be achieved with exposure of less than 1 year.

[670]

"Yes, the inhalation of asbestos fibres such as amosite increased the risk of lung cancer developing in Mr Cotton. The relative risk of lung cancer is estimated to increase 0.5 - 4% for each fibre per cubic centimetre per year (fibre years) of cumulative exposure. A cumulative exposure of 25 fibre years is estimated to increase the risk of lung cancer 2 fold. Clinical cases of asbestosis may occur at comparable cumulative exposures. 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. Heavy exposure, in the absence of radiologically diagnosed asbestosis, is sufficient to increase the risk of lung cancer. Cumulative exposures below 25 fibre ml years also are associated with an increased risk of lung cancer, but to a lesser extent. The presence of asbestosis is an indicator of high exposure. Results of air monitoring of such processes reported in the book 'Engineering Aspects of Asbestos Dust Control' by Rajhans (1982) [show] Mr Cotton's work with cement pipes in South Australia could have exposed him to 5 - 15 airborne respirable asbestos fibres per cubic centimetre and his exposure in the band drier room in Millennium Chemicals could be up to 10 fibres per cubic centimetre. Based on 10 fibre/cc and 8 years exposure, the cumulative exposure for Mr Cotton would be 80 fibre years. The relative risk increase would be 40% - 320%.

Mr Cotton was exposed to asbestos 25 years ago in 1975 when he worked with asbestos pipes in South Australia and later in 1990 which is about 10 years ago to friable asbestos cladding during his work in the band drier of Millennium Chemicals. His lag time from first exposure to development of lung cancer is 25 years and therefore is more than the minimum lag time of 10 years required to attribute the lung cancer to asbestos in the Helsinki Criteria. The New Zealand Report of the Asbestos Advisory Committee to the Minister of Labour 1991 states that the relative risk of smoking and cancer combined is 8.2 - 52.2."

[673]

349 Professor Wan was cross-examined about his assumption that Mr Cotton's asbestos exposure while working on cement pipes in South Australia could have involved up to 10 fibres/ml and his reliance upon the work by Rajhans (supra) for that conclusion. The relevant passages in the work by Rajhans and Bragg were tendered (Exhibit 59) which, at 68 and following, describe the dust emissions when working with asbestos in mining or milling, including scraping and shovelling. At 84 of that same exhibit there is a table describing typical exposures to be expected in normal machine operations, including hand sawing, machine sawing with a jigsaw or circular saw. The typical exposures for hand sawing were 2 - 4 fibres/ml, for machine sawing with a jigsaw 2 - 10 fibres/ml and for machine sawing with a circular saw 10 - 20 fibre/mls. It was therefore suggested to Professor Wan that his assumption of 10 fibre/mls exposure constantly during the cement laying processes in Adelaide may be an overestimate and, in my view, there is some force in that suggestion. However, Professor Wan was disinclined to place great reliance on precise numerical estimates of the extent of fibre exposure, no doubt recognising the great limitations of such attempts, and also because of his earlier statement that any such respirations are likely to be accompanied, to a great extent, by sub-microscopic fibres which cannot be measured by current methods. In a supplementary exhibit (59(2)), being a further extract from Rajhans and Bragg at 88 and 89, there is a discussion about asbestos exposure in houses, offices and other buildings. The authors made reference to a work which measured asbestos dust concentrations in a group of storehouses insulated with sprayed Crocidolite and Amosite. Those results showed the range of concentrations varying from 0.26 - 11.89 fibres/cc. They concluded that the concentrations of Crocidolite and Amosite dust that may occur when unsealed sprayed insulation of fallen asbestos debris is disturbed are likely to be in excess of the threshold levels. This is especially so for Crocidolite if the threshold level is to be held below 0.2 fibres/cc.

[695]

"Relative risk

It is impossible to state the cause of a condition, such as lung cancer, in an individual with certainty. This is because there are a variety of possible causes, and also cases for which no particular cause is known. For example cases occur in life-long non-smokers who have not been exposed to dusts or fibres; these cases are sometimes referred to as background cases. However, from epidemiological studies that have been conducted on groups of people, and analysed using statistical methods, it is possible to obtain information on the risk of exposures to various agents.

Risk is usually expressed in terms of the measure relative risk (RR). This is defined as The ratio of the risk of disease or death among the exposed to the risk among the unexposed. As an example it has been estimated that the relative risk in smokers compared with non-smokers is 15. Another example is that the relative risk of lung cancer due to asbestos exposure in a particular factory in London was estimated as 3. These are both average values and further analysis shows that the relative risk due to smoking depends on the amount smoked, and that due to asbestos exposure on the extent and intensity of that exposure. That is, for an agent that increases the cancer risk, higher exposures increase the risk more than low exposures.

Another measure used is attributable fraction among the exposed. This is defined as (RR - 1)/RR, so that a relative risk of 15 gives an attributable fraction of 14/15 = 0.93 or 93%. An interpretation of this figure is that 93% of the lung cancers in smokers are attributable to smoking (and 7% are background cases). Note that a relative risk of 1 indicates no excess risk, so that a relative risk of 15 may be divided into 1 (background) + 14 (excess). Thus, for an individual smoker who develops lung cancer, although it is not certain that the lung cancer was caused by smoking, one can say that the probability that it was due to smoking is 93%.

A relative risk of 2 gives an attributable fraction of 50%. That is, it is equally likely that the condition was due to the exposure or not. For relative risks higher than 2 then the exposure is the more likely cause, and for relative risk less than 2 the exposure is the less likely cause."

[715]

374 In the end I consider these experts accepted that the methodology to be adopted varied, depending upon whether the separate causes potentially acting in combination were entirely independent of each other in effect, or whether, as seems to have been generally acknowledged in this case, the separate causes potentially acting in combination were non-independent in the sense that the effect of each was greater in the presence of the other. All the epidemiological and statistical experts accepted that the correct methodology to move from an elevated relative risk to the probability that that relative risk caused the phenomenon (in Professor Berry's language to the "attributable fraction among the exposed" (Exhibit 145(1), p 2) is by the application of the formula (RR - 1)/RR. No matter what value is selected for RR the application of the formula will, of necessity, always produce a figure of less than 1. This is to be expected because no matter how high the RR may be, there always remains a possibility (progressively a smaller one) that the phenomenon may be due to some other factor and, hence, the calculation may approach, but never arrive at, the figure of 1.0 (ie 100 per cent). However, when in a case such as the present, where one is identifying two potential carcinogens to both of which the deceased is known to have been exposed (here tobacco and asbestos) and one calculates the RR for each and converts that to the probability of cause being due to that carcinogen alone, each resultant probability figure will necessarily be less than one. It is the next step which is, to say the least, enigmatic. In order to estimate the combined or "multiplicative" effect of the two carcinogens acting together, a number of the experts, specifically Professor de Klerk, Mrs Sowden and Mr Kottek, have multiplied those two factors (each being less than one) together. The inescapable result is that the "synergistic" or "multiplicative" effect is lower than the probability of either the more potent or the less potent factor alone. Thus, in the present case, if the risk of the probability that smoking caused Mr Cotton's lung cancer is 80 per cent (ie 0.80) and the probability that asbestos caused the disease is 16 per cent (0.16) then, on this methodology, the combined effect is 0.80 x 0.16 = 0.128 or 12.8 per cent - markedly lower than the probability that either of the carcinogens alone caused the disease. In the passages in the transcript, to which I have just referred, each of the three experts accepted that this runs counter to the qualitative evidence that the combined effect of smoking and asbestos exposure as a potential cause of lung cancer is greater than the effect of either carcinogen acting alone but explained, nevertheless, that it was correct statistically because the calculation addressed the three potential possibilities, namely:

[926]

Regulation 322: obliges any employer to ensure that no worker is exposed to an atmospheric contaminant listed in the schedule at a concentration which exceeds the level set out in the schedule. This prevention is required to be implemented, as far as practicable, by a suitable ventilation or exhaust system or by other suitable means but, if it is not practicable to avoid the atmospheric contaminant by any other means then suitable respiratory protective equipment must be provided.
Schedule 3 lists various atmospheric contaminants and the maximum time-weighted average exposure standards for them. The contaminants include four references to varieties of asbestos and the maximum exposure standard for each of those is as follows:
- Amosite - 0.1 fb/ml
- Asbestos (not otherwise listed) - 0.1 fb/ml
- Chrysotile - 1.0 fb/ml
- Crocidolite - 0.1 fb/ml
Regulation 803 is to be found in a section of the regulations dealing with specified hazardous substances and, in this particular instance, with asbestos. It obliges any employer in charge of a workplace to ensure that every asbestos surface is kept in a good condition; any repair or sealing necessary to prevent the breaking up of asbestos or the release of airborne asbestos is done promptly; and maintenance, replacement, removal or repair of an asbestos cement surface is carried out in the approved manner.
Regulation 804 contains an express prohibition against any person using, handling or causing or permitting another to use or handle Crocidolite or Amosite or a product containing Crocidolite or Amosite.
Regulation 815 imposes an obligation on an employer to ensure that the workplace is maintained in a clean condition and, in particular, to ensure that where there is a workplace at which an asbestos process is involved (defined by reg 801 to include the repair, maintenance and replacement of asbestos services and the cleaning and disposal of asbestos materials, among other things), that all machinery, apparatus, equipment and like furniture and fittings; the external surfaces of any exhaust system and cleaning equipment, and the floor, wall, ceilings or inside part of the roof and other interior surfaces are kept as far as practicable free of asbestos and other waste material. It specifically provides that in such circumstances the employer shall ensure that cleaning is carried out on completion of an asbestos process at least daily and by means of an approved vacuuming equipment or some other suitable method so that, as far as practicable, asbestos is not discharged into the atmosphere of the workplace.
Regulation 816 obliges an employer to ensure that a safety warning sign with the words "Danger - Asbestos" is prominently displayed at each entry to every asbestos processing area.
Regulation 823 creates an offence for any person to carry out or to cause or permit any other person to carry out asbestos removal work unless the person carrying out the work is licensed as required, has the approval in writing of the Commissioner to commence the work, and performs the work in accordance with the licence.

[938]

558 Turning to the factors which are germane to the plaintiff's case against the third defendant, based as it is on breach of contract, negligence and breach of statutory duty, it is plainly the case that Mr Cotton, and other workers, were expected, indeed required, to work at the Australind factory, and to work at times within the confines of the BDR without any protective equipment or respiratory masks or the like. It is also the case that it must have been obvious to the third defendant that there were very large areas of asbestos cement sheeting on the cladding, internal walls and the roof areas of the various buildings on the Australind site where Mr Cotton and his colleagues were working. Similarly, it was known to the third defendant that there was asbestos lagging on the steam pipes in the BDR and that it had been mixed and made up on the premises and applied to the pipes during an earlier stage (see the evidence of Mr Savage). There is evidence to show that the third defendant was aware of the existence of asbestos in lagging in the BDR well before the Matprolab's assessment of March 1990. Exhibit 95(1) is a copy of the minutes of a Safety Meeting of the third defendant held on 9 September 1987 which, at p 2, refers to samples of lagging having been collected from the top of the band drier and revealing asbestos in two of the samples. Exhibit 96 is a memorandum of the third defendant dealing with asbestos at the Australind site and dated 23 August 1988. This refers to a strike by all the contract personnel on this site employed by three-named contractors on 10 August 1988 over dissatisfaction with the owner's requirements to handle asbestos material. This led to the company contracting Amdel Ltd to undertake airborne asbestos fibre testing which was conducted on 12 and 16 August 1988 and these tests confirmed the presence of asbestos in various places. The report concluded by observing that contract personnel had raised concerns about their working environment being in close proximity to asbestos-related materials and that this concern was understandable based on the current publicity of asbestos in the media at that date. The presence of asbestos on the third defendant's work site continued to be a subject of complaint by employees and was raised from time to time at company safety meetings - 29 July 1988 (Exhibit 97).

[982]

Two extracts of the Hansard Reports of debates in the House of Assembly in South Australia in November and December 1968 discussing the hazards associated with asbestos dust including its potential to cause lung cancer. The Minister responsible for the Department of Public Health in South Australia stated that officers of that Department were then (December 1968) well aware of the hazards associated with exposure to asbestos dust. The debate also made reference to workers who had been exposed to asbestos dying of lung cancer.
Exhibit 85: A publication of the Department of Labour and Industry of South Australia: "Working Asbestos Safely", issued in June 1979 describing, at p 2, the dangers of grinding, sawing, drilling or abrading action on the finished asbestos product, including pipes, because of the fibres liberated which can lodge permanently in the soft lining of the lungs and also warning (at p 7) of the health hazards from asbestos if people do not abstain from smoking or at least refrain from the habit in the work area.
Exhibits 81(1) to (3): These are publications of the Department of Public Health In South Australia entitled "Good Health" in July 1957, April 1960, July 1960.
Exhibit 81(1) contains passages (at pp 28 - 29) to the effect that inhalation of asbestos dusts produce inflammatory conditions in lungs and produce characteristic peribronchiolar fibrosis. No asbestosis was found in the survey of asbestos workers in Adelaide at that time but none of them had been engaged in the work for more than two years.
Exhibit 87(2) adverts to the historical knowledge of the disease known as asbestosis (p 6) and (at p 3) observes that in the implementation of a safety programme, the safety officer's principal duties are to aim at the elimination of all known hazards, to develop safe working conditions and methods and to see that protective equipment is utilised.
In Exhibit 87(3) there is reference to the need for clean air and an observation that an ordinary person in leisurely activity breathes in and out about 1000 cubic feet of air each day. At p 3 it discusses inanimate dusts and identifies common types of harmful particles as including asbestos dust. At p 4 the publication, speaking of asbestos dust, says that the damage it causes to the lung is very similar to that produced by silica but that some authorities consider that the effects of asbestos may develop more quickly. In the same report the authors observe that the prevention of dust diseases of the lungs is best approached as an engineering problem in dust suppression.
Exhibits 88 and 89 are publications by the EWSD of South Australia in May 1958 and October 1959 relating to the procedures to be followed for the laying of asbestos cement pipes which are described as being manufactured by James Hardie & Coy Ltd. Although there is much detail about the procedures to be followed there are no recommendations or warnings about the potential danger of asbestos, nor of dust arising from cutting or rasping operations nor any recommendations to use a wet process or other dust suppression measures.
Exhibit 91 is a booklet "Safety Policy Rules and Instructions" for the EWSD published in 1964 as a guide to supervisors, but there is no mention made of any disease risk involved in working with asbestos cement pipes or the need for any special measures or precautions when working with asbestos products.
Exhibit 93 is a publication "Hardie's Textbook of Pipeline Design 1981" which describes the composition, manufacture, properties, uses and methods of handling of asbestos cement pipe but it does not detail the types of asbestos used in the composition of these pipes. At p 5-62 there is a short section dealing with dust precautions warning that in cutting AC pipes care should be taken to avoid the production of dust. This observes that if it is necessary to cut the pipe other than with a Wheeler cutter that should be done with a portable electric cutter with a water cooled diamond blade. Although not recommended if an abrasive type disc is to be used or it is necessary otherwise to work in conditions where dust is produced, respiratory protective equipment such as the 3M8710 mask must be worn. If using a powered field lathe the service to the machine should be kept wet to reduce the generation of the airborne dust.

[1103]

685 A court is not compelled to abandon the task of determining whether an alleged breach of duty has, in fact, caused loss or damage in situations where medical or other sciences are unable to identify the actual cause or the causal mechanism. There are many instances in which scientific understanding of natural phenomena is absent or incomplete but, even in those cases, the common experience of humanity may enable a decision, whether by inference or otherwise, of cause and effect to be made to the requisite degree of proof. The plaintiff has relied on a line of authority, adopting this approach, to support her present case. This authority includes the well-known observations of Dixon J in Betts v Whittingslowe [1945] HCA 31; (1945) 71 CLR 637 at 649; and his Honour's earlier remarks to similar effect (although in dissent) in Adelaide Stevedoring Company v Forst [1940] HCA 45; (1940) 64 CLR 538 at 569 - 570; Tubemakers of Australia Ltd v Fernandez (1976) 50 ALJR 720; (1976) 10 ALR 303; Western Australia v Watson [1990] WAR 248 and CSR Ltd v Culkin, unreported; FCt SCt of WA; Library No 940570; 18 October 1994. Certainly, the plaintiff is entitled to call in aid these authorities and the court must be astute to ensure that all inferences which may properly be drawn, even in the absence of scientific proof or probability, are drawn but whether in fact proof of elevated exposure to risk can be treated as allowing an inference that, on the probabilities, that elevated risk caused or contributed to the misfortune is another matter. Seltsam v McGuiness [2000] NSWCA 29; (2000) 49 NSWLR 262 and the cases referred to in [650] to [654] above are powerful reminders that elevation of risk and material contribution in fact are not necessarily the same thing but, as Commonwealth v McLean (supra) and other authorities such as Tubemakers (supra) reveal, the elevation of the risk may, in the particular circumstances, be of such a kind that the inference of causation can and should be drawn.

[1124]

to the extent, if any, to which smoking contributed to the development of the lung cancer, Mr Cotton's smoking habit did not constitute contributory negligence because it played no part in the contribution to his exposure to the carcinogen asbestos caused by the alleged breaches of duty of the defendants. In other words, if the event which caused his damage was exposure to asbestos because of the negligence of the defendants, his smoking habit was independent of that and did not lead him (at least knowingly) to neglect reasonable care for his own safety, by continuing to work in the environments in which his employers had exposed him;
that at no time during the period when he was smoking, did Mr Cotton fail to take adequate care for his own safety because of potential exposure to asbestos, having regard to his absence of knowledge of any association between asbestos exposure and smoking;
in any event the continuation of smoking by Mr Cotton was due to his addiction to tobacco and, therefore, did not constitute any failure by him to take reasonable care for his own safety;
at the time when he commenced smoking, and during the period leading to the establishment of his addiction to smoking, Mr Cotton did not know nor should he reasonably have known, that consumption of tobacco products posed any significant risk to his health;
until the diagnosis of his lung cancer, Mr Cotton did not know nor should he reasonably have known, that a smoker who was exposed to asbestos dust was subject to a materially increased risk of contracting lung cancer;
any lack of reasonable care for his own safety by Mr Cotton due to his use of tobacco products did not cause any additional injury or damage beyond the damage which was produced by the combination of smoking and tobacco exposure, where that combined effect was not known to him;
because of the material greater risk of developing lung cancer for a person exposed to asbestos who also smoked, the employers (first and third defendant) had failed in their duty to warn the deceased of that enhanced risk. This seems to be, in substance, a plea that the continuation of smoking by a person working in an environment involving asbestos exposure, could not be regarded as a lack of care for his own safety, unless the otherwise unknown degree of danger arising from the combination of those two carcinogens was brought to that person's attention by the employer;
for this last reason the alleged contributory negligence or assumption of risk by Mr Cotton in continuing to smoke, was not in fact any lack of care for his own safety nor any voluntary assumption of risk because it was a product of the employers' failure to discharge the alleged duty of care to warn him of the enhanced effects of the combination of tobacco and asbestos and that this was not known, nor could it reasonably have been known, to the deceased until the time of his diagnosis.

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