Bale v Seltsam Pty Ltd

[1995] QSC 306

IN THE SUPREME COURT

OF QUEENSLAND

Brisbane  No. 785 of 1995

Before the Honourable Justice White

[Bale v. Seltsam Pty Ltd]

BETWEEN:

JOYCE BARBARA BALE

(Plaintiff)

AND:

SELTSAM PTY LTD

(Defendant)

REASONS FOR JUDGMENT - WHITE J

Judgment delivered 14/12/1995

CATCHWORDS      PERSONAL injury - pleural mesothelioma - wife of asbestos worker 1962-5 - exposure to dust on clothes, car - foreseeability of injury - state of knowledge at relevant period.

Counsel:Mr R Stenson for plaintiff.

Mr S Doyle SC for defendant.

Solicitors:Nall Payne Craswell for plaintiff.

Ebsworth & Ebsworth for defendant.

Hearing dates:   16, 17, 18, 26 October 1995

IN THE SUPREME COURT

OF QUEENSLAND

No. 785 of 1995

BETWEEN:

JOYCE BARBARA BALE

(Plaintiff)

AND:

SELTSAM PTY LTD

(Defendant)

REASONS FOR JUDGMENT - WHITE J

Judgment delivered 14/12/1995

The plaintiff, Mrs Bale, was diagnosed in February 1995 as suffering from malignant pleural mesothelioma with a very limited life expectancy.  She issued a writ against her husband's former employers, formerly Wunderlich Limited, manufacturers of asbestos cement products, on 9 May 1995 seeking damages for negligence.
           In brief Mrs Bale alleges that she contracted malignant mesothelioma as a consequence of her personal and domestic contact with her husband during the years 1962-5 when he was employed by Wunderlichs in its plant at Gaythorne, a suburb of Brisbane.  She alleges that it was reasonably foreseeable that unless the defendant took certain workplace precautions she, as a member of the family of one of its workers exposed to asbestos fibres, was at risk to her health.
The statement of claim was delivered on 30 May 1995. Requests for particulars were made and given and the defence was delivered on 29 June 1995. On 13 September 1995 Dowsett J extended the limitation period pursuant to s. 31 of the Limitation of Actions Act 1974 to 27 February 1996 and made other interlocutory orders. The action was entered for trial on 10 October 1995 and was heard on 16 October and following. A commendable degree of co-operation was demonstrated between counsel and their instructing solicitors both in being ready for trial quickly and in agreeing on a number of matters.
           Quantum has been agreed between the parties in the sum of $94,916.10.
Facts
           Mrs Bale was born on 18 September 1939 and is 56 years of age.  She married her husband, Henry Bale, in 1957.  They have two daughters born in 1959 and 1963 respectively.  When they married Mr Bale did National Service followed by a period at Brandon Timbers before commencing work at Wunderlichs at the Gaythorne factory.  Since leaving the employ of the defendant he has worked for Olympic Tyre and Rubber and has generally engaged in driving work, particularly trucks.  Mrs Bale had various jobs prior to the birth of her children including with a printer.  There was no evidence at the trial as to her employment since.
           Mr and Mrs Bale first lived in a flat in Hamilton then in a house at Mitchelton and then moved to their present home at Deagon where they have lived for more than 30 years.  The flat at Hamilton was constructed of fibro sheeting (which contains asbestos) inside and out and was painted and in good repair.  The Mitchelton house was built of wood.  The Bale's home at Deagon is of fibro sheeting including corrugated sheeting on the roof.  Over 20 years ago Mrs Bale helped her husband carry out renovations and extensions to the house.  She helped by holding fibro sheeting whilst Mr Bale cut it with an angle grinder and a fibro cutter and assisted him whilst the sheets were being nailed in place inside.  She was about 6 feet away from the site of the cutting outside and was involved in cleaning up afterwards.  This incident formed part of the facts pleaded against the defendant.  Dr Basden, a chemist, carried out an analysis of certain asbestos sheeting which was provided to him by Mrs Bale's solicitors.  His report concluded that it was highly probable that the sheeting was made by another manufacturer and that its chemical composition was such that it was unlikely to have caused Mrs Bale's malignant mesothelioma.  In submissions her counsel expressly did not seek to rely on this event as a probable cause of Mrs Bale's injury.
           The evidence given by Mr and Mrs Bale was virtually unchallenged.  Mr Bale's description of the process at the factory was supplemented by the evidence of Mr Warner Johanssen, the works manager at the relevant time.
           In 1961 Wunderlichs installed a new plant for asbestos fibre treatment in a new shed at its Gaythorne premises.  The shed was also used as a storage area for bags of asbestos which originated in Canada and South Africa as well as Australia.  Previously the asbestos had been treated at the factory in the dry form.  The new process was a wet process which, together with extractors, was intended to eliminate much of the dust which had been generated under the previous system.
           The process for the production of asbestos-cement sheeting commenced with the operator opening bags of asbestos which had been delivered to him by forklift from storage.  As received in the bags the asbestos fibre was insufficiently refined.  The operator tipped the dry fibre onto conveyor belts which operated below floor level.  The hood or cover over the conveyor belt was designed to prevent the operator putting his head above the belt.  A duct in the hood carried dust up to a dust collector.  As correspondence, to which I shall refer later, demonstrated this part of the process continued to be a source of unacceptable levels of dust although Mr Bale never worked in this part of the factory.  The conveyor belt then dropped a measured amount of the asbestos fibre into a large enclosed unit described as an edge runner with an exhaust connected to the dust collector.  This unit ground and wet the asbestos for about two or three minutes after which a hutch opened and the asbestos dropped onto a covered conveyor which carried it across a roadway into the main factory.  The damp asbestos was then emptied into a hopper and bagged by an operator.  The bags were piled onto a trolley, taken to another part of the factory and awaited use in the beater unit.  If the asbestos in these bags dried out before beating the process had to be started again.
           The beater was a large tub-like unit into which cement or ground sand and water were added mechanically and to which the asbestos fibre was added manually.  A large paddlewheel pushed the mixture around for about 20 minutes.  It was then dropped in a liquid state into a stirrer where it remained until going into the machine that made the sheeting.  About 12% of the blend in the sheeting was asbestos.
           The process just described was in operation during Mr Bale's period of employment at Wunderlichs between 1 June 1962 and 30 August 1965.  Mr Bale worked in three different positions during this time:  at despatch; in the mixing section; and as a tester.  The job at despatch involved regular daytime working hours.  Mr Bale despatched or unloaded orders for fibro asbestos products.  This despatch area was inside the main factory.  Mr Bale did not regard it as a particularly dirty job.  As an operator in the mixing section Mr Bale was required to work shiftwork.  He would take the already opened bags of damp asbestos off the trolley and tip them into the mixer, fold the bags over and replace them on the trolley.  For one week in a three week shift he was required to clean the mixer by hand.  This involved getting into the unit, scraping it down by hand and then hosing out the debris.  This was a particularly dirty job and Mr Bale would be covered with the mixture, particularly down his front and on his arms.  At the end of the shift the damp mixture would dry and his clothes would be covered in cement and asbestos dust.  He recalled the asbestos fibres pricking and sticking into his arms, which he removed with tweezers and which sometimes caused small festering sores.
           The final position which Mr Bale held at Wunderlichs was as a tester.  This was a quality control position to test the strength of the product.  Its area was located directly underneath the mixing department.  In each area in which Mr Bale worked it was the responsibility of those on the job to sweep the area clean of dust before going home.  Mr Bale said the floor was never damped before sweeping because wet floors were dangerous.  He described this as dusty dirty work in each of the three sections.  Whilst he worked in the mixing section particularly dust accumulated in the pockets of his trousers and shirts.
           Mr Bale drove a utility to work which he parked in the work's car park some 100 metres away from the main factory.  He said that this was not a particularly dust-prone area.  However when he was on night shift he would park his vehicle inside the factory after 5.00pm and leave it with the windows down.  As a consequence the vehicle became very dusty.  Smoko and meal breaks were taken seated in the utility.  Mrs Bale cleaned the utility every few weeks or monthly by wiping over the interior with a cloth and vacuuming it.  She hosed down the tray and wiped the exterior cabin with a cloth.  She travelled in the utility at least once weekly.  On those occasions it would be dusty and she would wipe the seats before getting in.
           Mrs Bale said that during the whole time her husband worked at Wunderlichs he came home very dirty with greyish dust covering his clothes and in his hair.  She would usually greet him with a hug or a kiss before he changed.  On those occasions when he did not immediately shower and change after coming home he generally sat at the kitchen table and she would clean the dirty marks on the chairs after he had gone.  Mr Bale's clothes were his own clothes, not provided by Wunderlichs and Mrs Bale did the laundry for the whole family.  His clothes were kept and washed separately from other laundry.  Before washing she would shake the dust from his clothes.  Mrs Bale took them outside and shook them with both hands held up in front of her body.  Dust would fly out.  Depending on the season, the clothes were long or short sleeve shirts, long trousers or shorts, socks and underclothes.  Mr Bale did not wear a washable hat or indeed any hat at all.  Mrs Bale washed his clothes two or three times per week.
           Mrs Bale could not recall living near an asbestos dump or any other asbestos works apart from the defendant's works at Gaythorne at any time in her life.  There was no suggestion in the evidence that dust was emitted from the factory premises such as to expose Mrs Bale to any environmental risk during this period.
Particulars of negligence
           The relevant particulars of negligence pleaded against the defendant together with the further particulars are as follows:

"(a) Failing to warn Henry Valentine Bale of the dangers associated with exposure to asbestos fibres in circumstances when it knew that such exposure was hazardous to health".

The dangers particularised to include the development of various lung diseases and disorders including lung cancer, mesothelioma, asbestosis and other pleural diseases of which the defendant ought to have warned Mr Bale from the commencement of his employment in 1962.  The plaintiff pleads that the defendant, through Mr Johanssen the factory manager, had knowledge of such dangers from 1960 and from scientific and medical literature appearing from 1962.

"(b) Failing to warn the plaintiff of the dangers of exposure to asbestos fibres brought home by Henry Valentine Bale from the defendant's workplace".

The particulars are that the plaintiff ought to have been warned by the defendant from the commencement of employment by Mr Bale that any exposure to asbestos fibres and dust was hazardous to health and was known to cause various lung disorders including mesothelioma.

"(c) Failing to take all necessary steps to ensure that the plaintiff would not be exposed to asbestos fibres in the process of laundering the work clothes of one of its employees, namely, Henry Valentine Bale".

"(d) Failing to ensure that its employees did not leave the defendant's workplace until their work clothes were free of dust".

The protection of the plaintiff included providing Mr Bale and other employees with overclothing and ensuring that they did not leave the factory without first removing the overclothing and leaving it in lockers; ensuring that the overclothing was laundered by the defendants in such a way as to protect those who carried out the laundering from exposure to asbestos dust; ensuring that the system of work was such that the overclothing was not at any time contaminated with significant quantities of dust containing asbestos fibres; providing employees with showering facilities and ensuring that no employee left the workplace at the conclusion of a shift without first utilising showering facilities to remove any asbestos dust and fibres; providing and maintaining equipment and work practices which tested and monitored the levels of airborne asbestos fibres within the factory on a regular basis; retaining or employing an industrial hygienist or similar expert to enable the defendant to become conversant with current scientific knowledge as to the nature and extent of the dangers to health of asbestos fibre exposure and the necessary steps to eradicate risks to health of its employees and their families associated with asbestos fibre exposure; instituting and maintaining a system of cleaning the factory premises using dustless methods such as approved vacuum cleaners; warning the plaintiff and Mr Bale of the serious risks associated with asbestos fibre exposure in dust or generally and warning Mr Bale of the risk to his family of carrying those fibres and dust home on his person or overclothing; and the installation and use of adequate suction fans effectively to remove asbestos fibres from the air within the factory.
           The other particulars of negligence are:

"(e) exposing Henry Valentine Bale to such heavy concentrations of asbestos fibres that his clothing, by completion of a shift, was covered in dust and powder containing asbestos fibres;

(f) failing to take any or any reasonable steps to prevent the plaintiff being exposed to asbestos fibres in circumstances when it knew or ought to have known that such exposure by any means was exceptionally hazardous to the health, not only of its employees, but to all members of the community, including the families of its employees;

(g) failing to take any or any adequate steps to prevent the accumulation upon the person and clothing of Henry Valentine Bale of dust and powder containing asbestos fibre;

(h) causing or permitting the plaintiff to be exposed to harmful quantities of asbestos fibres."

The Issues
           The major issues requiring determination are:

.Could the defendant foresee or ought it reasonably have foreseen that a person in the position of Mrs Bale would be likely to suffer personal injury as a consequence of its operations at its Gaythorne factory?

.If some personal injury to Mrs Bale was reasonably foreseeable was malignant mesothelioma of a class or kind of injury which was reasonably foreseeable?

.If it was, did the defendant fall below the standard of a reasonable manufacturer in its response to the perceived risk?

Causation
Mrs Bale carries the burden of proving on the balance of probabilities that the asbestos dust brought home by her husband from his work and inhaled by her caused her to contract malignant pleural mesothelioma.  There is a low risk of contracting malignant mesothelioma in populations unexposed to asbestos dust estimated at about one or two cases per million adults of the population per year.  Whilst not expressly conceding causation, the defendant did not seek to resist the conclusion that there was a body of evidence from which it could be inferred that it was the inhalation of asbestos dust from her husband, his clothes and his car derived from his work place which has caused Mrs Bale's condition.  The evidence demonstrates that exposure to very small amounts of asbestos dust may be sufficient to cause malignant mesothelioma in a person susceptible to that condition.  The defendant did not seek to argue that it was necessary for Mrs Bale to be exposed over the whole period from 1962 to 1965.  The case proceeded on the basis that any exposure during that period may have been sufficient.
           The other matter concerning causation about which there was little debate was the kind of asbestos used at the Gaythorne factory in the relevant period.  Mr Bale said that when he moved to the testing section at Wunderlichs his senior told him that blue asbestos was used at the Gaythorne plant.  Mr Johanssen, the former works manager, now retired, said that it was not used in the relevant period.  No disclosed documents deal with this.  A document relating to dust counts at Wunderlichs' Rose Hill, NSW factory makes reference to blue asbestos in 1958 but that cannot be determinitive.  However, it was not submitted by the defendant that blue asbestos was the only form of asbestos whose fibres, if inhaled, would cause malignant mesothelioma.  The case proceeded on the basis that whatever the asbestos used at Gaythorne, (and the one most commonly used in Australia at the time was amosite known as brown or grey asbestos) it was capable of producing malignant mesothelioma.  In those circumstances I do not propose to deal with causation further.
Overview of Submissions
           The plaintiff sought to demonstrate from the evidence of a number of expert witnesses that in the period 1962 to 1965 there was a body of scientific evidence available to the defendant had it turned its mind to the issue, which would have alerted it to the dangers from asbestos dust to people in the position of Mrs Bale.  This, in effect, was a submission that low levels of exposure to asbestos dust could be foreseen as productive of personal injury.
           The defendant submitted that, while the dangers of inhalation of asbestos dust were well known for workers exposed to heavy levels of dust, the link between malignant mesothelioma and asbestos inhalation was first established by the work of a South African pathologist, JC Wagner, published in 1960.  The defendant submitted that even though those results related to non-workers nonetheless they had been exposed to heavy levels of asbestos dust.  The defendant maintains that it was not until 1965, with the publication of a paper by ML Newhouse & H Thompson, that the risk of contracting malignant mesothelioma to a person exposed to low levels of asbestos dust first became recognised.

Asbestos
           In its natural state asbestos is rock or stone.  There are a number of minerals which are given the collective name asbestos.  They are each of different chemical and physical properties and are used industrially for different purposes.  Asbestos has quite extraordinary properties of durability and lightness.  It resists fire and is regarded as virtually indestructible.  Although its properties were well known for about two thousand years, it was not exploited systematically for industrial use until the end of the nineteenth century.  To be of use the rock must be crushed into fibre form.  The milling process was rarely completed at the mine site and required further break down at the factory where its ultimate industrial destination was determined.  This activity was productive of substantial amounts of dust.
           Microscopically the fibres of the various forms of asbestos are quite different.  The asbestos which is recognised to have the most harmful properties medically is crocidolite (blue asbestos).  Much less so is amosite (brown or grey asbestos) while chrysotile (white asbestos) in its pure form is considered relatively harmless.  It is generally believed that exposure to chrysotile with its curly fibre, uncontaminated with amphibole (crocidolite, amosite or tremolite having a straight fibre) may not detectably increase the risk of contracting malignant mesothelioma above the background risk in the community generally. 

Diseases associated with Asbestos
           Dangers to health associated with the inhalation of asbestos fibres have been known since the end of the last century with the publication of a report by the British Chief Inspector of Factories.  The condition asbestosis was not named until 1927.  A number of different diseases are now known to be caused by the inhalation of asbestos dust.  The first four are characterised as non-malignant.  The remaining two are malignant.  They all depend, among other things, on individual susceptibility.
Asbestosis.  This disease is caused by prolonged and/or heavy exposure to asbestos dust apparently of any type although crocidolite (blue asbestos) is the most hazardous.  It is a scarring or fibrosis of the internal lung tissues.  The lungs thicken and stiffen over time causing shortness of breath.  Its consequences can be mild or so severe as to be completely disabling leading to death.  Its onset is dose related either as to intensity or length of exposure.  In 1934 W Wood and S Gloyne found that the shortest exposure to asbestos dust in a factory which eventually led to asbestosis was 6 months.  The more usual period was found to be in the vicinity of five years emerging some 15 to 20 years after exposure.  In more recent times exposure of some two to three months at the Wittenoon mine in Western Australia has been sufficient to contract the disease.
Pleural Plaques.  These are rounded raised gristly patches on the inside chest wall generally associated with exposure to asbestos dust which may be much less than necessary to cause asbestosis.  These are shown on x-ray but are generally without symptoms.  Pleural plaques may be a forerunner to the development of asbestosis but on their own they are commonly regarded as an indicator of work with asbestos in the past.
Pleural Effusion.  This is the outward manifestation of an inflammation of the pleura.  Fluid accumulates in the chest cavity outside the lungs and embarrasses breathing.  It is usually acute and settles after a relatively short period.
Diffuse Pleural Fibrosis.  This may occur in the absence of exposure to asbestos but commonly it is associated with it.  It is probably preceded by pleural effusion and pleuritis.
Lung Cancer.  It is a tumour which occurs in the air sacs and the bronchial lining.  The correlation between lung cancer and asbestosis was suspected for many years and confirmed in 1955.  It seems to be generally accepted that its risk is greatly increased in people with asbestosis who are smokers.
Malignant Pleural Mesothelioma.  This is a tumour of the membrane lining surfaces of the lungs, internal chest walls and upper diaphragm.  Malignant mesothelioma can occur in the peritoneum (the membrane lining the gut and internal abdominal walls).  The microscopic structure of a mesothelioma tumour is distinct from that of a lung cancer as is its mode of spread.  It requires a smaller exposure to asbestos containing amphibole (crocidolite, amosite or tremolite) than the other known asbestos related diseases and has a long induction period from 15 up to 50 years.  Smoking is not believed to increase its risk.  Until the use of electron microscopy and immuno chemical stains in the 1980's it was very difficult to diagnose.  Some writers doubted its existence as a primary tumour even into the 1960's.  Once it becomes symptomatic it is fast acting, incurable, fatal within a short period and extremely painful.  It continues to be a rare condition.
Knowledge of asbestos related diseases
           The expert witnesses provided written reports or statements, produced relevant literature and gave oral evidence directed generally to the state of knowledge from 1962 to 1965 of the danger of contracting malignant pleural mesothelioma from exposure to small amounts of asbestos dust.
           From the nineteenth century there were concerns for the health of workers exposed to lead, coal, silica and other atmospheric extractive dusts although recognition of the dangers associated with the inhalation of asbestos dust did not come until towards the end of the century.
           There is little doubt that the community at large had by 1962 been made aware of the generally harmful effects of the inhalation of significant amounts of asbestos dust for those who worked in the industry.  The important work of Merewether and Price:  'Report on the Effects of Asbestos Dust on the Lungs and Dust Suppression in the Asbestos Industry' was published in 1930 in the United Kingdom where there were great numbers of workers employed in the asbestos textile industry.  The report was not confined to the textile industry.  That report was instrumental in bringing about the first regulations controlling asbestos workplace atmospheres in the United Kingdom in 1931 which came into force in 1933.  According to Dr Basden's research, the first case of asbestosis recorded in Australia was that mentioned in the 1933 Report of the Director-General of Public Health in New South Wales.  In 1934 Merewether recommended preventive measures in the asbestos industry to reduce the risk of asbestosis.  These included localised exhaust ventilation, enclosure of dusty operations and wet methods of manufacture.  Papers were published in the 1930's which tended to show that even relatively short exposure to heavy doses of asbestos dust by workers could eventually cause asbestosis (Wood & Gloyne).
           In 1938 Dreessen and others published a major report on asbestosis in the textile industry in the United States.  For the first time an attempt was made to calculate a safe level of asbestos dust particles in the atmosphere.  The authors concluded that an atmospheric concentration of less than five million particles per cubic foot would be unlikely to cause the onset of asbestosis.  This figure in due course found its way into various workplace regulations around the world.  Victoria was the only state in Australia for many years to regulate the atmospheric count for harmful substances.  In 1956 Victoria proclaimed works or factories in which asbestos was used, manipulated, crushed or pulverised as carrying on a dangerous trade.  The regulations forbade an occupier and/or an employer to allow concentrations of substances in excess of the quantities set out and provided for the use of respirators and other protective measures.  These followed earlier regulations made in 1945.
           Papers seeking to make a link between lung cancer and asbestosis were published from about the mid-1930's, throughout the 1940's with the link finally confirmed in a seminal paper by R Doll in 1955.
           The International Labour Organisation's Third International Conference of Pneumoconiosis Experts was held in Sydney in 1950 and attracted significant media coverage.  Its focus was mainly upon silicosis and coal miners' pneumoconiosis but it also dealt with asbestosis.  The participants included industry representatives as well as scientists.  A major survey involving some 4,000 workers in dusty trades conducted by the industrial hygiene division of the Victorian Health Department in 1956 (the results of which were reported in the Melbourne Age in some detail) was reported to have shown a disturbingly high incidence of asbestosis among workers regularly handling asbestos.  At least by the 1950's there is evidence that some workers at Wunderlichs factory (and others in Queensland) were experiencing asbestosis after quite prolonged employment in the industry and x-rays were monitoring their progress.
           By 1960 I conclude that, for those with some little interest in the subject, asbestosis was known to be a possible consequence of prolonged and heavy exposure to asbestos dust in the work place.  It was also known to those who investigated further that those who had contracted asbestosis could also develop lung cancer.  Since pleural plaques were virtually symptomless only those involved in the field of thoracic medicine were likely to be aware of the condition.  Although malignant mesothelioma of various organs was known amongst a handful of specialists its identity as a primary tumour was not widely known or accepted and it was a rare condition difficult to diagnose.  It is to that emerging knowledge that I now refer at some length.
Malignant Mesothelioma

(a)The Literature

It is necessary to examine the literature because it is through a close examination of what was being written, it is submitted for the plaintiff, that Wunderlichs ought to have become aware of the risks to which it was exposing Mrs Bale.
           From footnotes in some texts tendered by the parties and from other reading I have become aware of other studies generally in the field concerning the dangers associated with the inhalation of asbestos dust.  I have confined my consideration of this submission by the plaintiff by reference only to the material tendered as evidence by the parties.  In other asbestos cases there may be other evidence which may lead to different conclusions.
           A Pneumoconiosis Conference was held in Johannesburg in South Africa in February 1959.  Its papers were published in 1960 including those by pathologists Wagner and Sleggs which described an association between exposure to asbestos and malignant mesothelioma.  They published a joint paper with Marchand in the British Journal of Industrial Medicine in August 1960 entitled "Diffuse Pleural Mesothelioma and Asbestos Exposure in the North Western Cape Province".  That article has been variously described as "seminal" or "famous" by the  expert witnesses in this case.  The precis of the article which appears at its commencement is as follows:

"Primary malignant tumours of the pleura are uncommon.  Thirty-three cases (23 males, 11 females ages 31-68) of diffuse pleural mesothelioma are described: all but one have a probable exposure to crocidolite asbestos (Cape blue).  In a majority this exposure was in the Asbestos Hills which lie to the west of Kimberley in the north west of Cape Province.  The tumour is rarely seen elsewhere in South Africa."

The article indicated that in the 1950's a number of cases of malignant pleural mesothelioma suggested that asbestos might be implicated.  Of those, one patient had asbestos in his lungs and 10 came from a hospital to which suspected cases of tuberculosis were referred from a large asbestos mining area.  The authors wrote:

"This hypothesis could not be supported at once from the original histories obtained by the patients, for they included housewives, domestic servants, cattle herders, farmers, a water bailiff, an insurance agent, and an accountant, none of whom were working on the asbestos mines at the time."

The authors undertook a detailed investigation of the patients' past occupation and place of residence.  An association with asbestos exposure was discovered in all but one case.  They wrote:-

"This is a preliminary publication and the problem is being intensively investigated."

Eight case histories of the 33 originally investigated were summarised in the paper, illustrating various aspects of the disease and the different levels of exposure to asbestos dust.  Several of the histories related to women who were not miners but who lived in or near mining towns.  Of some interest was Case 15, a woman whose father had a long mining history.  She went to school in the Copper Belt where she spent most of her youth.  Case 16 was that of a farmer who went to a village school near an asbestos mine.  He transported asbestos in donkey wagons for two years when a boy and often slept on the bags.  He worked for only one month in an asbestos mine.  Case 24 was of an accountant who had spent his early childhood in the asbestos belt.  His only other contact with asbestos was auditing the books of an amosite mine in the Transvaal.  Of the 33 cases investigated eight showed the presence of asbestosis.  Of the remaining 25 cases 18 were born in the vicinity of the mines and two arrived in the district as infants.  Of those 18 people 11 had a definite childhood exposure to the dust and two were exposed industrially in later life.  Two patients with childhood exposure later worked in the asbestos mines.  Three cases had arrived in the region at an older age but were employed either on the mines or in transporting asbestos.  A further three of those 25 had industrial exposure and in only one case did the relations deny any exposure at all to asbestos dust.  The authors indicated by way of an addendum that by the end of June 1960 a total of 47 cases of mesothelioma had been identified.  In 45 of those cases a possible association with exposure to crocidolite had been established.
           The paper was important not just for the connection which it made between malignant mesothelioma and exposure to asbestos dust but because it also tended to confirm the existence of primary malignant tumours of the pleura.  For many years there was a vigorous school of thought which suggested such tumours to be secondary in origin.  There was some attempt in the paper to identify which kinds of asbestos fibres were associated with the malignant tumours.  That was much less conclusive but tended to suggest that it was confined to blue asbestos or Cape blue (crocidolite).  There was considerable questioning of the experts at trial as whether these findings could be regarded as "preliminary".  The authors certainly said so.  They were scientists and while there remained much work yet to be done they raised interesting issues for consideration.  Even though most of the cases had little occupational exposure to asbestos dust the levels of dust were as high as in some occupations.
           A discussion held at a clinicopathological hospital conference in London was printed in the British Medical Journal for 30 April 1960.  It is entitled "Complications of Asbestosis".  The participants discussed a patient who had worked in an asbestos factory for 11 years and was diagnosed as having asbestosis and rheumatoid heart disease.  He also had a carcinoma of the right lower bronchus and metastases in various locations.  Dr Hugh-Jones, a thoracic specialist, in considering the carcinoma observed that most reports had stressed the frequency of sqamous carcinoma with asbestos.  He said that there was no question of the present carcinoma being a mesothelioma.  He described asbestos at p. 1350 as "very toxic and produces not only pulmonary fibrosis but reactions in the pleura and even in other organs".  He noted that another hazard of exposure to asbestos was mesothelioma of the pleura.  He added "this rather rare tumour may draw attention to the fact that a patient has worked in asbestos dust".  Dr Hugh-Jones concluded:

"Asbestosis was first described in this country by M Murray in 1907.  After that, in 1930, Merewether and Price reported the dangers of asbestos dust in the lungs and made recommendations for dust suppression.  Thereafter there was a great improvement.  In the factory where our patient worked the utmost precautions are now taken to prevent asbestosis occurring.  It is a disappearing disease.  Nevertheless, asbestos dust is most toxic, and the amount needed to cause asbestosis is not known, so constant vigilance and new preventive methods are needed if this disease is to be abolished".

I mention this reprint of the discussion not because it added to knowledge about malignant mesothelioma and asbestos exposure but because it sounded a warning about the unknown aspects of the toxic effects of asbestos.
           An article appeared in The Lancet of 3 December 1960 entitled "Asbestosis and Abdominal Neoplasms" by Dr Keal.  In his summary he noted the high incidence of cancers in people with asbestosis.  He particularly drew attention to the occurrence of cancers in two patients whose sputum contained asbestos bodies many years after removal from exposure but who had no other evidence of asbestosis.  In the body of his article he mentioned that primary mesothelial tumours were rare and added, "This type of tumour is more common in patients with asbestosis".
  A short article in the 8 September 1962 edition of the South African Medical Journal by Thompson appeared under the title "Mesothelioma of Pleura or Peritoneum and Limited Basal Asbestosis".  That was an abstract of a paper presented at the Research Forum of the University of Capetown on 14 June 1962.  Thompson noted that it was accepted by a majority of pathologists that mesothelioma was an entity in itself and that diffuse or malignant mesothelioma had been shown to be associated with pulmonary asbestosis in Canada, Holland, South Africa and Germany.  In his own practice he wrote that he encountered 7 examples of mesothelioma and none had asbestosis clinically or radiologically and only one had a history of occupational exposure to asbestos.  He concluded that it was likely that the enormous increase in the world consumption of asbestos and its use in a wide variety of industrial products made it possible for an increasing number of people manufacturing, handling or using those products to inhale enough asbestos fibres to produce what he described as "this limited basal asbestosis" without having any clinical or radiological evidence of it.  He added that in the modern home asbestos may be present from the roof to the pipes in the basement, but suggested that the home hazard from asbestos might be theoretical rather than practical to the occupant but not to the builder.  This was a particularly prescient comment, but not more widely circulated for some years.
  A letter appeared in the British Medical Journal of 3 November 1962 from WJ Smither Chairman of the Asbestos Research Council and two members of the Medical Research Council's Pneumoconiosis Research Unit.  They referred to and cited the Wagner articles in the South African Medical Journal and the British Journal of Industrial Medicine and wrote:

"There appears to be no correlation between the severity of any pulmonary asbestosis and the occurrence of these tumours.  In a number of cases the exposure to asbestos dust appears to have been minimal, and the only histological evidence of asbestos exposure is the presence of a few asbestos bodies and fibres in the lung tissues.  However, a detailed occupational history has, in nearly all cases, revealed some contact with asbestos fibre."

The writers asked for information concerning any patient in whom a mesothelioma tumour had been diagnosed and asked for the information to be sent to the Director of the Medical Research Council's Pneumoconiosis Research Unit where a register was being compiled.
           In the 24 November 1962 issue of the British Medical Journal, McCaughey, of the Department of Pathology at Queen's University Belfast together with Wade and Elmes of the Department of Therapeutics and Pharmacology wrote under the title "Exposure to Asbestos Dust and Diffuse Pleural Mesotheliomas".  They reported a number of cases of diffuse pleural mesothelioma researched by them.  They had analysed histologically 15 cases looking for asbestos bodies.  They found them in 12 and in only one case was the asbestos plentiful.  In the remainder they were few and a prolonged search was needed for their detection.  The occupational histories showed that in four cases there was an intermittent exposure to asbestos usually through occupation in shipyards or engine rooms.  The authors concluded:  "In most of these cases exposure to asbestos was not continuous or prolonged and in some instances there was a considerable gap between the last exposure and the onset of symptoms due to the tumour."
  An article appeared in The Medical Journal of Australia for 15 December 1962 under the heading "Malignant Pleural Mesothelioma in an Asbestos Worker" by Dr JC McNulty, a chest physician at the Kalgoorlie District Hospital.  He referred to and cited the Wagner article in the British Journal of Industrial Medicine in 1960 and noted the authors' comment that there was circumstantial evidence of "at least transitory asbestos exposure" in 24 cases of malignant pleural mesothelioma occurring 20 to 40 years after the exposure to the dust.  Blue asbestos had been mined in Western Australia since about 1946 and a number of miners had developed asbestosis, silicosis and a mixed pneumoconiosis containing elements of both.  Dr McNulty reported what he believed to be the first case of mesothelioma outside South Africa.  The man had been a mill worker in an asbestos mine from 1948 to 1950.

"The relatively short period of exposure to blue asbestos dust confirms an impression received from Wagner et alii (1960, 1961) that these tumours may arise after transitory exposure to crocidolite in susceptible persons."

Dr McNulty referred only to blue asbestos emphasising that it was a very harmful and lethal fibre and that its dust urgently required further experimental study.
           A major article by Hourihane appeared in Thorax (1964), the major research journal for chest medicine, entitled "The pathology of mesotheliomata and an analysis of their association with asbestos exposure".  The article primarily focused upon the recognition and diagnosis of primary pleural tumours.  In his summary Dr Hourihane wrote:

"A study of the pathology of 34 cases of primary tumours (mesotheliomata) of the pleura and peritoneum shows these to be distinct and recognisable neoplasms which can be distinguished from primary carcinomata of the lung or either viscera.

The association of these tumours with asbestos bodies in lung tissue is confirmed.  Many of the cases gave no history of industrial exposure, and it is possible that temporary or relatively trivial exposure may have occurred."

The next significant development in the link between non-worker exposure to asbestos fibres and mesothelioma was a paper by Newhouse and Thompson given to a conference held at the New York Academy of Sciences in October 1964 devoted to the biological effects of asbestos.  That paper was entitled "Mesothelioma of Pleura and Peritoneum Following Exposure to Asbestos in the London Area".  Their paper was subsequently published in the 1965 British Journal of Industrial Medicine.  The month is not clear but the paper was received in February and publication would be at least several months later.  The synopsis contained the following:

"A series of 83 patients from the London Hospital with a diagnosis of mesothelioma confirmed by necropsy or biopsy has been studied for possible exposure to asbestos.  The series consisted of 41 men and 42 women; 27 of the patients had peritoneal and 56 pleural tumours.  The earliest death recorded was in 1917, but only 10 of the series died before 1950 and 40 between 1960 and 1964.

In 76 of the series full occupational and residential histories were obtained.  40 gave a history of occupational or domestic (living in the same house as an asbestos worker) exposure to asbestos ...  None of the 17 suspected cases of mesothelioma, rejected on pathological grounds, was found to have any exposure to asbestos.  There was also evidence that neighbourhood exposure may be important.  ... The interval between first exposure and the development of the terminal illness of mesothelioma range between 16 and 55 years ..."

The cases studied fell into a number of groups, namely, factory workers; laggers and insulation workers; relatives of workers and persons living within a half a mile or less of an asbestos factory.  Six had no known exposure to asbestos however the authors noted that they were unable to obtain an exhaustive history.  The defendant concedes that after the publication of that study the link between exposure to low levels of asbestos dust and malignant mesothelioma had been made and impliedly that it ought to have thereafter taken preventive measures.  Mr Bale ceased employment in August 1965 with Wunderlichs.
           Although outside the period with which this action is concerned an important article appeared in the British Medical Journal in 1966 by Hourihane, Lessof and Richardson entitled "Hyaline and Calcified Pleural Plaques as an index of exposure to asbestos:  a study of radiological and pathological features of 100 cases with a consideration of epidemiology".  The researchers had collected 56 cases of pleural plaques found at necropsy and 50 cases found on x-ray examination.  They conclude in summary:

"A close association between exposure to asbestos and the development of pleural plaques has been shown.  A cause and effect relationship is probable.  The most extensive lesions are radiologically detectable, and the disease asbestosis is then also present, despite the absence of any other radiological abnormality.

The sources of asbestos are considered and evidence is presented to suggest that there is a widespread non-industrial community exposure.  Mesotheliomata are common in patients with pleural plaques, and it is suggested that there is a dose response relationship between the asbestos and the development of these neoplasms.

The question of a relationship between lung cancer and asbestos is left open, but the value of radiological surveys for pleural plaques is emphasised in any study of this problem.

Asbestos is not the sole cause of pleural plaques, but it is certainly the most common."

I have referred in considerable detail to the literature which was put to, discussed with and tended through the expert witnesses.  I was left with the impression that every effort had been made, particularly on the part of Dr Basden and Dr Oliver who gave evidence on behalf of Mrs Bale, to identify every item of literature which made mention of asbestos and mesothelioma from whatever source in the English speaking world.  The witnesses' evidence was that in the period under consideration the Australian Medical Journal would have been read by most medical practitioners in Australia and the British Medical Journal was subscribed to and read by at least the specialists.  The British Journal of Industrial Medicine was a specialist research journal and although it was available in Australia the number of subscriptions taken would have been quite limited.  There is no doubt that it was a journal for the specialist.  It was subscribed to by Dr Rathus in Queensland and Dr Ferguson in New South Wales both of whom were witnesses.  The South African Medical Journal was not likely to be available in Australia without considerable difficulty.  Some medical practitioners, including Dr Ferguson, took The Lancet.
           As can be seen, the period of Mr Bale's employment at Wunderlich's co-incided with important medical research linking asbestos exposure to mesothelioma and, by the end of the period, revealing that the exposure could be well below occupational levels.

(b)The Witnesses

The plaintiff called five expert witnesses.  Dr WA Oliver is a thoracic physician.  He graduated in medicine in Sydney in 1962 and worked in Queen Mary's Hospital in London from 1965 to 1966 where he saw a number of cases of malignant pleural mesothelioma either in workers or in families of workers associated with particular asbestos plant.  Dr E Rathus, now retired, was a specialist in chest diseases who was Director of Industrial Medicine in Queensland from 1957 to 1982.  Dr K Basden is a retired senior lecturer at the School of Chemical Engineering and Industrial Chemistry at the University of New South Wales with a particular interest in dust suppression and dust diseases.  Mr Gordon Stewart is a retired industrial hygienist who worked in that capacity with Mt Isa Mines Limited from 1965.  Mr Peter Russell, now retired, was formerly a safety officer with James Hardie Pty Ltd, another producer of asbestos-cement products from 1948 to the 1970's.
The defendant called Dr David Ferguson, emeritus Professor of the University of Sydney and a specialist in occupational health.
           I shall consider the evidence of Dr Rathus first because he was both a witness of fact and an expert witness.  Dr Emanuel Rathus was Director of Industrial Medicine in Queensland from 1957 until 1982.  He specialised in chest diseases in South Africa after the second World War and came to Queensland in 1952.  He became a member of the Mesothelioma Surveillance Program in the 1970's which was chaired by Dr Ferguson.  In 1952 there were two large asbestos sheeting manufacturers in Queensland - James Hardie and Wunderlich.  There were other much smaller enterprises utilising asbestos in their products.  Dr Rathus had a small staff and access to the Government laboratory chemists.  In his position as Director of Industrial Medicine he could advise and recommend but had no coercive powers.  There was no relevant legislation in force apart from the general provision in the Factories and Shops Act 1900 concerning the provision of adequate ventilation.  Dr Rathus first visited Wunderlichs in May 1957 and thereafter visited probably twice a year in his early years as director and subsequently no less than once a year.  The same frequency was true for James Hardie and other asbestos factories.  Documents produced under subpoena from the Department of Health at the trial record the written dealings between the Department through Dr Rathus and Wunderlichs in the period to the end of the 1960's.  Not surprisingly, given the passage of time, Dr Rathus was unable to be at all precise as to dates unless documents covering certain events were available.
           The plaintiff alleges that Dr Rathus raised with Mr Johanssen at some time either prior to or during Mr Bale's period of employment the need to keep the employees' work clothes at work and have them laundered safely and to require the men to shower before leaving the works.  I shall return to that evidence in due course.  After his first visit to Wunderlich's on 21 May 1957 Dr Rathus reported to the Director-General of Health that he found an unacceptably high level of dust particles in areas of the Wunderlich factory and made recommendations for the provision of an exhaust hood over the asbestos well on the ground floor where the teasing processes were carried out.  The factory was still using the dry method of processing the fibre.  He recommended the routine annual x-ray of all employees of the firm including all new employees as soon as possible after engagement in order to exclude any possible findings of disease.  In its reply Wunderlichs expressed gratification that Dr Rathus had noted "that the asbestos hazard has considerably improved" since the last inspection.  Wunderlichs wrote that it did not routinely arrange x-rays for all employees but only those who had the highest exposure to asbestos fibre and asked whether this was sufficient.  The recommendation concerning the provision of an exhaust hood was referred to head office (in New South Wales) but it was expected that the directors would "favourably consider some scheme for reducing the dust hazard at the point in question".
           After Dr Rathus visited Wunderlichs on 6 December 1960 the company was informed of the results of his visit by the secretary to the Director-General of Health.  He wrote:

"Dr EM Rathus, Director of Industrial Medicine, has reported that your firm has made great progress in the designing of equipment calculated to depress dust contamination of the atmosphere to an absolute minimum.

He states that some cases of asbestosis have been discovered at your firm but they probably occurred when the less modern methods of work prevailed.  Surveys in the future will no doubt reveal the effectiveness of the present system."

The writer went on to deal with some intense noise exposure to workers and recommended protection.
           In evidence Dr Rathus explained the positive tone of such letters as to encourage and compliment where there was some entitlement to it in order to enhance personal relations with, as he put it, "the people whom I was brow-beating into spending lots of money" with respect to industrial health and hygiene.  Similar positive expressions were also included in his reports to the secretary to the Director-General.  That must be seen in the context of the administrative arrangements of the government of the day whereby his report to the Director-General was translated into the third person virtually without change by the secretary to the Director-General and conveyed to the manager of the factory under consideration.  Dr Rathus knew that what he wrote to the secretary would be transliterated to the company concerned.
           A letter written by Dr Rathus dated 8 August 1966 to the works manager at Wunderlichs, although outside the period in question, provides some insight into the way Dr Rathus dealt with what he regarded as an industrially unhygienic plant.  He praised the firm for the "tremendous amount" that it had done to enclose the train of processing of asbestos fibre.  He noted that improvement over the old system was "quite remarkable".  He expressed concern about the quantity of dust at the point where the asbestos fibre was introduced at the inception of the operation and made it clear that the exposure of the operator to the asbestos dust was unacceptable.  Although the tone is encouraging and conciliatorily the reader could have no doubt, in my view, that it was a stern message about the failure of the company to eliminate a serious health hazard.
           Again a letter from Dr Rathus to Mr Johanssen dated 13 October 1966 serves to show that the focus was very much on the protection of workers in the factory from the contraction of asbestosis.  Dr Rathus reported on dust count tests carried out at the factory.  Although the counts were below the suggested maximum allowable concentrations for asbestos dust Dr Rathus commented that no doubt from time to time they exceeded that which was allowable.  He added that from his own personal observation visually there was sufficient asbestos fibre "floating around to be a hazard over many year's exposure".  He pointed out to Mr Johanssen that asbestos has an unenviable reputation and that, by reference to the literature, it appears that no matter what was done cases of asbestosis would still arise where the fibre was capable of invading the lungs.  He recommended that in order to obviate these hazards there should be a rotation of men from hazardous to non hazardous positions; the absolute enclosure of all processes; the compulsory wearing of face masks; and where specific dusty jobs were undertaken for short periods air supply hoods should be supplied.  He noted that because asbestosis had a long incubation period it would not be possible to see how effective such a program might be under 10 to 15 years.  This was the first letter expressing concern at the generally hazardous nature of asbestos and making wide ranging suggestions to eliminate the danger.
           Dr Rathus was a member of the National Health and Medical Research Council and a member of its Occupational Health Committee from 1957.  That committee reviewed recommended maximum concentrations of atmospheric contaminants associated with occupational exposure from time to time and in particular in 1961, 1963 and 1964.  The secretary was Dr Gordon Smith then senior to Dr Feguson.  They looked closely at the threshold limit values adopted by the American Conference of Governmental Industrial Hygienists in May 1963.  Recommendations were made as to how Australia should seek to fit in, adopt or otherwise deal with these recommendations.  In the review dated 3 March 1964 appears a comment:

"Because of local legislative requirements and other factors, it would not be practicable to include the values for mineral dusts as shown in the US Schedule (Table 4), but the problem of standards of dust is ..... one which could be examined by the Committee."

Table 4 related to mineral dusts and included silicates which included asbestos.  The millions of particles per cubic foot of air, based on impinger samples counted by light-field technics was a maximum of 5.  This was the figure contained in the Victorian legislation but Queensland had no such measurement requirements.  This maximus of 5 million particles per cubic foot, it will be recalled, was published by Dreessen and others in the 1930's as the safe occupational limit.
           In September 1966 an investigation of James Hardie's factory was undertaken by the Department of Health to look at the problems of asbestos fibre contamination of the working environment and the possibilities of asbestosis developing among workers.  The tests suggested that in certain places the fibre content was unacceptable.  Dr S McCullagh, James Hardie's medical officer, proposed coming to Brisbane to discuss the problems with Dr Rathus.  In his reply to Dr McCullagh, Dr Rathus wrote:

"In fact I think the asbestos firms in Queensland, and in Australia in general, to date have enviable reputations compared with what one knows of the overseas situation."

During this period from time to time Dr Rathus would bring visiting health experts and medical students to visit the Wunderlich factory in Brisbane to show them how an efficient modern factory could handle such a dangerous substance with safety.
           In his statement prepared for this litigation dated 18 September 1995 Dr Rathus said that in the late 1950's/early 1960's he knew of cases where adverse health conditions were caused by limited exposure to asbestos even by non workers.  That was not developed by him in his oral evidence.  He said that in his opinion in 1962 Wunderlich knew enough of "these dangers" to have required its workmen not to wear clothes home because they knew that some their workmen left the factory covered in dust.  Mr Johanssen does not recall that particular conversation and in oral evidence Dr Rathus agreed that it was impossible to pin him down to dates, even years.  For him the problem was a continuing one.  In a letter dated 2 June 1967 Dr Rathus wrote to Mr Johanssen as follows:

"As you are aware there has been general concern in the asbestos industry about the problems of asbestosis.  Its impact on the working population has become quite clear over the decades and with a very much larger use of asbestos in various ways the ramifications of the problem have become if anything more complicated.  I refer of course to the strong suspicion that mesotheliomata (pleural tumours) are strongly suspected of being connected with asbestos exposure.  This refers not only to the working population but also to the general community.

It is my privilege to emphasise these matters and I think that it is only reasonable to bring these matters to your attention."

Dr Rathus had numerous conversations with Mr Johanssen over the years.  Needless to say not everything was put in writing when he returned to his office.  However Dr Rathus agreed that if matters were not trivial and related to serious questions of health he would have conveyed his concerns in writing.  That is what he did on 2 June 1967.  Dr Rathus was and is an enthusiastic and vigorous proponent for occupational health and safety.  Asbestos and lead were the matters that he was most concerned with in his early years in Queensland.  He read widely and knew what was going on in his field.  He subscribed to the British Journal of Industrial Medicine and read the Wagner article when it first appeared.  He was aware that Dr Wagner had given a paper in Sydney in about 1962 but was unable either to attend or to speak to him.  Nonetheless I think it unlikely that he made the link between exposure to low levels of asbestos dust and the contraction of some kind of disease be it mesothelioma or anything else until after the circulation of the Newhouse and Thompson article towards the end of 1965 and did not bring Mr Johanssen's attention to these problems until about the time that that letter was written in June 1967.
           Towards the end of 1967 it appears that the member of parliament in whose electorate the Wunderlich factory was situated had asked a number of questions of the Minister for Health about asbestosis.  Again it is outside the relevant period but is sufficiently contemporary to assist in understanding how an expert in the field viewed the dangers of asbestos.  Dr Rathus provided a report to the Director-General in respect of those matters.  It needs to be viewed as providing ammunition for the Minister who was being challenged about how little the government was doing to protect workers in the asbestos industry.  Dr Rathus noted that over the years both Wunderlichs and James Hardie had accomplished a great deal and spent an enormous amount of money on the installation of new machinery and new enclosed processes but that neither firm had completely solved the problem of dust control.  Dr Rathus noted Victoria was the only State which had any regulation of the asbestos industry and only with respect to the number of particles of asbestos dust in the atmosphere.  Dr Rathus concluded that the situation was not a happy one for asbestos workers but that he could see no alternative but to go on in the pattern already established of inspections and recommendations.

           There is no reference in any of the contemporary documents that employees should not wear their working clothes home and that they be laundered by the employer.  Dr Rathus made mention of difficulties in getting workers to use face masks and there is no doubt that there would have been difficulty in implementing showering practices.  Mr Bale said that everyone was keen to leave the factory premises as quickly as possible at the end of the shift.  Nonetheless, if the risk were appreciated the employer could have found an appropriate way to enforce the hygiene.
           Dr Oliver is a thoracic physician.  He was a medical registrar in Australia in 1964 and was not then particularly interested in the management of lung disease.  He took an advanced course in medicine in Sydney in 1965 and he recalled people in his profession talking about the increasing numbers of malignant mesotheliomata but did not associate this with asbestos exposure.  It was not until he went to London and started working at Queen Mary's Hospital which had a large number of patients from the Cape Asbestos Factory at Barking in its catchment area that he became aware that the association between mesothelioma and asbestos exposure was well known.  Some of the patients seen at the hospital had only domestic exposure or lived down wind from the factory.
           Dr Oliver concluded in his report tendered in the trial that if Dr McNulty knew of the Wagner paper when he worked in Kalgoorlie in 1962 it would be surprising if the defendant did not know of this and the cautionary letters in the British Medical Journal and the investigations proceeding in London.  He commented that if he had been working in this field in 1962 he would have been concerned about the two letters in the British Medical Journal about low dose asbestos exposure and mesothelioma.  Dr Oliver particularly pointed to the letter of 3 November 1962 in the British Medical Journal from the chairman of the Asbestos Research Council who was an industry person.  He concluded that industry itself was getting suspicious and that "red flags", as he expressed it, were going up.
           Mr Gordon Stewart, a consultant industrial hygienist, is a chemist with a major in biology.  He was first employed in the field of industrial hygiene in 1954 as a scientific officer in the industrial hygiene division of the Department of Health in Victoria.  He was involved in the administration of the occupational health and safety aspects of the various Health Acts from time to time, including regulations relating to dangerous trades.  His particular duties involved assessing the level of environment hazard derived from contamination of the workplace by toxic gases and dust.  He was employed from 1965 by Mt Isa Mines Limited as their industrial hygiene engineer and a significant amount of his work with that company related to the measurement of the atmosphere in respect of lead particles.  In his affidavit of 18 September 1995 which formed the major part of his evidence in chief, Mr Stewart swore that it was common in the early 1960's for employers in industries known to produce potentially hazardous chemical agents such as dust to employ industrial hygienists.  Formally trained industrial hygienists, as I understood the evidence, were not to be found in Australia until about the mid-1980's.  However in the early decades of the century the Commonwealth and one or two States established divisions dealing with industrial health directed by medical practitioners.  They had an unsteady history which is set out in exhibit 4, an article written by Dr Ferguson for the Medical Journal of Australia in July 1994 dealing with the history of occupational medicine in Australia.  It is clear from his article that the emergence of occupational health as an aspect of medical studies is a rather recent innovation.  Despite the lack of formal qualifications a person, quite often the chemist in the relevant works, according to Mr Stewart, was given the responsibility of taking dust measurements and dealing with the matters required under the legislation in Victoria.  Mr Stewart was able to refer to people carrying out the functions of industrial hygienist in the early 1960's in Mt Isa Mines, at the BHAS smelter at Port Pirie, on the waterfront, in association with the Wheat Board where poisons were used to kill weevils, and in the aluminium industry.  Because of the passage of time he was unable to be more particular.  Mr Stewart said that asbestosis was "a big issue" when he first joined the Health Department in Victoria in the 1950's.  Whilst he was employed in Victoria and by Mt Isa Mines he had ready access to books and journals held by those organisations or by university libraries.  He himself accessed the QUT, University of Queensland and State public libraries as a consultant in more recent years.  In the early 1960's he was aware of general medical publications such as the British Medical Journal, the Lancet, the Journal of the American Medical Association and the Australian Medical Journal and of particular industrial medical publications such as the British Journal of Industrial Medicine, the Journal of Occupational Medicine and the Archives of Environmental Health.  As an industrial hygienist at the time he was aware of the serious effects upon health of the inhalation of asbestos and that that had been known for decades.  He was also aware of theories of the correlation between the inhalation of asbestos and various cancers.  When he worked at Mt Isa Mines he had a general brief to protect the community from the effects of the mine process but particularly in the case of exposure to lead.  As he recalled, it was not until between 1965 and 1970 that Mt Isa Mines required its employees to shower and change before leaving the site to prevent the wider distribution of lead in the community.  This must be seen against the long understood risk of lead poisoning.  Mr Stewart, although stating that he was very much aware of the developing concern about asbestos as an occupational health problem in the period 1954 to 1984, and his recollection of particular medical journals and discussions with colleagues, nonetheless he does not say that in his work as a scientific officer or indeed after he commenced work in 1965 with Mt Isa Mines that he became aware through the general medical publications to which he said he had access of the risk to members of the public from exposure to low levels of asbestos dust.
           Mr Peter Russell was employed by James Hardie from 1948.  He started work as a cadet engineer and studied chemical engineering at the University of Sydney part time.  Although he did a great many subjects towards that degree it appears that he never completed it.  Towards the end of 1960 he took up the position of safety and fire officer with that company at its Camellia factory.  He was responsible for safety in the production of brake linings, insulation and asbestos-cement product factories.  His main task was to concentrate on the asbestos dust problem which existed within those factories.  Previously there had been a safety officer whose job it was to take dust measurements and count the particles under a microscope.  Mr Russell swore an affidavit dated 19 September 1995 in which he said that when he was appointed to this position he read what was available to him at James Hardie and became concerned about the seriousness of the asbestos dust problem in the factory.  To broaden his knowledge he researched various public libraries and public health department libraries to learn as much as he could about the dangers of asbestos dust.  He said that he became aware through his reading in the late 1950's and the early 1960's of a possible link between asbestosis and cancer and between exposure to asbestos dust and mesothelioma.  He became aware of two cases of health problems by a wife and child said to be as a result of exposure to asbestos dust carried home on work clothes.  He did not elaborate in oral evidence.  He became aware that different individuals had different susceptibilities to asbestos dust and that even fairly minimal exposure to asbestos dust could be dangerous to health.  He recalled having access to the Wagner article shortly after it was published.  He said he was given the article (exhibit 8) reporting a discussion on the complications of asbestosis in the 30 April 1960 volume of the British Medical Journal, to which I have earlier referred, by Dr McCullough who was James Hardie's medical officer.  Mr Russell recalled that James Hardie had a series of reports of a conference held in France in 1964 at which the report of Dr Wagner was discussed and recalled that he delivered a lecture based on his 1960 paper in Sydney in either 1962 or 1963.  Mr Russell had regular meetings with individuals in the district in which the Camellia factory was situated to discuss safety issues and asbestos related diseases.
           Mr Doyle sought in cross-examination to impugn Mr Russell's recollection of these matters by suggesting that it was unlikely that he could recall that he was aware of these things from as long ago as 35 years.  Mr Russell has been called on a number of previous occasions in respect of actions against James Hardie in respect of asbestos related matters.  There is a risk that he may have merged his recollection as to what happened in the early 1960's with what he has learnt subsequently but I am persuaded that Mr Russell was aware of the Wagner article shortly after it was published, that he had passed to him other articles to which I have referred at that time and that he endeavoured to qualify himself to fulfil the role of safety officer in a diligent fashion.  However Mr Russell did not say that at any time he drew the conclusion that exposure to very low levels of asbestos dust were likely to constitute a risk either to workers or to those outside the factory.  There is no suggestion that he sought to give that advice to James Hardie or indeed that he discussed things of that kind with other colleagues.  That suggests to me that whilst he may have had access to the Wagner article in the early 1960's and other articles he did not draw the conclusions which it is argued that the defendant ought to have drawn had it perused those articles or sought advice.
           Dr KS Basden, retired senior lecturer in the School of Chemical Engineering and Industrial Chemistry at the University of New South Wales had a particular interest in industrial dusts from about the beginning of the 1970's.  He undertook an extensive survey of the available literature in respect of the dangers of asbestos from the turn of the century until the mid to late 1960's.  He himself became aware of that literature only from the 1970's but his report was valuable in so far as it conveniently collected what was available.  Dr Basden was of the opinion that there was a substantial body of knowledge concerning the physiological effects of asbestos dust inhalation in the period 1962-1964 which together with the statutory requirements, at least in other States than Queensland, if heeded by the defendant, would have caused it to have taken precautions so as to eliminate the risks of the inhalation of asbestos fibres by Mrs Bale.  This was contrary to a view which he had expressed before the New South Wales Dust Diseases Tribunal in November 1990 (exhibit 28).  Propositions were put to him on that occasion from a work by Lee and Sellicoff entitled "Historical Background to the Asbestos Problem" reported in Environmental Research Vol 18 at p. 300.  This exchange occurred at t/s p. 321 of exhibit 28.  Beginning with the quotation the following appears:

"Q.'The decade of the 1960s provides a convenient time at which to terminate a historical review of asbestos disease.  With admirable hindsight from the late 1970s we can see that the essential evidence had already been reported but not yet assembled or gested with sufficient credibility to be entirely convicing.'  Do you agree with that as an assessment of the association of asbestos and mesothelioma in the 1960s.

A.Yes.

Q.With few exceptions he says:  'The evidence at that time rested on scattered reports of small numbers of cases and the cases themselves suffered from being either selected or simply those that happened to come to the attention of the reporter.'

Do you agree with that.

A.Yes.  Well, those are the words of Sellicoff, yes.

Q.Do you agree with what he wrote.

A.Yes.  There's no reason for me to disagree, no.

Q.Do you agree that in those scattered reports to which he referred, the author proceeding:  'The population base from which the cases came were seldom mentioned.  The significance of pleural changes and the occurrence of mesothelioma in persons without a distinct history of exposure remained in considerable doubt.  The idea that asbestos could be at least a co-factor in the production of bronchogenic carcinoma was far from fully accepted.'

Do you agree with that.

A.I'm just wondering - I'm grappling with it a bit because of my non-medical background but I think that would probably summarise the situation fairly well.

Q.Would you agree with this next sentence.  Are you familiar with the word 'parenchymal.'

A.No, I'm not.

Q.Would you assume that it means a disease associated with --- an organ as distinct from its subservient structures.

A.Well, yes, I'd accept that.

Q.Well, taking that to be the meaning, do you agree with this as written by those authors, 'That parenchymal asbestosis was very likely to occur in those that had been exposed to heavy dosage in the early years of the industry was clear enough, but what effect environmental controls that had been influenced in the 1930s might have upon its future prevalence was not known.'  Do you agree with that.

A.Yes.

'The possibility that quite low dosages might have grave consequences 30 or more years after first exposure was still unproven.'  Do you agree with that.

Yes.

'Many things were needed to confirm the suggestions that were emeging from the studies up to that time.'  Do you agree.

Yes.

'Most importantly, systematic epidemiological investigation was needed of large cohorts drawn from various types of industry with the inclusion of adequate control populations.'  Do you agree with that.

Yes.

Q.'Some of these were already organised but it was too early for the results to be meaningful.'  Do you agree.

A.Yes.

Q.'We now know' that is these authors writing in 1979 - 'We now know that much of the negative evidence stems from coming to conclusions prematurely before the slow processes of carcinogenesis had had a chance to make themselves evident.'  Do you agree.

A.Yes.

Q.'We now know also that reduction of heavy exposure that lead to early death would reveal such slowly developing diseases as mesothelioma and carcinogenic carcinoma with increasing clarity.'  Agree.

A.Yes.

Q.'But foreknowledge was not available at the time although some investigators suspected that the auguries were not good.'  Agreed.

A.Yes.

Q.Would you not agree that it was not until the very end of the 1960s at the earliest that the scientific community came to accept that mesothelioma could be caused by exposure to asbestos at much lower levels than was known to be necessary to cause asbestosis.

A.Yes, I would agree with that."

Dr Basden suggested that his answers needed to be looked at in context.  An examination of the transcript before the Tribunal really does not indicate that his answers were qualified in any way.
           The real value of Dr Baden's report and evidence was that he has collected together much of the available literature and legislation chronologically in a careful and systematic fashion.  He made no profession to having medical expertise and indeed qualified his answers to the cross-examiner in the Dust Diseases Tribunal in that way.  Of interest is his reference at p. 14 of his report to an article in Australian Factory for 1 March 1958 at pp. 36, 38 and 57 by WF Cooper entitled "Toxic Agents in the Factory" where the following appears:

"Asbestos is another destroyer of lung tissue and the maximum permissible concentration is 2½ million particles per cu. ft.; that is, 87 c.c.  The prevention of silicosis and asbestosis revolves itself around suppression and exhausting it, plus personal protection of workers by respirators.  Pre-placement and periodic medical examination are essential with radiological review."

There was no evidence as to the circulation of this journal.  However it must be indicative of information being disseminated to the industry to which I have earlier referred.
           Dr David Ferguson was called to give evidence on behalf of the defendant.  He has been closely involved in thoracic medicine as it affects occupational health for many years.  Amongst many appointments he has chaired the Mesothelioma Surveillance Program from 1977.  In his report (exhibit 26) he suggests that in the years 1962-65 the primary asbestos industries (being mining, milling and the manufacture of asbestos products) were likely to have been aware of the risk of asbestosis in workers continually exposed over long periods to asbestos dust inhalation.  That seems to me to be expressed rather conservatively in view of the studies which had been undertaken in Victoria and relevant conferences held in Australia concerning dust diseases at which there was participation by industry.  It seems quite unlikely that industry would not have been aware of the extensive work that had been done in the United Kingdom in relation to asbestosis in the 1930's and 40's.  Dr Ferguson suggested that the British Journal of Industrial Medicine would have had very limited circulation in Australia being received only by the State divisions of occupational health or industrial hygiene and by some university medical schools and libraries.  But he took it and read it together with the other usual medical journals to which reference has been made.  He was of the view that it was not until the publication of the paper by Newhouse and Thompson in 1965 that research and academic workers in the field became strongly conscious of the risk of mesothelioma from exposure to relatively small doses of asbestos.  He suggested that the knowledge contained in that paper took several years to percolate into medical practice in the field and to the practitioners advising industry.  He noted that there was no immediate government action in Australia and crocidilite importation into the country was not prohibited for another decade.  It is relevant to note that the "Asbestos Rule" requiring protection for asbestos workers and removal and laundering of work clothes in their factory was introduced and became effective in Queensland only from July 1971 and that, it seems, at the insistence of Dr Rathus.  Dr Ferguson emphasised the rare occurrence of mesothelioma and that its gradual emergence was attributable to the long induction period of between 30 and 50 years after first significant exposure in the decades following the 1940's.  He concluded that since the state of knowledge in Australia in 1962-1965 amongst medical scientists about this risk was minimal it could not be expected that industry in Australia would be as well informed.  He said that it was not common practice in 1962-1965 in Australia to require on-site showering and laundering of work clothes in dust exposed employees although anything to reduce dust inhalation was good hygiene.
           He was taken in cross-examination to a number of general articles which he had contributed on industrial and occupational medicine.  In an article written for the World Health Forum in 1991 under the heading "Asbestos:  Insufficient Action, Overreaction and Action for Tomorrow" he wrote:

            A starting point for a manufacturer using asbestos in its manufacturing process as did Wunderlichs would be statutes regulating the industry and any regulations made thereunder.  The Queensland Factories and Shops Act 1901 as amended and the regulations are expressed in broad terms as to ventilation and would have given no guidance.  From there many options were available.  It could have designated one of its own officers to search out and maintain a watching brief into matters of safety concerning asbestos dust; it could have employed someone like Mr Stewart; it could have expressly sought the advice and assistance of the Department of Health's Industrial Medicine Division because even though small, it had a dynamic and enthusiastic director.  Ought it to have done so?  Mr Doyle submitted for Wunderlichs that the defendant's conduct was no different from that of other asbestos cement manufacturers in Australia at that time.  The response to such a submission was given as long ago as 1860 by Cockburn CJ addressing the jury in Blenkiron v. Great Central Gas Consumers Co 2 F&F 437 at p. 440; 175 ER 1131 at p. 1132:

"It is not enough that they [the company] do what is usual if the course ordinarily pursued is imprudent and careless; for no one can claim to be excused for want of care because others are as careless as himself; on the other hand, in considering what is reasonable, it is important to consider what is usually done by persons acting in similar business."

Dr Ferguson suggested in his article, to which I have referred, and in oral evidence that the spirit of the age was essentially one of laissez-faire.  From the limited evidence available to me, I think it true to say that Queensland had had major mining industries in which, in the not too distant past, the immediate safety of the workers had been secured.  In the 1950's and 1960's concern was being directed with greater urgency towards more indirect questions of safety such as dust disease outside the traditionally recognised ones of coal, gold, silver, lead and sand.  The knowledge of the devastating effects of asbestosis was known, but after the introduction of the wet method Wunderlichs were not entirely without justification if they thought that the major risk had been dealt with although there were still points in the factory where quantities of dust were permitted to float.  I am persuaded that Wunderlichs was under an obligation to all who might reasonably have been affected by the conduct of the factory processes and to embark upon acquitting that duty it needed to undertake investigations into what was known about asbestos dust.
           At the relevant time it may be taken to have been understood that exposure to prolonged or high dosages of the dust could lead to asbestosis.  The essential question is, I think, whether Wunderlichs could have reasonably understood between 1962 and the middle of 1965 that there was a risk that exposure to low dosages of asbestos dust could produce harmful results in individuals and if it did, that someone like Mrs Bale, removed from the factory, was reasonably exposed to the risk.  Windeyer J in Mt. Isa Mines Limited v. Pusey (1970) 125 CLR 383 observed at p. 397:

"Forseeability here [in the duty sense] predicates the foresight of a reasonable man.  The reasonable man is not here anyone on the Clapham omnibus.  He is a man who notionally stood in the shoes of the defendant and had such knowledge, and capacity for care and foresight, as that defendant actually had and in addition such as a reasonable man in that position is expected to have.  ... He is not a seer who can foretell future occurrences that are quite unlikely according to the natural and ordinary course of events.  Happenings that were fortuitous, in the sense that no reasonable man would have thought of them as within the range of possible consequences, cannot be said to have been reasonably foreseeable.  And knowledge after the event, when it is easy to be wise, cannot show that the event was foreseeable.  Fullagar J spoke of this in Ray v. Broken Hill Pty Co Ltd (1957) 97 CLR 419 at p. 422:

"The fact of the happening of the accident is, of course, itself a relevant consideration, but, in considering whether it ought to have been foreseen, it is wrong to take as the standard of comparison a person of "infinite-resource-and-sagacity."

It is plain that a growing suspicion was emerging during the period under consideration about the connection between mesothelioma and the inhalation of asbestos dust.  However until the Newhouse and Thompson article published in the course of 1965 there was no published material which identified dosages as low as that inhaled by Mrs Bale with the contraction of harmful disease.  The period from 1960 to 1965 was at the very forefront of medical science on this subject.  Although most of the articles to which reference has been made might have been obtained on a conscientious search for information about the adverse properties of asbestos on individuals, nonetheless, it is in my view of significance that neither Dr Ferguson, who was an acknowledged expert in the field, nor Dr Rathus, whom no one could accuse of being unduly conservative in his endeavours in this area, having read the literature, made the links sufficient to foresee the risk of harm from such low dose exposure.  The comment by Dr Rathus on the x-rays of Wunderlichs workers in August/September 1966 that one of the men "had exposure up to about 25 years ago - nil since (wet process) - Would explain pattern" is clearly suggestive of a view that the level of exposure within the factory after the introduction of the wet process would be insufficient to cause asbestosis.  Mr Stenson for Mrs Bale submitted that both Mr Stewart and Mr Russell who worked in the field were aware of the literature.  Nonetheless I was not persuaded that either of them were aware of the risk of contraction of injury from exposure to low doses of asbestos fibre or that they made the necessary connection between that and the exposure of a class of persons in the position of Mrs Bale.  Indeed neither gave evidence that they made any recommendations or spoke to any persons of this connection at the relevant time.  Any suggestion that they may have understood this link I think must be regarded as wisdom after the event.
           I am not here concerned with scientific certainty.  It has no place in considering liability for negligence.  Both Professor Ferguson and Dr Rathus (as well as Mr Russell and Mr Stewart) were operating in the field of industrial and community health and safety and I did not discern in their approaches to these questions that they needed to be satisfied to the level required for acceptance by the medical/scientific community of a connection between low dose exposure to asbestos and the eventual onset of mesothelioma in their approach to their work.  As I have said, no evidence of Mr Stewart or Mr Russell would lead me to the conclusion that they would have made the necessary connection at any time during the relevant period.  The focus then was still upon reducing the level of dust within factories to an acceptable level and would have been far higher than that which would have been sufficient to contract mesothelioma in a susceptible individual.  As Mr Doyle has submitted, it is significant that MIM did not introduce laundering facilities such as are alleged the defendant ought to have had in place at Gaythorne in the relevant period until between 1965 and 1970 and that was for the control of lead dust well known for its poisonous quality.  Mr Stenson has submitted that at least by 1964 the necessary connection had been made.  By this I take him to be referring to the conference held in New York at which Newhouse and Thompson presented their conclusions.  However, that conference was in October 1964.  There is no evidence as to who the participants at the conference were or whether it was reasonable that Wunderlichs should have had someone attending.  The paper itself was not published until towards the middle of 1965 and the proceedings were not published until December 1995.
           Mr Stenson submitted that even if injury by the contraction of mesothelioma was not foreseen in the relevant period it was reasonably foreseeable that a person in the position of Mrs Bale might contract pleural plaques.  There really was very little evidence as to the amount of inhalation of asbestos fibres which was necessary to bring about that condition.  There was no evidence as to whether the amount of asbestos inhaled by Mrs Bale was likely to have produced pleural plaques in her.
           Something was sought to be made by the defendant of the fact that none of Dr Ferguson, Dr Rathus or senior scientists of the Health Departments in either New South Wales or Queensland took care that they wore special clothing when visiting these factories.  It think little can be made of this.  Many instances can be produced from experience that even when fully aware of risks "scientists" are prepared to take them.
           As will be apparent from the foregoing I have formed the view that between 1962 and August 1965, the period of employment of Mr Bale with Wunderlichs, it was not reasonably foreseeable that a person in the position of Mrs Bale would sustain personal injury of any kind as a consequence of her shaking out and laundering her husband's work clothes or in cleaning his car of the asbestos dust that had accumulated in it.
Like class or kind of harm
           Although my finding on the question of foreseeability of harm has disposed of the action, nonetheless, in view of the time that was devoted to it in submissions I should deal with this further question, namely, accepting that Mrs Bale is a member of the class whom Wunderlichs ought to have foreseen as being at risk of harm from the way in which it conducted its business, was the contraction of mesothelioma harm of a class or kind which was reasonably foreseeable.  Mr Doyle submits that it was not, while Mr Stenson submitted that if contraction of pleural plaques was foreseeable that condition was sufficiently similar to mesothelioma.
           Mr Stenson submitted that (1) since not as much exposure to asbestos was required to cause pleural plaques as to cause asbestosis and (2) because it was known that pleural plaques could occur from the inhalation of asbestos well before 1960 and (3) because both pleural plaques and mesothelioma occur in the pleural cavity and have a number of features in common, the defendant had sufficient understanding of a risk of personal injury of a similar kind when it exposed Mrs Bale to the inhalation of asbestos fibres in the way that it did.
           It is necessary to look more closely at the medical evidence.  The major distinction between mesothelioma and asbestosis according to Dr Ferguson is that the former is a cancer while the latter is a degenerative disease associated with scarring or fibrosis in the lungs.  The malignant mesothelioma with which this case is concerned is a tumour arising from the pleura or the lining of the lung whereas asbestosis is a disease affecting the internal lung tissue.  Pleural plaques prior to 1960 were and still are associated with asbestos.  They differ from mesothelioma in the first instance because they are non-malignant.  They are composed of fibrous tissue or scar tissue of a gristly nature or appearance.  They amount to a thickening of the pleura in irregular patches which tend to occur on the inside lining of the chest, particularly along the lines of the ribs and not the visceral pleura which coats the lungs.  They tend to occur in the dome of the diaphragm but may also occur on the outside of the heart cavity.  Pleural plaques occur as a result not only of heavy exposure to asbestos but they are more likely to occur in that circumstance than with lighter exposure.  They are often forerunners of asbestosis.  In themselves they do not appear to create any disability and in almost every case Dr Ferguson concluded that the subject was unaware that he or she had anything wrong.  He described them as "a badge of office" for asbestos workers.  Dr Rathus was quite clear that malignant mesothelioma was not medically the same as asbestosis and gave a similar description of the differences as did Dr Ferguson.  It seems clear from a medical point of view that pleural mesothelioma and pleural plaques arising from the inhalation of asbestos fibres are not the same.
           The question is whether in law it is sufficient to show that a reasonable manufacturer in the position of the defendant who could foresee a risk of some personal injury to Mrs Bale (and in this case it appears to be limited to pleural plaques) associated with the inhalation of asbestos or whether it is necessary to show that what was foreseeable was the risk of injury by the contraction of mesothelioma.  Mr Doyle submitted that there is a difference in approach in recent developments in England to that of the High Court.  The distinction is said to arise between the approach of the High Court in Mt Isa Mines and Jaensch v. Coffey and the House of Lords in Page v. Smith [1995] 2 WLR 645. Those cases concerned claims for damages due to nervous shock. Before turning to them something generally needs to be said about what is meant by "of the same class kind or character". The cases where this has been discussed, particularly Hughes v. Lord Advocate [1963] AC 837; Doughty v. Turner [1964] 1 QB 518 and Smith v. Leech Brain & Co Ltd [1962] 2 QB 405 need not be repeated here.
In Mt Isa Mines Barwick CJ held at p. 390:

"But the rarity of such an injury in the circumstances does not in my opinion deny the foreseeability of an injury of the class of which it forms one.  That it is sufficient that the class of injury as distinct from the particular injury ought to be foreseen as a possible consequence of particular conduct in order to establish liability for damages of the particular injury is well established.  (See eg Chapman v. Hearse)"

Professor Fleming commented in The Law of Torts (8th ed.) at p. 213:

"Clearly it is a matter of judgment where to draw the line, and in problematical cases this will depend largely on what outcome the court wishes to reach.  Overriding, perhaps, is the guiding principle that the hazard should not be defined with over-much particularity, less the unique feature inherent in every case disqualify the injury from falling within the description of the apprehended risk."

In Page v. Smith, a collision occurred between the cars driven respectively by the plaintiff and the defendant due to the fault of the defendant.  Neither the plaintiff nor the occupants of the defendant's car sustained physical injury, however, the plaintiff who suffered from recurrent myalgic encephalomyetitis (chronic fatigue syndrome) claimed that as a consequence of being involved in the collision he suffered a recrudescence of the condition.  His evidence was that prior to the collision he was recovering from a severe attack of the condition and expected to return to work as a teacher, but that as a consequence of the collision the condition had become chronic and he would be unable to work again.  The condition was characterised as "non physical" and therefore fell to be considered by reference to the authorities generically described as the nervous shock cases.  In the House of Lords, Lords Keith and Jauncey dissented in separate judgments holding that for a duty to be owed to the plaintiff injury of nervous shock must be reasonably foreseeable and on the facts it was not.  They did not consider that the earlier authorities from which this principle was derived could be distinguished on the ground that the sufferers were bystanders or so-called secondary participants in the accident.  The majority (LJJ Ackner, Browne-Wilkinson and Lloyd) found this distinction to be compelling.  They were concerned that were the law to persist in drawing a sharp distinction between physical and psychiatric injury it would limp too far behind medical science.  Lord Lloyd concluded at p. 667 that

"Nothing will be gained by treating them [physical and psychological injury] as different "kinds" of personal injury so as to require the application of different tests in law."

Since physical injury was said to be reasonably foreseeable, then it followed that any harm which could be described as personal injury was not beyond the risk.
           Perhaps the question here is whether the law should adopt the distinctions made in medical science classifying conditions and diseases.  I think that it ought not.  However, it is unnecessary for me to consider the clearly different approaches between the majority and the minority in Page v. Smith and the implications for the approach to primary participant plaintiffs who sustain injury by nervous shock.  What the majority do underline is that it is inappropriate to concentrate on fine distinctions between the harm that might have been foreseen and the harm that was actually sustained irrespective of the approach that might be taken to the need to foresee injury by shock.  I am of the view that were it foreseeable that some particular physical harm could have been sustained to someone in the position of Mrs Bale from the inhalation of asbestos fibres that would be sufficient.  A recent decision of Holland J in Margereson v. JW Roberts Ltd (unreported decision, 1991 M800 and 1993 H6610 given in October 1995 and kindly provided by the Library Services of the Lord Chancellor's Department, Leeds) relies upon the approach of the majority in Page v. Smith to the question of what kind of physical injury if any must be foreseen.  The plaintiffs (one deceased) claimed damages for personal injury arising out of the contraction of malignant mesothelioma caused by environmental exposure to asbestos dust emitted from the defendant's factory premises in Leeds.  The first plaintiff's exposure was as a resident in a nearby street from his birth in 1925 to 1943 and again from 1948 to 1957.  The second plaintiff had a childhood residence in the immediate vicinity of the factory from 1938 to 1951.  The court found that there was little attempt internally to comply with the Asbestos Industry Regulations of 1931 which followed the Merewether and Price report in 1930.  What efforts there were simply exhausted the dust into the surrounding streets.  The evidence revealed that significant amounts of asbestos dust accumulated in the streets and drifted into the surrounding houses; that children played in the streets and jumped on the sacks of asbestos which were in the loading bay on the street and which emitted clouds of dust.  The court found that at no relevant time was mesothelioma a concept known to medicine nor the potential for it being caused by lesser levels of exposure to asbestos.  However Holland J found that the levels of asbestos dust in the immediate curtilage of the defendant's factory were much the same as those within the factory.  Accordingly it was reasonably foreseeable that persons subjected to that level of asbestos dust would be likely to contract asbestosis if susceptible to the disease.  That the plaintiffs contracted mesothelioma rather than asbestosis did not relieve the defendants of liability because personal injury was foreseeable.  With respect, the conclusion on the facts with which Holland J was concerned seems irresistible.
           Dr Ferguson said that the attitude of occupational physicians was that unnecessary exposure to a hazardous substance, even at a level which was believed would not cause disease, was undesirable and it was good industrial practice to keep the exposure down to a level that was reasonably attainable.  Without more, this cannot give rise to liability.
Breach of Duty
           I should then mention something about the standard of care of a manufacturer should some harm have been found likely.  The defendant in effect did nothing apart from the introduction of the wet method and some exhaust fans.  Was this reasonable in the light of the risk to Mrs Bale?  The evidence at the time was that pleural plaques were understood to be symptomless.  The elimination of the risk to those outside the factory premises was easy to effect.  Showers were already provided as required under the Factories and Shops Act and it would not, I think, have been a difficult matter to arrange for the supply of clothing at the factory and lockers for the workers to store their street clothes.  If called upon to do so I would conclude that the defendant was not entitled to take the risk of Mrs Bale contracting pleural plaques (or any other physical injury) and that by doing so it would have fallen below a reasonable standard of care for a manufacturer in the period under consideration.

Conclusion
           It is with regret that I have come to the decision that I have.  It has not been an easy one, particularly in light of my conclusion that I could find no real evidence that Wunderlichs took any great care for their employees' health and wellbeing during the relevant period.
           Mr and Mrs Bale both gave their evidence in a most restrained fashion.  There was scope for exaggeration by both of them as to the quantities of dust which were emitted both at the factory and at home.  Mrs Bale and her family face a bleak future.  It was not until a detailed examination was undertaken of the extensive medical and scientific literature together with cross-examination of the witnesses that the true position, as I saw it, was revealed.  It was not inappropriate for Mrs Bale to bring her action.  The case has been conducted on both sides as far as I can tell with all due expedition and economy.
           The formal order is that the plaintiff's action against the defendant is dismissed.