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OUTER HOUSE, COURT OF SESSION
[2007] CSOH 138
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OPINION OF LORD UIST
in the cause
HELEN WRIGHT
Pursuer
against
(FIRST) STODDARD
INTERNATIONAL PLC and
(SECOND) NOVARTIS GRIMSBY LIMITED
Defenders
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Pursuer: Marshall, Solicitor; Thompsons
First Defenders: R A Smith QC, Comiskey,
Dunlop; Simpson & Marwick WS
2 August 2007
Introduction
[1] The
late James McHardy Wright ("the deceased") was born on 7 March 1925 and died on 20 April
2000.
The cause of death given on his death certificate following a post mortem
examination carried out by Dr Jeannette McFarlane, Consultant Forensic
Pathologist in the Department of Forensic Medicine and Science at the University of Glasgow, was bronchopneumonia due
to pulmonary fibrosis. The deceased worked as a boiler man for the first
defenders' predecessors James Templeton & Co Limited ("Templetons") between
about 1957 and 1974 and for the second defenders, formerly known as Ciba-Geigy
Limited, between about 1975 and 1990. This action is brought by his widow
solely in her capacity as his executrix. She avers that the deceased contracted
asbestosis as a result of being exposed to significant quantities of asbestos
dust while in the employment of Templetons and the second defenders due to
their negligence and various breaches of statutory duty. At the outset of the
proof it was intimated that the pursuer had reached an agreement with the
second defenders and was no longer proceeding against them. The proof therefore
proceeded against the first defenders only. As they were the only defenders at
the proof I shall refer to them from now on simply as "the defenders".
[2] The
issue which was addressed in the evidence was whether the deceased had
contracted asbestosis. The evidence led consisted of evidence of the degree to
which he was exposed to asbestos dust while in the employment of Templetons and
medical evidence dealing with the question whether he had contracted
asbestosis. The evidence of exposure came from four witnesses, one of whom
provided hearsay evidence of the deceased, and the medical evidence came from a
total of eight doctors. The medical evidence can conveniently be subdivided
into (i) clinical evidence; (ii) radiological evidence; and (iii) pathological
evidence.
Asbestosis
[3] Asbestosis
is a serious, long-term lung disease caused by the inhaling over a long period
of dust from asbestos (a naturally-occurring fibre which was formerly widely
used for various industrial purposes, including insulation). Asbestos fibres
settle in the lungs and cause extreme irritation, resulting in thickening and
fibrosis (scarring) of the lung tissue. As changes in the lung occur slowly the
condition can take 20 years or more to develop. The main symptoms are
increasing breathlessness (especially when exercising), coughing, chest pain
and a feeling of tightness in the chest. Lung function may be damaged so much
that respiratory failure results. Other symptoms that sometimes occur are nail
abnormalities and clubbing of the fingers. Clubbing occurs when the fingers
become thicker and broader and the tip of the nail curves. A history of
exposure to asbestos is important in the diagnosis of asbestosis. Steps taken
in the diagnosis of asbestosis consist of lung function tests showing fibrosis
of the lungs and breathlessness, a chest x-ray or CT scan and a biopsy of lung
tissue for examination.
Cryptogenic
Fibrosing Alveolitis
[4] Cryptogenic
Fibrosing Alveolitis ("CFA") is a progressive fibrosing inflammatory disease of
the lung of unknown aetiology. It affects men more than women and the median
age at diagnosis is in the seventh decade. It is characterised by inflammation
and fibrosis of the pulmonary interstitium and peripheral air spaces. The word
"cryptogenic" indicates that it has no known cause. The condition is known in
the USA as idiopathic pulmonary
fibrosis. The typical patient with CFA presents with gradually increasing
breathlessness, sometimes associated with an irritating cough; on examination
by the doctor finger clubbing is usually present and crackles are audible on
auscultation. Investigation typically shows widespread nodular, irregular and
chest shadows on the chest radiograph, and functionally there is a reduction of
lung volumes (a restrictive ventilatory defect), of carbon monoxide transfer
factor and of arterial oxygen tension. Asbestosis is one of a number of
conditions whose symptoms are similar to those of CFA. (See generally Roland du
Bois, Cryptogenic Fibrosing Alveolitis and Cryptogenic Organizing Pneumonia,
7/20 of process, and Crofton & Douglas, Respiratory Diseases (5th
Ed), Chapter 41, Pulmonary Fibrosis, 7/22 of process).
The evidence
of exposure
[5] The
evidence of exposure came from Miss Victoria Cameron (31), a para-legal in the
firm of Thompsons, the solicitors for the pursuer, John Affleck (63), who
worked in Templetons from about April 1956 until June 1981, the pursuer and
Robin Howie (59), an occupational hygienist. I proceed to deal with the
evidence of each of these witnesses in turn.
(i) Miss Victoria Cameron
[6] Miss
Cameron took a statement (7/38 of process) from the deceased when she visited
him at home on 13 July 1999. She visited him again on 11 August 1999 when, at his request, the original statement was
revised. She thereafter had the revised statement typed out (6/23 of process)
and the deceased signed it on 19 August 1999 after having made several
manuscript amendments to it. It was accepted by the defenders that the revised,
signed statement had evidential status: Highland
Venison Marketing Ltd v Allwild GmbH 1992
SLT 1127. That statement, as amended by the deceased, so far as relevant to the
question of exposure, and with appropriate syntactical and grammatical
corrections, reads as follows:
"On 22 October 1998 I had quite severe chest pain and breathlessness and
was attended by my GP on the same day. My GP immediately sent me to the
Victoria Infirmary. They admitted me right away and started doing tests. I
assumed it had something to do with my angina. While I was in Coronary Care the
Doctor asked me if I had ever worked with asbestos. I told him I had and he
then told me he thought I had asbestosis but would do further tests to confirm.
Then, on 12 November 1998, while I was in hospital, I was told I had
asbestosis. As soon as I heard this news my wife and I were very shocked and
extremely worried. They told me at the hospital that there was nothing that
could be done about my condition.
Since being diagnosed I feel
that I have deteriorated and I am now dependent on oxygen.
For the majority of my
working life I have been surrounded by asbestos.
When I left school at the
age of 14 I started working as an apprentice hairdresser with Anderson
Hairdressers in Aberfeldy. I was not exposed to asbestos in this job. I worked
there until 1941.
I then worked for the
Forestry Commission in Perthshire. This job involved planting trees. I was not
exposed to asbestos. I worked there until 1943.
From 1943-1947 I worked In
the Royal Navy and then in the Merchant Navy from 1947-1956. I worked with the
boilers in both the boiler rooms and the engine rooms. I would have to check
the boilers and alter the temperature when necessary. I would open and close
the valves and check gauges. The boilers, pipes and engines would be lagged
with asbestos and I was exposed to it every day. We never knew the dangers of
asbestos. We were never given any protection such as masks. Fresh air was taken
down to the boiler and engine rooms by fan trunking from the upper deck.
When I left the Navy I went
to work at Silcox Animal Feed in Renfrew. I worked as a machine operator and
did not work with asbestos. There was, however, asbestos on the pipes and
boilers. I worked there from 1956-1957.
I then went to work as a
boiler man with Long John Distillers in Glasgow. I worked there for a few
months in 1957 in the boiler rooms. Again the boilers and pipes were lined with
asbestos.
I then went to work at
Templetons' Carpet Factories in Glasgow. I worked there from
1957-1974. I started off working there as a spare man. I would be working in
factories all over Glasgow - about 5-6 of them. I
would run the turbines and work in the boiler rooms as previously described. The
turbines and the boilers would be lagged with asbestos and I was therefore in
contact with it every day. I would also have to remove the asbestos from the
pipes and the boilers when the inspectors were coming. We would be told by the
bosses that the inspectors were coming and we would cut the wires which held
the asbestos onto the pipes and boilers and take the asbestos off. We would use
pliers to cut the wires. We would then put the asbestos into bins until the
inspectors had gone. I think it was white asbestos. Then, depending on how bad
the old asbestos was, we would put it back on the pipes and attach it using the
wire. If the asbestos was no good we would use new stuff. We were never given
any protection.
For a few months in 1974 I
went to work at Beechams in Irvine. Again the pipes and
boilers would have been lagged with asbestos and I would be in contact with it
all day.
Then, for another few months
in the same year, I worked at Coca-Cola in Irvine. Again the pipes and
boilers would be lagged with asbestos and I would be in contact with it all
day.
I then went to work at
Ciba-Geigy in Paisley. I would again be working as a plant operator on the
boilers, turbines, ice plants and effluent. Again the boilers and pipes were
all lagged with asbestos. I would therefore be in contact with it every day. I
believe they are now taking the asbestos away from the factory. I worked there
from 1975-1990."
(ii) John Affleck
[7] Mr
Affleck worked for Templetons from about April 1956 until June 1981. He worked
there as an apprentice, leading hand, chargehand and plant engineer. He worked
in all their factories in the east end of Glasgow, of which there were
approximately six. The factories were in Templeton Street, Fordneuk Street, Tulloch Street, Craignestock, Kerr Street, Bernard Street, and the newest one at
Dixons Blazes. The initial job of the factories was carpet manufacturing, but
they also did their own spinning and washing trains. He was in the maintenance
division, which was concerned with boiler plant, turbines and line shafting.
The boilers generated steam to drive the turbines and heat the factories. The
bulk of the boilers were coal-fired and the newest one was oil-fired. Engine
men operated the turbines and boiler men operated the boilers. The boiler men
had to raise steam, using the coal fire method, to generate power and drive the
turbines. Within the factories the boilers were normally located nearest the
roads for access to coal supplies. One type of boiler, known as the Yarrow, was
50 feet high and consumed 15 tonnes of coal per hour. The boilers, all the
pipework and the turbine jackets were insulated with asbestos. He knew the
deceased, who was initially a spare boiler man and then became stationed in the
Bernard Street factory for the bulk of his
time. In the Bernard Street factory there was a
coal-fired boiler known as a Lancashire boiler, which was a bit smaller than the Yarrow
boiler. The asbestos was disturbed during the annual overhauls which took place
during the Glasgow Fair fortnight. All the purpose-made jackets were taken from
the valves to give access to open up the valves. The jackets consisted of a
canvas cover filled with an asbestos lining of some type. There were a series
of clips on both sides of the cover wired together and they were stripped off
and laid aside. The work was done basically by the maintenance division, but
there were never enough people in the maintenance division for them to go
through everything, so the boiler men and engine men were brought in to help as
general labourers. The deceased was one of the men who helped. If repairs
required to be made to boilers, pipes or turbines at any other time an
assessment was made and another company was brought in to do the work. The
conditions in the boiler rooms were pretty grim. The factories were old and,
apart from coal dust, the boiler rooms had ash, quite considerable amounts of
asbestos which was broken due to wear and tear and poor ventilation. At the
time the workers were ignorant of the danger of asbestos. Access was pretty
poor and occasionally people would walk along the asbestos pipe to gain access
to another boiler. It was the boiler man's responsibility to keep the working
area of the floor clean using a brush and shovel and mops. At that time no particular
measures were taken to suppress dust. After 1975 there was a symposium at Edinburgh University to promote awareness in
industry of the danger of asbestos. After that workmen doing temporary repair
work like taping or painting were instructed to use pressurised masks.
[8] In
cross-examination Mr Affleck explained that his main base was in the Tulloch Street factory but that he moved
around doing maintenance for all the factories. The deceased's base was the Bernard Street factory but as spare man he
moved around other factories. The Dixon Blazes factory was situated in Crown Street and came into operation in
1965 or 1966. It was the biggest weaving section but could not handle spinning,
which was done in the other factories. The deceased worked in the Dixons Blazes
factory for at most a year or a year and a half from the time of its opening
until he left Templetons. He would doubt if there was any asbestos in the
Dixons Blazes factory: it had pre-formed metal clad insulation and boilers. The
deceased qualified as a boiler man but there was no position for him and he
filled in when holidays or sickness occurred. He was a spare boiler man for
about four years before he became a full boiler man, when he spent time first
in the Tulloch Street factory and then in the Bernard Street factory. The
boilers were stoked mechanically from the basement up into the hoppers, the
hoppers fed the grates, the grates were fired off and it was his job to keep
the fire up at the front. The steam pressure would be 250 psi, no less
than 230 or the turbines would slow. The steam was superheated. It was the
deceased's job to make sure there was an adequate temperature and in turn an
adequate pressure. In the Glasgow Fair fortnight the deceased went into general
labouring, working under instruction with the engineers during the annual
overhaul and doing pressure tests at the end of the fortnight. He would
probably have had to remove the insulation round the valves. The steam drums
and the boilers were all covered in permanently sealed asbestos, which was
never taken off. The end drums had manhole covers which could be taken off, but
when they were taken off "the weight of them" could fall and break the asbestos
insulation. That had to be cleared up. At the end of the Fair fortnight an
assessment was made for outside contractors to come in and do repair work: they
would come in and remove the damaged area and do repairs to it. The deceased
never directly got involved in any kind of insulation repair work. When he
worked with the maintenance division during the Fair fortnight he was not in
direct contact with asbestos but it would be in the atmosphere.
[9] In
re-examination Mr Affleck stated that asbestos would have been in the
atmosphere where the deceased was working not just during the Fair fortnight
overhaul but all the time. Asbestos dust would have been in the atmosphere
probably through fair wear and tear and damage by others or possibly some
things falling against the pipework or the boiler work. The deceased and
possibly others were present when the "monkey dung" men were in the boiler room
carrying out an operation involving a mixture of insulation and plaster of Paris which was
mixed up in a bucket, plastered onto the pipework, netted, covered and painted.
That was something that happened "fairly now and then". The deceased had to
climb up and down ladders to look at site glasses to see the water levels in
the boilers and probably had to pass through the area where there was
insulation on the steam drums etc. The floor had to be cleared at the end of
the shift.
(iii) The pursuer
[10] The
pursuer met the deceased in 1956 and married him in 1957. He was a chief stoker
in the Merchant Navy when she met him and, as she put it, "he gave up the sea
for me". He began working for Templetons in December 1957. He went round five
factories as a spare man. He also went to the Dixon Blazes factory when it
opened. He eventually got a stationary place in Dixon Blazes. He stripped the
lagging off the boilers preparing them for inspection. She herself had been in
the Tulloch Street factory and seen round it:
there were lagged pipes all round it.
[11] In
cross-examination she stated that the deceased worked for Templetons from 1957
to 1974 apart from a short period of about a couple of months. For five years
he was a spare man covering all the factories in Bridgeton. After that he worked more
or less in one factory, Tulloch Street. He went to Dixons Blazes
but was in Tulloch Street most of the time. As a
spare man he looked after the boilers and prepared them for inspection, no
matter which factory he was in. He looked after the turbines as well. She
thought he worked in Dixons Blazes towards the end of his employment for over a
year or maybe more, but she did not pay much attention to Dixons Blazes and
could not remember that far back. She knew that boiler inspections happened
frequently. The factory would not be shut down as there were other boilers
running. She surmised that they went on holiday in June.
(iv) Robin Howie
[12] Mr
Howie is an occupational hygienist. He is a graduate of the Institute of Physics (1973) and joined the Institute of Occupational Medicine in 1970. He holds a diploma
in occupational hygiene (1982). His particular areas of interest are exposure
to asbestos, noise and heat. He has done a lot of experimental work on airborne
fibre respiration. He was familiar with the deceased's occupational history.
With regard to the deceased's work in the Royal and Merchant navies, ships were
at that time steam-driven and the pipes were well insulated with materials like
asbestos. Stokers in both the Royal Navy and Merchant Navy were quite heavily
exposed to brown asbestos. There were three forms of asbestos on a ship: (1)
"monkey dung" (a papier-mâché mess); (2) pre-formed sections; and (3) spray
asbestos. Under reference to 6/33 and 6/34 of process, two papers by PG Harries
entitled respectively "Asbestos Hazards in Naval Dockyards" (1968) and
"Asbestos Dust concentrations in Ship Repairing: A Practical Approach to
Improving Asbestos Hygiene in Naval Dockyards" (1971), he stated that the dust
concentration on board ship would have been in excess of 1,000 fibres per
millilitre. The deceased would probably have been exposed to dust from others
working with lagging and from lagging in the general environment. Dust was
generated through vibration from machinery and general repairs. Everyone was
exposed to asbestos dust from the activities of other individuals. The second
paper, 6/34 of process, was the gold standard of the period and table 5 on page
246 summarised asbestos dust concentrations in miscellaneous processes
associated with pipe lagging. Harries measured dust concentrations during
deliberate disturbance of asbestos within ships. He measured the levels in both
the operative and general environments. Removing asbestos covers would generate
between 100 and 500 fibres per cubic centimetre. The concentration would be low
from sweeping the boiler room daily, from broken and brittle insulation and
from climbing ladders and walking along pipes.
[13] In
cross-examination Mr Howie stated that he would expect a high level of dust to
be generated from the re-fitting of naval vessels as the asbestos had to be
removed. He would judge anything above 50 fibres per millilitre as being
high. As lagging on hot pipes became dry and pliable it had to be broken in the
process of removal. He estimated the deceased's exposure as 50-100 fibres
per cubic centimetre when working directly with asbestos.
The background
to the medical evidence
[14] Before
I turn to look at the medical evidence it is appropriate to consider the
history of the deceased's illness as provided by himself in his signed
statement and by the pursuer in her evidence.
[15] In his
signed statement 6/23 of process, in addition to what he said about his health
in the first three paragraphs in the excerpt quoted above, the deceased stated:
"Since being diagnosed with
asbestosis I have gone down from over eleven and a half stones to under nine
stones. I have to use oxygen and can't walk far at all. Even going from one
room to another in the house is a struggle. We have had a chair lift put in and
that helps a bit although I still have three stairs to go up when I get to the
landing. I can now do nothing around the house. I used to help my wife with
jobs around the house and now I can't. My wife does all the housework and
cooking. My sister-in-law helps with the shopping as my wife is not able to
leave me for a long time. I used to enjoy doing a lot of joinery and woodwork.
I do not have the energy to do this any more. My wife has to take care of me
completely - she washes and clothes me. She helps with my medication and the
exercises the hospital have given me to help clear the fluid from my lungs."
[16] The
pursuer stated that when the deceased worked in Ciba-Geigy he travelled to work
by bicycle and when he was breathless she used to follow him out of the house
at 4.45 am. She remembered his having been breathless when they
went on holiday in about 1985. He retired in 1990. Before that she had to go to
the doctor with him because he was so breathless. When they moved to
Thornliebank in about 1996 he was not well at all. He lay at the radiator with
pains in his back. He used to be good at DIY but he became unable to do it. He
suffered from pernicious anaemia. She had to bathe him as he was not able even
to wash himself. When she got him downstairs in the house (in 1998) he would
just sit on the settee. He coughed, but not a lot. He had pains and was very,
very breathless. In October 1998 he was admitted to the Victoria Infirmary for
over three weeks. The doctors had a consultation and all said to her that he
was suffering from asbestosis. When he got out of hospital he could not do
anything for himself. He was bedridden. He used oxygen cylinders until provided
with a machine. Nurses came in to see him once a week. When he died she thought
he did not weigh even eight stones. In cross-examination the pursuer explained
that the deceased had trouble breathing from the time of his retirement until
his death.
[17] The GP
records are 7/4 of process. They cover the period from 22 February 1978 until the deceased's death. The entries show that the
major conditions from which he suffered were noise exposure hearing loss from
1985, angina and pernicious anaemia from 1987 and tinnitus from 1983. On 29 September 1989 he was admitted for four days to the Royal Alexandra Hospital in Paisley with severe chest pain
suggestive of angina and the discharge letter (page 63) stated that chest x-ray
was normal. A letter to the GP from a consultant physician and cardiologist at
the Victoria Infirmary dated 30 March 1990 (page 60) stated that his chest was clear. An entry
by the GP on 18 December 1995 stated: "X3 chest pain
'sharp' secs only after chest infection - nil since Thurs, chest clear." On 1 February 1996 the GP wrote: "Flu-type symptoms -chest tightness,
cough with dark yellow sputum (1/52). Chest poor AE but nil focal." On 16 February
1998
the entry reads "Unconscious episodes for a few moments over the last 6/12". On
22 October 1998 the GP was called to see
him as an emergency after he had had central sharp chest pain overnight. The
entry recorded that he had had influenza the previous week, that he was sweaty,
coughing and suffering from shortage of breath. He was admitted as an emergency
to the Victoria Infirmary and was an in-patient there until his discharge on 13 November 1998. The discharge letter from a specialist registrar in
Gastroenterology dated 18 November 1998 (pages 32-33) stated that he had
been admitted with episodes of severe chest pain associated with some dyspnoea
with a questionable pleuritic component which had been persisting for some
months but which had been worse in the two days prior to admission. The letter
went on to state as follows:
"He remained symptomatic and
it was difficult to distinguish how much of his symptoms related to ischaemic
heart disease and how much related to respiratory disease. It was felt that his
chest x-ray appearances could relate to pulmonary fibrosis and as he had a
greater than 10 year history of exposure the question of asbestosis and
pulmonary fibrosis was raised.
An Exercise Tolerance Test
was performed which was discontinued after 1 min 28 secs because of severe
chest pain and shortness of breath without changes in his ECG. His CT scan
suggested possible asbestosis with interstitial fibrosis and his pulmonary
function test showed a restricted defect."
On 10 February 1999 Dr D R H Vernon, Consultant
Physician in Respiratory Medicine at the Victoria Infirmary, wrote a letter to
the GP (page 27) which contained the following statements:
"I saw your patient at the
Chest Clinic. He seems to be waiting for an assessment re DSS claim for
asbestosis..... His CT scan is strongly supportive of that diagnosis. There is
pleural thickening, pleural plaque formation with some calcification and
interstitial fibrosis. Of course he also has the occupational exposure to
asbestos......
Finger clubbing is present
and there are bilateral basal inspiratory crackles on auscultation."
[18] On 14 July 1999 Dr Vernon wrote a letter to the GP containing the
wrong GP's details and the wrong address and date of birth for the deceased,
but which clearly related to the deceased. The letter related to the deceased's
claim for benefits. In it Dr Vernon stated:
"I saw your patient and his
wife at the Chest Clinic. He is as you know trying to get some compensation for
his pulmonary fibrosis, is likely to be asbestos (sic). He has a history of exposure and he has evidence of asbestos
related pleural plaques. It seems much less likely that he has a coincidental
cryptogenic fibrosing alveolitis. He does not have any evidence to suggest that
it is related to arthritis. RA factor and ANA are negative and I do not think
he has overt evidence of arthritis. He does have finger clubbing of course and
he certainly has basal crackles on auscultation.... He additionally has
significant ischaemic heart disease and has had a previous bypass graft."
On the same date Dr Vernon wrote to the pursuer about
the deceased's benefits claim in the following terms:
"Further to our conversation
at the Hospital clinic, I write to confirm that my clinical feeling is that it
is likely that your husband has asbestosis. He has an occupational history
which suggests exposure to asbestos. He has evidence on his x-rays and CT scan
of asbestos related plaque formation and he has evidence of pulmonary fibrosis.
It seems that the medical adjudicator felt that the total history of asbestos
exposure was not adequate to cause asbestosis but that it could account for the
pleural plaques. Whether that is the (sic)
sustainable argument or not I do not know but I am sure that Thomsons would
advise you. I would have thought on a balance of probabilities that the most
likely cause of his fibrosis is his occupational asbestos exposure."
The clinical
evidence
(i) Dr Jill Fowlie
[19] Dr Jill
Fowlie (39) was the deceased's GP. The deceased became her patient on 21 October 1995, when she noted his past medical history (7/4 of
process, page 48). She saw him relatively infrequently until his acute
admission with chest pain on 22 October 1998 and thereafter increasingly
frequently. She saw him at home on 19 November
1998,
a week after his discharge from hospital, and noted bilateral course basal
crepitations. She saw him again on 30 November
1998
when she noted that he had worked for Templetons' Carpet Factory and had a
discussion with him about asbestosis following upon the above letter of 18 November 1998 from the specialist registrar. Under reference to
that letter she explained that 1 minute 28 seconds for an exercise
tolerance test was not very good. She personally had not thought that the chest
pain from which he was then suffering was typical of angina. On 21 December 1998 there was recorded a request for a wheelchair for the
deceased, presumably because he was breathless. By April 2000 he was terminally
ill and died in hospital. In cross-examination Dr Fowlie accepted that the
deceased had gone from being able to go to the surgery to death in 18 months.
(ii) Dr Gavin Boyd
[20] Dr
Gavin Boyd (64), a consultant physician with a special interest in respiratory
medicine, who had retired from the National Health Service three years
previously, was led as a witness for the pursuer. He had, along with Dr Frank
Moran, established the Cardio-Pulmonary Laboratory at Glasgow Royal Infirmary.
He had considered the GP and hospital records, the post-mortem report, the
statement of the deceased and the reports from the other consultant medical
witnesses, but not the x-rays, and produced his reports 6/4 and 6/16 of
process. He began by explaining the features which a physician looks for to
diagnose asbestosis. The crucial first step was a significant degree of
exposure to asbestos. Then he looked for the symptomatic evidence, namely, a
shortage of breath and restriction of respiratory function and mobility.
Occasionally there was a cough and a small number of patients developed
clubbing of the fingers. As the disease progressed an examination of the lungs
revealed crackles. Radiological examination would disclose fibrosis and damage,
bilateral in the lower lobes and encroaching on other areas as the disease
progressed. Where the patient survived for a period there would be pleural
changes and evidence of asbestos bodies in the lung.
[21] Dr Boyd
then went through the deceased's GP records. The deceased had a clearly
documented history of ischaemic heart disease from 1966 when he had been
admitted to hospital with chest pain. In 1987 he had had an acute ischaemic
incident. When re-evaluated in 1991 he had unequivocal evidence of ischaemic
heart disease with symptoms of a varying nature. He had a problem with
restriction of breath and of activity. He was cycling to work with shortage of
breath, which meant he was capable of reasonable activity. His deafness was
evaluated. His cardiograph was normal on exercise (later borne out by the
post-mortem findings of recanalisation). He had evidence of chest infections
from 1991 onwards and had been prescribed a broncho-dilator, although it was
not clear why. In 1995 he had claudication, discomfort in the legs on walking
due to lack of blood supply. On 29 November 1995 he had a chest infection
which was treated by Augmentin. This was a short-lived episode of chest pain.
He received regular injections for pernicious anaemia. When the GP saw him on 22 October 1998 she thought he had an infection. Dr Boyd did not
think that any of the previous medical history could be related to lung
fibrosis. The deceased had had recurring episodes of angina and lung
infections. He cycled to work and "had to be dragged to the doctor". He could
well have underplayed the severity of his problems. While shortage of breath
could be linked with lung fibrosis, chest pain could not.
[22] Dr Boyd
then referred to his first report dated 12 August 2001 (6/4 of process), which
concludes with his opinion, the last sentence of which reads: "It is my
opinion, on a balance of probabilities, that the overall findings in this case
are consistent with a diagnosis of asbestosis rather than the other types of
interstitial pulmonary fibrosis such as cryptogenic fibrosing alveolitis." The
deceased had had constant but low grade exposure to asbestos. That was very
important as it offered an explanation for the fibrosis. He had pleural plaques
and pleural thickening. He had all the features of lungs damaged by the
fibrotic process. The global picture was one of asbestos exposure, asbestos
damage to the lungs, fibrosis and elevated (although not greatly) asbestos counts.
The interesting thing was how rapidly his condition had progressed, but it was
not known for how long the fibrosis had been established: it could have been
undetected at a lower level for quite a long time.
[23] Dr
Boyd, after reviewing reports from the defenders' experts, produced a
supplementary report dated 12 May 2004. The last two paragraphs of
his opinion in that report read as follows:
"This man had a history of
low level but repeated exposure to asbestos over many years and evidence of
widespread pulmonary fibrosis identified clinically, radiologically and
histo-pathologically. The diagnostic criteria for asbestosis were satisfied.
There was also evidence of asbestos-related pleural disease. Cryptogenic
fibrosing alveolitis is a disease which is associated with inflammatory
fibrotic changes in the lung where the cause is unknown.
In the context, therefore,
of a long occupational history of exposure to asbestos, the presence of
asbestos-related pleural disease, the histo-pathological and clinical features
in keeping with a diagnosis of asbestosis together with the radiological
appearances that, in my view, favour asbestos-related abnormalities rather than
features of cryptogenic fibrosing alveolitis, it remains my opinion, on a
balance of probabilities, that this man suffered from asbestosis as a result of
the occupational exposure to asbestos material during the course of his working
life."
He thought that the fibrosis must have been
established sometime before October 1998, when the deceased was admitted
to hospital. As he put it, "you can live with a problem in the lung until it
catches up with you". The patient could compensate until there was no spare
left to compensate with. By October 1998 there was something seriously wrong as
there was a major clinical deterioration and there were major pathological
abnormalities. The fibrosis must have been established sometime before
then. He accepted the view of the
defenders' respiratory physician Dr Crompton in his report (7/29 of
process, page 3) that rapid progression to death within two years of diagnosis
of pulmonary fibrosis was a point in favour of a diagnosis of CFA. In his view
CFA had a history of moving to fatality within five years of diagnosis. The
main question was, why did the deceased deteriorate so rapidly? He believed it
was because of the long-standing damage to his lungs. The presence of asbestos
bodies in the lungs was supportive of asbestos-related disease. If the levels
of asbestos bodies in the deceased were increased, he felt comfortable with a
diagnosis of asbestosis. He did not believe that asbestosis could be excluded
if the level of asbestos bodies in the deceased was not significantly
increased.
[24] In
cross-examination Dr Boyd accepted that the first time fibrosis of the lungs
entered the diagnostic frame was in October 1998. From 1987 onwards the
deceased's chest had been noted to be clear on repeated examinations. The entry
"chest clear" was a factor against crackles, but the significance of sparse
crackles might not have been recognised. Crackles were an early sign of
fibrosis. Viewed alone, they developed in this case sometime after 1995-6.
Evidence of disease was present after 1995-6. There was nothing in the
evolution of the deceased's problems to show that something had gone wrong with
his lungs till October 1998. The progression of the clinical problem thereafter
advanced rapidly, as indicated by the letters from Dr Vernon in the GP
records throughout 1999 and early 2000. He was not so sure that the fibrosis
was deteriorating rapidly. He believed that there were other factors aiding the
deceased's decline as well as the progression of pulmonary fibrosis. He
accepted that the rapid development of CFA was a feature for differential
diagnosis. Over 90% of patients with CFA had finger clubbing, fewer with
asbestosis. In the literature there were one or two cases of rapidly advancing
fibrosis which was asbestosis. He thought that it might not be correct to
isolate the feature of rapidity of progression of the disease, but accepted
that CFA advanced more rapidly than asbestosis. Heavy exposure to asbestos
superimposed on individual susceptibility could lead to a rapidly advancing
disease. There were variables. You had to be careful about how you related
epidemiological evidence to the individual. We would not be debating the issue
if it were clear cut. The deceased had evidence of a raised and significant
number of asbestos bodies. He accepted he did not mention infection in his
supplementary report, but it was an issue which emerged from his own experience
of dealing with cases of pulmonary fibrosis. He saw the deceased's decline as a
mixture of fibrosis and infection. The mention of infection was a development
of his view on further reflection by him. He did not consider infection crucial
but was just trying to insert an element of caution into the view that the
deceased's decline was all attributable to pulmonary fibrosis. He had never
come across a case of asbestos where there had been 20-25 years from the last
exposure to asbestos and 18 months from diagnosis to death. He was aware there
was a latency period. He went along with the concept that a certain level of
exposure to asbestos was needed to cause asbestosis and also that the level of
exposure affected the severity of the condition. There was a shift away from
the view that fibrotic changes ceased with exposure. In general you would
expect that the longer the period from the last exposure the slower the disease
would progress. He had not had a case where asbestosis had progressed slowly,
then rapidly. He would not expect asbestos-related conditions to develop in a
florid form late on, but there had been cases where they had. There was
spectrum of clinical responses and some cases could be extreme. Fibrosis which
appeared 20 years after the last exposure to asbestos was not typical of
asbestosis, but clearly it could occur. He thought that in this case the
fibrosis would be expected to become apparent before the 1990s.
[25] Dr Boyd
was referred to the following sentence in the report of his former colleague Dr
Francis Moran, a consultant in respiratory medicine and witness for the
defenders, dated 29 May 2004 (7/9 of process, page 4):
"Fibrosis occurring in or
around 1998, progressing as rapidly as did that of Mr Wright and
accompanied by gross finger clubbing, is incompatible with a diagnosis of
asbestosis but is entirely compatible with a diagnosis of cryptogenic fibrosing
alveolitis."
He disagreed with the definitive view there expressed
by Dr Moran. He relied upon the occupational history of asbestos exposure and
the asbestos bodies found in the deceased's lungs. He thought the latency
period could well extend to 30 years, but beyond 30 years was stretching it.
Pleurisy had a time lag of 30 years. In his experience green glass appearances
on CT scan were not indicative of any particular disease process, but were
common in CFA and uncommon in asbestosis. They were more in keeping with CFA,
but the deceased had not responded to steroid treatment and that would shade the
argument away from CFA. On his interpretation as a clinician over 40 years
pleural thickening was more a feature in asbestosis. He thought the asbestos
exposure to which the deceased had been subjected could be described as low
grade exposure over many years. Under reference to the reports (6/5, 6/6 and 6/7 of process) from Dr Rodney
Burnett, a consultant histo-pathologist led for the pursuer, he accepted that
asbestos body counts in cases of asbestosis are usually extremely high. The
asbestos body count in cases of asbestosis was greater than in cases of pleural
plaques. His own position was set out in the opinion expressed in his
supplementary report and quoted above. He disagreed that a low asbestos body
count favoured a diagnosis of CFA as asbestosis had been recorded without the
presence of asbestos bodies. The presence of asbestos bodies very firmly
weighed the diagnosis in favour of asbestosis. As a physician he had grave
difficulty with another diagnosis in this case. He was not in a position to comment
on the expected fibre count. He would use the fact that they were at a raised
level as possible support for an asbestos problem. The literature indicated
that if you found asbestos bodies in the lung that moved the diagnosis away
from CFA. The level of asbestos bodies in the lung in asbestosis need not be
very high - it could be low or even absent.
[26] In
re-examination Dr Boyd was referred to an entry in the medical records dated 23
October 1998 (the day after the deceased's acute admission to hospital) which
stated "chest clear this am" (bilateral crepitations having been noted the
previous day) and stated that that bore out what he had been trying to explain,
that the level of crackles would vary from time to time. In the hospital records of 14 April 1999 there was an entry stating "CT scan shows plaques and
fibrosis". An entry of 14 July 1999 stated "possible
coincidental CFA".
(iii) Dr Graham Crompton
[27] Dr
Graham Crompton (69) was a respiratory physician led on behalf of the
defenders. He had been a consultant physician in the Respiratory Unit at the Western General Hospital, Edinburgh from 1969 to 1999 and a
part-time senior lecturer at Edinburgh University for the same period. His
reports are dated 10 April 2002 and 10 September 2004 and are respectively 7/5
and 7/29 of process. The first report was a short one based exclusively upon an
examination of the deceased's hospital records from the Victoria Infirmary. In
it he stated as follows:
"Investigations revealed
radiographic evidence of bilateral pleural plaques (CT scan and ? chest
x-ray) and also pulmonary fibrosis. The pulmonary fibrosis was, understandably,
thought to be asbestosis because of the bilateral pleural plaques. However, the
Benefits Agency did not accept a diagnosis of asbestosis apparently because it
was thought that the history of asbestos exposure was insufficient to cause
asbestosis.
The alternative diagnosis to
explain the pulmonary fibrosis was cryptogenic fibrosing alveolitis in a man
who had pleural plaques caused by the inhalation of asbestos fibres. The
chances of anyone developing asbestos-related pleural plaques and the rare
condition of CFA are very small, but this man's disease apparently progressed
very rapidly and he died on 20.04.2000. Such a rapid disease progression is
much more in favour of CFA than asbestosis, and therefore it is entirely
possible that this poor man had CFA and also had evidence in the form of
pleural plaques of previous asbestos exposure......
...... Since the relatives
requested an autopsy .......... I would expect that an asbestos fibre count per gram
of dried lung tissue must have been performed. This would almost certainly
distinguish between asbestosis and CFA."
[28] In his
second report, having read Dr Boyd's second report, the radiological report of
Dr Sproule and the pathology reports of Drs McFarlane, Burnett, Thomas and Gibb
(referred to below), he expressed the opinion that on the balance of
probabilities the clinical, radiographic and pathological evidence made a
diagnosis of CFA in a man who had coincidental asbestos-related pleural plaques
very much more likely than asbestosis. The basis of that opinion is set out in
the body of his report as follows:
"Points in favour of a diagnosis of asbestosis
·
History of asbestos exposure
·
Pleural plaques with some calcification detected by x-ray and
CT scanning
Points in favour of a diagnosis of cryptogenic fibrosing
alveolitis
Rapid
progression of disease to death within two years of a diagnosis of pulmonary
fibrosis being established.
·
Scanty asbestos bodies found by pathological examination of
lung tissue in a man known to have been exposed to asbestos.
·
An amphibole fibre count of 1.21 million fibres per gram of
dried lung. This count is just above the background level, and was expected in
a man with a history of asbestos exposure, but some 50 times less than one
would expect if the diagnosis was asbestosis.
·
I believe that there are occasional cases of rapidly
progressing asbestosis but as far as I am aware this only occurs within a few years
of massive exposure to asbestos. In these cases on would expect to find
numerous asbestos bodies and very high amphibole fibre counts."
[29] In his
oral evidence Dr Crompton explained that asbestosis was fibrosis of the
interstitial tissues of the lungs caused by the inhalation of asbestos fibres.
CFA was formerly known as interstitial pulmonary fibrosis, a term which
involved lots of diseases of different aetiology. CFA was an entity in itself
and was inflammation of the alveoli (the little air sacs or balloons at the end
of the tubes known as the broncheoli) leading to fibrosis. Its cause was
unknown. CFA was rare but not extremely rare. When he worked at the Western General Hospital they had a register of
semi-rare diseases and there were 15-20 cases of CFA annually in south east Scotland. In CFA patients died quite
quickly after the diagnosis was made. It was estimated in 1995 that it was
responsible for 1,500 deaths a year in the UK. He personally had seen
many more patients with CFA than with asbestosis, which was more common in the
west of Scotland. CFA and asbestosis had
common features. They started in the bottom of the lungs. It was not possible
at that stage to differentiate between them clinically. The progression in the
two diseases was different: in CFA death occurred within five years, no matter
what treatment was given. The pathology of the two diseases was different: in
asbestosis asbestos bodies were found quite easily, whereas they were rarely
found in CFA. When he wrote his first
report he was unconvinced that the deceased had asbestosis and therefore
decided to wait for the pathology. Dr Gibbs' laboratory in Cardiff was a reference laboratory
for the UK and he had a tremendously
good reputation. As the deceased had bilateral pleural plaques and there was no
cause of them other than asbestos, he must have been subjected to asbestos
exposure, but he could not say what the amount or degree was.
[30] Dr
Crompton was then referred to entries in the GP and hospital records and to Dr
Boyd's report. He explained that crepitations (referred to by the Americans as
"Velcro crackles") came on at an early stage in both conditions before changes
were visible on chest x-ray. On a consideration of the GP records, he thought
it was highly unlikely that the deceased had any form of interstitial fibrosis
in 1990. Entries in the GP records showed that his chest was clear on 20 March 1990, on 27 January, 30 March and 7 April 1992 and 18 December 1995. The fact that on the last
date he had chest pain lasting for seconds only was not of any significance. If
there had been any pathology the pain would have lasted for some time. It was
highly unlikely that he had any form of interstitial pulmonary fibrosis then as
"you do not get chest pain coming and going with interstitial pulmonary
fibrosis: once there, it's there all the time". In relation to the entry of 1 February 1996 which mentioned sputum, "you don't expect dark yellow
sputum in interstitial disease". If at that time the deceased had had
established pulmonary fibrosis one would have expected the GP who listened to
the back of his chest to hear crackles. He must have had finger clubbing for
some time prior to October 1998, probably in 1997. Clubbing came on at an early
stage in fibrosis, but he could not say if it appeared before crackles. It
appeared in 50% of patients with CFA and in under 50% of patients with
fibrosis. He read Dr Vernon's reference to "evident finger clubbing" as meaning
that it was gross. He thought that the
deceased's CFA commenced somewhere between 1995 and 1998. He could not say
anything more than that, except that if the GP was correct that the chest was
clear on 18 December 1995 then the onset would maybe
have been between 1996 and 1998. The progress in this case was rapid even for
CFA: it was on the rapid end of the CFA scale. It was extremely unlike any case
of asbestosis he had ever heard of. He expected asbestosis to progress slowly
over 15 to 25 years. The progression of the disease here was atypical of
asbestosis. He relied heavily on the rapid progression of the disease as
tilting the diagnosis in favour of CFA (see W R Parkes, Occupational Lung
Disorders, 3rd Ed, 1994, 7/19 of process, which he described as "the
gospel of occupational medicine as far as clinicians are concerned"). He would
expect some asbestos bodies to be present in the lung tissue because there were
pleural plaques. Had this been a case of asbestosis, then, from what he read in
the books, he would have expected the asbestos fibres to be abundant. Sparse asbestos
bodies would favour CFA rather than asbestosis. He believed the deceased died
of CFA, not asbestosis. So far as Dr Boyd's opinion (6/16 of process, para 10
of review) on the radiological findings was concerned, it was not in the least
against a diagnosis of CFA. He had seen ground glass opacification on the CT
scan and it was very much more common in CFA.
[31] In
cross-examination Dr Crompton accepted that there were only two possible
diagnoses in this case - asbestosis or CFA. With regard to Dr Vernon's
diagnosis, he would have liked to have asked Dr Vernon for his opinion when the
deceased died 6 months later after a very rapid progression. It was
accepted that pleural plaques were indicative of a very significant asbestos
exposure. There was no other cause for pleural plaques. A diagnosis of
asbestosis would not be made without the presence of pleural plaques. Under
reference to literature put to him by Mr Marshall (7/14 of process) he stated
that he had not appreciated that slightly more people with asbestosis had
ground glass appearance on CT scan. None of the asbestos-related diseases
produced cough, sputum or wheeze until an extremely late stage. The deceased's
bronchial problems recorded in the GP notes related to flu. His breathlessness
pointed to heart disease. There was no evidence of anything other than heart
disease as a cause prior to 1998. The post-mortem report showed that he had
complete occlusion of one of his coronary vessels, which had recanalised. All
people with coronary artery disease got tightness of the chest and shortness of
breath. He did not think these symptoms indicated that the deceased had early
fibrosis. The fact that the deceased's chest was clear on repeated examinations
prior to October 1998 virtually excluded fibrosis before then. There was no
finger clubbing until early 1999. He thought the disease process commenced from
1995-6 onwards and was recognised at the acute episode which occurred in
October 1998. There was no evidence that the disease process commenced before
1995-6. There was x-ray evidence in 1992 that fibrosis was not present, and if
it did not show up on a lung x-ray it would not cause shortness of breath. With
regard to crackles, they were heard on the day the deceased was admitted to
hospital, 22 October 1998. The doctor who examined
him in hospital the following day and noted "Chest clear this am" did not hear
the crackles, but they were back again two days later on 25 October 1998.
[32] In
re-examination Dr Crompton said that some workers exposed to asbestos got no
lung problems, while others did. The deceased's lung problems arose many years
after he was exposed to asbestos. Had his disease been asbestos one would have
expected it to have appeared very much earlier. There was no ready explanation
for the "chest clear" entry on 23 October 1998, but it was possible that
fluid in the lungs masked the crackles. Fibrosis of the lungs could not cause
chest pain - full stop. Nor could it cause intermittent shortage of breath.
Once fibrosis was established the patient had some degree of shortage of
breath, and it then got worse and worse. Gross finger clubbing was rarely seen
in asbestosis. The change in the deceased's finger clubbing described by Dr
Vernon in the notes reflected the rapid progression in the fibrosis itself.
Pleural plaques did not change into something else or cause something else.
They showed that there had been exposure to asbestos. There was no reason why a
man with pleural plaques or pleural thickening could not have some unrelated
lung disease. A letter of 15 February 2000 from Dr Vernon referring to
"pulmonary fibrosis of whatever cause" indicated that he was less certain than
when he had formerly thought that it was asbestosis.
(iv) Dr Francis Moran
[33] Dr
Francis Moran was a consultant physician at Glasgow Royal Infirmary until his
retirement in November 1994. He was in administrative charge of the Department
of Respiratory Medicine at Glasgow Royal Infirmary and Belvedere Hospital from 1982 and of the Second
Floor Medical Unit at Glasgow Royal Infirmary from 1980. He was called as a
witness for the defenders. He had produced three reports, 7/9, 7/30 and 7/31 of
process, dated respectively 29May, 28 July and 13 August
2004.
At the time of his first report he had not seen the x-rays or CT scan. The
conclusion which he expressed in his first report was that the deceased's death
was caused by terminal aspiration pneumonia occurring in the presence of, and
partly as a result of, apparently severe and diffuse end-stage pulmonary
fibrosis caused by cryptogenic fibrosing alveolitis. He could not exclude a
possible contribution from 1998 onwards to his general deterioration and the
terminal event. He added to that in his evidence by stating (as he did in an
earlier passage of his report quoted above) that the rapidity of the
progression of the disease in this case was completely incompatible with
asbestosis. If the deceased's first exposure to asbestos was in 1943, then his
comment had even more force. It was the first, not the last, exposure to asbestos
that mattered. Asbestos caused fibrosis by remaining in the tissues for a long
time, causing an inflammatory reaction. The greater the exposure in a person
who had developed asbestosis, the more advanced the degree of fibrosis was
likely to be. There was generally a relationship between the number of fibres
found (on lung tissue examination) and the degree of exposure. There was not a
good correlation between the intensity of exposure and the appearance of
pleural plaques. Plaques became more and more visible on x-ray or CT scan as
the years went by due to calcification, and new plaques appeared. He was taken
through the hospital records and stated that they provided no evidence of
crackles in the lungs before 1995-6. So far as the "chest clear this am" entry
on 23 October 1998 was concerned, one could
only speculate on the accuracy of the observation. The chest x-ray taken around
that time showed fibrosis. It was unlikely crackles would disappear and come
back again in a case of established fibrosis. The precise mechanism of crackles
was controversial, but it was the fibrosis itself which caused the crackles. It
was likely that the deceased had a combination of problems. (Later in
cross-examination he stated that if the patient was in pain and could not take
a deep breath it may be difficult to hear crackles.) The evidence of very rapidly progressing
finger clubbing was absolutely consistent with CFA and inconsistent with
asbestosis. The only other condition that would cause that degree of finger
clubbing was a lung tumour.
[34] In his
second report Dr Moran commented on the x-ray and CT scan films. He expressed
the opinion that the CT scans confirmed the presence of bilateral calcified
pleural plaques consistent with occupational exposure to asbestos beginning
more than 30 years before 1998 and of extensive bilateral interstitial fibrosis
of the lungs, the appearances of which, including the possible component of
alveolitis, were entirely consistent with the diagnosis of CFA made by him and
others on the basis of the clinical history and pathological findings. He added in evidence that he would not expect
alveolitis in a case of asbestosis.
[35] In his
third report Dr Moran dealt with Dr Boyd's second report and the pathological
findings of Dr Gibbs. Commenting on the latter, he stated that "Dr Gibbs'
finding in this case of an asbestos fibre count approximately 1/50th
of that to be expected in a case of asbestosis leaves, in my opinion, no room
for doubt......Dr Gibbs' department has a probably unsurpassed experience in
this field." He went further in his evidence when he stated "I believe Dr Gibbs
is the world expert in this field".
[36] In
cross-examination Dr Moran stated that he would not expect alveolitis in
asbestosis but that it is an active feature in CFA, although he would not be
surprised to find that someone had described a small amount of alveolitis in
asbestosis at one point or another. The deceased's negative chest examination
was the one consistency throughout his medical records. He would expect always
to find crackles in association with pulmonary fibrosis. Finger clubbing was
more common in CFA than in asbestosis and occasionally preceded it. In
asbestosis there was less finger clubbing and it occurred late on. His guess
would be that fibrosis was present from maybe late 1996, but maybe not because
it was known that it was rapidly progressing. One possible cause of
breathlessness from 1985 onwards was fibrosis.
[37] The
last statement was immediately retracted by Dr Moran in his first answer in
re-examination when he stated that the medical records did not support fibrosis
from 1985 onwards as they did not record progressive breathlessness from any
cause, and he would have expected it to have been picked up had it been
present. Pain in the chest, which was also present, was not normally associated
with fibrosis.
The
radiological evidence
[38] Only
three radiological films of the deceased were taken - two x-rays, one on 22 October 1998 and one on 29 October
1998,
and a CT scan on 5 November 1998. The radiological evidence
related to what was found on these films.
(i) Dr Michael Sproule
[39] Dr
Michael Sproule (38) was a consultant radiologist at the Western Infirmary and Gartnavel Hospital in Glasgow with a particular interest
in chest radiology. He was led as a witness on behalf of the pursuer. He had
examined the three films of the deceased's chest and produced a report 6/14 of
process. He set out a summary of his findings in his report as follows:
"1. There are focal areas of
pleural thickening in both hemithoraces, some of which contained calcification.
In some areas the pleural thickening has an irregular outline and is therefore
consistent with thickening of the subpleural interstitium caused by pulmonary
fibrosis. However, in other areas the outline is smooth and is consistent with
parietal pleural thickening due to previous asbestos exposure.
2. There is moderately
severe pulmonary fibrosis in both lungs with relative sparing of the apices.
Given the presence of benign pleural plaques the appearance is suggestive of
asbestosis. However, it is not possible on CT scanning alone to ascertain
aetiology of pulmonary fibrosis with any certainty. The appearance could
therefore be due to cryptogenic fibrosing alveolitis with coincidental pleural
plaques due to previous asbestos exposure."
He explained in his evidence that his findings of lung
fibrosis were not specific to any aetiology: there were no lung features
specific for either CFA or asbestosis. He thought asbestosis the likeliest
cause because of exposure, which he described as the single most important
factor, and pleural disease.
[40] The
x-ray of 22 October 1998 showed both lung fields to
be grossly abnormal. This was a non-specific finding, but consistent with
pulmonary fibrosis. There was ground glass shadowing present, that is, a
veil-like density partially obscuring the pulmonary vessels. There was also a
reticular abnormality (a lace-like pattern consistent with underlying lung
fibrosis) present in both lungs, particularly in the mid and lower zones. The
second x-ray, taken on 29 October 1998, was a portable film not
directly comparable with the first, but showed no difference in the lungs from
the first. It was easier to see the reticular abnormality in the second than in
the first x-ray. His findings on examination of the CT scan were stated thus in
his report:
"The subpleural parenchyma
of both lungs is abnormal. The lower zones are the most severely affected with
relative sparing of the apices. There is a prominent reticular abnormality,
ground glass shadowing and early honeycomb formation. The appearance is typical
of moderately severe pulmonary fibrosis. The prominent ground glass opacity
suggests an element of active alveolitis."
[41] In
cross-examination Dr Sproule stated that only the pleural plaques pointed
reliably in the direction of asbestosis rather than CFA. The type of exposure
was more important than the amount. The latency period for asbestosis was
probably from at least ten years up to 40 years from exposure to asbestos.
Active alveolitis was more common in CFA than in asbestosis (70% as opposed to
50%). On being referred to the opinion expressed by Dr Wightman in his report
that, while honeycomb shadowing was quite commonly present in the late stages of
asbestosis, it was usually accompanied by prominent parenchymal bands, he
accepted that the parenchymal bands in this case were "not pronounced" and "not
a prominent feature", but did not think they were a reliable discriminator for
either asbestosis or CFA. He thought an absence of bands would be more
suggestive of CFA.
[42] In
re-examination Dr Sproule referred to two statements in the abstract of the
article 7/36 of process ("High resolution computed tomographic assessment of
asbestosis and cryptogenic fibrosing alveolitis: a comparative study"), namely:
(1) "Band-like intra-pulmonary opacities, often merging with the pleura,
were seen in 19 patients with asbestosis but in only two with cryptogenic
fibrosing alveolitis." and (2) "Pleural thickening or plaques were seen in 21
patients with asbestosis and in none with cryptogenic fibrosing
alveolitis."
(ii) Dr Arthur Wightman
[43] Dr
Wightman (62), a witness for the defenders, was a consultant radiologist with
special responsibility for chest and ENT radiology at the Royal Infirmary of
Edinburgh since 1 April 1975. He had also examined the
three films of the deceased's chest and produced his report 7/32 of process. He
concluded that the deceased's interstitial fibrosis showed certain radiological
features that supported the strong clinical and pathological evidence for CFA
rather than asbestosis. After stating that there were bilateral pleural plaques
typical of plaques arising from previous asbestos exposure, he expressed his
opinion on the radiology as follows:
"The CT scan shows evidence
of interstitial fibrosis. Two radiological features favour CFA over asbestosis
as the cause for this. First, 'ground glass' change is rare in asbestosis and
common in CFA. In interstitial fibrosis it signifies the presence of active
alveolitis, and this was confirmed on the histology of the post mortem lung
(page 2 of Dr Thomas's report of 4 February 2003). Second, while honeycomb
shadowing is quite commonly present in the late stages of asbestosis, it is
usually accompanied by prominent parenchymal bands. In this case the pronounced
honeycomb shadowing is accompanied by sparse bands only, a feature more in
keeping with CFA."
He went on to express the opinion that the deceased's
rapid progression so long after his first exposure to asbestos was inconsistent
with asbestosis and that examination of the histology showed an asbestos body
count significantly below that associated with asbestosis.
[44] In his
oral evidence Dr Wightman stated that he had seen Dr Sproule's report and the
deceased's hospital records. The plaques in the pleura were consistent with
exposure to asbestos. The pleural thickening was secondary to fibrosis, not
restricted to asbestosis and therefore could not help to differentiate between
asbestosis and CFA. The fibrosis was moderately extensive at the time the CT
scan was taken. The fibrotic changes were slight in the upper zones but the
distribution of the fibrosis did not help as the two conditions had a similar
distribution of fibrosis. In the early stages of asbestosis the fibrosis was at
the back of the chest, but as this was not an early case that did not apply.
There was no infection in the deceased's lungs at the time of the CT scan.
[45] Ground
glass change referred to areas of the lung that looked like an opaque window or
a veil of whiteness on radiological examination. The lung normally showed up as
black on radiological examination. This ground glass change showed inflammation
of the walls of the alveoli, causing alveolitis. This was a definite and
unequivocal change which was a strong pointer in favour of CFA. It was common
in CFA but rare in asbestosis. By the time the fibrosis had reached this stage
he would expect crackles to be heard as they appeared before signs on x-ray.
[46] In late
asbestosis with honeycombing he would expect the parenchymal bands to be
numerous. The honeycombing change was the main change on the deceased's scan
and the main evidence of fibrosis. In asbestosis it was usually associated with
numerous parenchymal bands (of which there were not many here) and not with
ground glass change (which was present here).
[47] In
cross-examination Dr Wightman said that the x-ray of 22
October 1998 showed patchy shadowing at the base of the right lung. This
corresponded with the abnormality of fibrosis subsequently shown on CT scan.
One might have mistaken it for pneumonia, but the CT scan disproved pneumonia.
The deceased might have had tracheobronchitis superimposed on existing
fibrosis. Pneumonia was denser than ground glass change and obscured the lung
markings. There had to be some active outpouring of fluid into the alveoli to
cause ground glass changes. More
established fibrotic change was represented by honeycombing. He had seen patients
with overwhelming fibrosis and would not describe the deceased's fibrosis as
having reached that stage.
[48] In
re-examination Dr Wightman said that this was certainly not early fibrosis: it
was established and moderately severe. His expectation was that there would
probably be further fibrotic change before death but he could not be certain.
In his letter of 26 November 1999 Dr Vernon had stated: "His
fibrotic process in the lungs is clearly progressing fairly rapidly." Asbestos
was quite indolent and remained static or produced only a minor change over
three to four years.
The
pathological evidence
(i) Dr Rodney Burnett
[49] Dr
Burnett (57), a witness for the pursuer, was a clinical diagnostic
histopathologist at the University of Glasgow Department of Pathology at the
Western Infirmary, Glasgow. He had particular interests in respiratory and
gynaecological pathology and in the audit of histopathological diagnosis and
particular expertise in asbestos-related diseases. He produced three reports, 6/5, 6/6 and 6/7
of process dated respectively 5 March 2001 and 29 April and 7 May 2002.
[50] A
histopathologist is a pathologist who examines tissue and tissue sections by
microscopy. The procedure is that small pieces of tissue are selected at the
post mortem examination and are then preserved, fixed and embedded in paraffin
to form blocks from which sections (thin slices) are cut for examination under
a microscope. The thin slices are mounted on glass and stained by haematoxylin
and eosin (abbreviated as H & E), which is the standard stain, or by
another method. In this case the lung sections were subjected to the Perls
Prussian Blue reaction, which is used to demonstrate iron deposits in diseases
and for the easy identification of asbestos bodies.
[51] Dr
Burnett's first report was based upon his histological examination of material
obtained from the deceased's post mortem examination. Eighteen histological
paraffin blocks were provided and H & E sections were cut from each of
these. Fourteen of these sections were of lung tissue, although the site and
side were not indicated. The remaining four sections consisted of pieces of
myocardium. His examination of the lung tissue disclosed the acute disease
process of extensive pneumonia and a terminal superimposed exudative and
disquamative alveolitis, the features of which were those of adult respiratory
distress syndrome (ARDS). These acute changes reflected only the terminal
illness but were superimposed upon well established and very extensive
pulmonary fibrosis present to some extent in all the sections. At its most
severe there was confluent fibrosis with honeycomb formation. Some degree of
pleural thickening and fibrosis was present in virtually all of the sections.
The appearances of the pulmonary fibrosis were consistent with a diagnosis of
asbestosis. Asbestos bodies were identified in the lungs but were sparse. The
fibrosis, the pleural plaques and the asbestos bodies were convincing evidence
of asbestos exposure. His one caveat was that the number of asbestos bodies
identified even after protracted searching was quite low and he would have
expected to see more in a case of asbestosis, particularly of this degree of
severity. From his reading of the autopsy report it appeared unlikely that
material was taken for an asbestos fibre count. The most that he could say,
therefore, was that asbestosis was the most likely diagnosis and it would be
important to get a thorough and independent assessment of the occupational
history, clinical history and examination and the radiological findings in the
case.
[52] His
second report was a response to a letter from the solicitors for the pursuer
asking whether an asbestos fibre count should be attempted. He stated that such
a count was possible on the material retained within the paraffin blocks
produced from the autopsy tissue. He appeared to express a lack of enthusiasm
for an asbestos fibre count, pointing out that the process was irreversible and
would result in complete destruction of the tissue used, describing it as "a
relatively crude technique at the best of times" and commenting that the
presence of any asbestos bodies on histological examination implied a very
significantly raised asbestos fibre count. The last point which he made was
this:
"There are good reasons why
there may be significant discrepancies between the asbestos body count and the
asbestos fibre burden in cases of asbestosis. Asbestosis is generally accepted
to be mainly due to serpentine asbestos (Crysotile) whereas asbestos bodies are
almost invariably formed from amphibole asbestos fibres. The presence of
asbestos bodies in cases of asbestosis therefore depends largely on the degree
of contamination of the white asbestos by amphibole varieties (usually brown
asbestos - amosite) since white asbestos fibres do not normally form asbestos
bodies. You will note therefore that there is scope for considerable variation
in asbestos body numbers in cases of asbestosis although they are almost
invariably present because of the very high exposure rates in these
individuals."
[53] His
third report took the form of a response to a faxed message from the solicitors
for the pursuer in which he said that he agreed with them that it would be
inappropriate and indeed possibly unhelpful in this case to attempt asbestos
fibre counting. He stated that it was generally accepted that the presence of
pleural disease in the form of either diffuse visceral pleural thickening or
parietal pleural plaques was strong evidence favouring a diagnosis of
asbestosis. He continued:
"A major factor present in
asbestosis cases is the absolutely enormous exposure to asbestos dust and
despite relatively more efficient clearance of serpentine asbestos from the
lungs asbestos fibre counts in cases of asbestosis are usually extremely high.
Asbestos body counts are also usually high in asbestosis because although the
amphibole contamination may only represent a tiny proportion of the total fibre
load, this load is so large that significant numbers of asbestos bodies will be
formed and these tend to persist in the tissue for several decades. You will
appreciate, therefore, that there are multiple often conflicting dynamic
factors at play here and the situation is both complicated and also, it must be
said, imperfectly understood (certainly by me!).
My position, therefore, and
this is the one which I would adopt in court, is that the histological findings
are entirely compatible with a diagnosis of asbestosis and that there is ample
pathological evidence of significant asbestos exposure. You will appreciate
that that is as far as I can actually go. I know of no way to disprove the
possibility that a man previously exposed to asbestos goes on to develop the
entity known as idiopathic fibrosing alveolitis / pulmonary fibrosis. On the
other hand I do not believe that it is possible to make that diagnosis in these
circumstances anyway, unless it can be done on clinical grounds."
[54] In his
oral evidence Dr Burnett went through Dr McFarlane's post mortem report (6/2 of
process) and commented on it. The finding of bilateral pleural plaques was a
good indication of previous exposure to asbestos. Due to widespread
consolidation (pneumonia) the deceased's lungs were about twice as heavy as
they ought to have been. The honeycomb change in the lungs meant that the
surface of the lung looked like the surface of a honeycomb as it was lined with
cysts, which was a feature of end stage fibrosis. The examination of the heart
indicated ischaemic heart disease, although there was no evidence of damage to
the heart muscle. Dr McFarlane retained lung tissue which she had made into
paraffin blocks, he had received them and cut a section from each of them. He
had no idea where the blocks came from in the lung, but he presumed the person
who took them had taken them had taken a fair section from both lungs. Asbestos
bodies are feriginous bodies consisting of fibres coated with protein (deposits
of iron and sometimes calcium) which stained dark blue when the Perls technique
was performed. In this case he had identified asbestos bodies within the lung tissue.
They were sparse, not all over the place and he had to look for them. He had to
spend half an hour or an hour looking. There were not many, but he had to look
for them. It was possible to spend all morning looking at one slide for
asbestos bodies, but he did not have to do that in this case. Once you saw
asbestos bodies there was no point in doing a fibre count. He was not a fan of
fibre counts. His research group had published on the topic in the last year
(6/17 of process). Their conclusion was that fibre counting was not very
reliable. Asbestos fibres and asbestos bodies were different. Only a small
proportion of fibres from blue or brown asbestos ever became bodies. If
asbestos bodies were seen there was no need for fibre counting. Once asbestos bodies
were identified that meant that the person had been occupationally exposed to
asbestos.
[55] He was
aware that in this case there was a dispute about the presence of asbestos
bodies and he had therefore reviewed the slides. He had found four asbestos bodies
without any difficulty whatsoever and had photographed them. The photographs
were produced as 6/18, 6/19 and 6/20 of process. 6/18 showed three photographs
of a single asbestos body magnified 1000-1200 times. Three fields were shown at
different focus depths marked on the slide. 6/19 showed two photographs of a
second asbestos body: it was the white line running the whole length of the
photographs. 6/20 consisted of two photographs, showing two asbestos bodies
from the same slide. At that point he stopped looking.
[56] Dr
Burnett's opinion was that it was not possible to tell the difference between
the fibrosis of asbestosis and the fibrosis of end stage CFA on either gross or
histological examination. CFA was a clinical syndrome, not a specific disease:
it was a process of pulmonary fibrosis leading to respiratory failure and
death. The word "cryptogenic" meant that its cause was not known: the trouble
with it, therefore, was that it was a non-diagnosis, it meant pulmonary
fibrosis of unknown or unascertained cause. He did not feel that a diagnosis of
CFA could be made when there was ample evidence of asbestos exposure. It was
known that the deceased had a history of asbestos exposure: he had pleural
plaques, pleural thickening and asbestos bodies in his lung, so in some ways it
was perverse to say that, as well as that, he had a completely different
pulmonary fibrosis of unknown cause.
[57] In
cross-examination Dr Burnett accepted that CFA was a well recognised clinical
syndrome. It was probably caused by a wide variety of different agents. If the
cause of the fibrosis was known the condition ceased to be CFA. Its old name
was idiopathic pulmonary fibrosis. Medical literature had attempted to
distinguish between CFA and asbestosis. Lots of people got pleural plaques and
did not go on to get asbestosis: they could have CFA also. Apart from the
asbestos bodies, there was no way he could tell the difference histologically
between end-stage CFA and asbestosis. The number of asbestos bodies present in
this case meant that the fibre count must have been elevated at least 100
times.
[58] With
regard to his histological examination, he would have looked at all 14 lung
sections, but searched for asbestos bodies only until he found two or three. He
could not say how many asbestos bodies he found out of how many sections. A
good guess was that it might have taken him 45 minutes to find two or three
asbestos bodies, then he would have stopped as there was no point in looking at
any more. There was no point in photographing more than four bodies. He had to
look for them, which was why Dr Thomas (the defenders' pathologist) did not see
them at all. He could not remember how many sections he looked at for asbestos
bodies, but the evidence from the Perls showed that he was averaging one body
per section. For his first report he looked at all 14 sections, but not for
asbestos bodies. He normally used a medium power microscope which magnified by
200 times. When he was searching for asbestos bodies he did "an H & E and a
Perls" on 13 sections (one of the fourteen having been sacrificed for the
asbestos fibre count). He photographed the asbestos bodies, magnified 1100
times, in oil. On each of the sections he looked at he found at least one
asbestos body. He did not look at anywhere near all of the sections. The longer
a deceased survived after exposure to asbestos, the lower the asbestos body
count would be as the fibre and body counts fell as the years went by. One or
two asbestos bodies per Perl stained section meant that the asbestos body count
was markedly elevated.
[59] Dr
Burnett was referred to a paper by Roggli and Pratt (7/13 of process) entitled
"Numbers of Asbestos Bodies on Iron-Stained Tissue Sections in Relation to
Asbestos Body Counts in Lung Tissue Digests" in which the authors stated that
"the presence of more than one asbestos body on light microscopy has been
recommended recently as one of the morphologic requirements (together with
peribronchiolar fibrosis) for the tissue diagnosis of asbestosis". He stated
that the authors were referring to the number of asbestos bodies per gram,
which was not helpful in this situation. Basically he thought they were saying
that you needed two bodies' worth per section for a diagnosis of asbestosis.
The paper dated from the early 80s and the material they were looking at was of
people subjected to high exposure who had died early and who would have had
much higher counts. The asbestos fibre and body count in a person who survived
for 30 years decayed. He accepted that in general terms the greater the
asbestos exposure the greater the pulmonary fibrosis would be. There was a
large element of idiosyncrasy in the response to asbestos both in pleural
disease and in asbestosis. In this case he would have expected to see more asbestos
bodies with this degree of severity. His view of the statement by Roggli and
Pratt "The Pneumoconiosis Committee of the College of American Pathologists has
specified that the minimum criteria for the histologic diagnosis of asbestosis
include the identification of peribronchiolar fibrosis and at least two asbestos bodies in tissue sections" was that that
would be fine back in 1983 and was the classic diagnosis of asbestosis based on
much higher asbestos body counts than the count in the case of the deceased. He
accepted that there was a quantitative or semi-quantitative basis for
establishing asbestosis through histological sections. He conceded that it
might have been wise for him in this case to have noted how many asbestos
bodies could be found in each of the sections but he was working on the basis
that if he could identify asbestos bodies the deceased had had a significant
asbestos exposure. He went on to say: "You can argue whether or not the amount
is sufficient to cause asbestosis using classical 20 year old definitions if
you want to, but the point I am arguing is that this man has quite clearly had
significant exposure to asbestos and all the authorities agree that if you are
averaging one body per Perl section that is about a hundred times greater than
background exposure". He accepted that the paper by Roggli and Pratt had not
been superseded and pointed out that the number of papers written about
asbestosis in the last five years was virtually none because the disease had
virtually disappeared, all the people who had it having died. He was unhappy
with the fibre count because it did not correspond with the fact that asbestos
bodies could be seen on their own. The
only way he could put it was that the fibre count was wrong. The conclusion
from the fibre count was that the exposure level was just at the upper limit or
just outside the upper limit of normal and this did not correspond with the
presence of asbestos bodies. With classic asbestosis a lot more asbestos bodies
were generally seen.
[60] Dr
Burnett was referred to the passage in his third report in which he mentioned
"more efficient clearance of serpentine fibres from the lungs" and explained
that serpentine asbestos was the common type of white asbestos used in large
amounts. It had curly fibres which were rapidly cleared from the lungs (their
half-life being about six days) and did not form asbestos bodies, but it was
invariably contaminated by amphibole (blue and brown asbestos), which was
inhaled. Only amphibole asbestos formed asbestos bodies. In this case there
were far too many asbestos bodies for a person who had not been exposed to
asbestos. A person's asbestos body count fell with time.
[61] Dr
Burnett was then referred to the report of Dr Thomas, the defenders'
pathologist, dated 7 September 2004 (7/28 of process), which
incorporated his two previous reports of 4 February and 30 May 2003. In his report of 4 February
2003
Dr Thomas had said that he would expect to find a minimum of one or two
asbestos bodies per histological section, that he could find no definite
asbestos bodies in this case and that there was no substantive evidence to
support a diagnosis of asbestosis. In his report of 30 May 2003 Dr Thomas said
that he had identified a single asbestos body in 28 tissue sections after two
thorough periods of examination, that he thought the tissue burden was likely
to be well below that seen in cases of asbestosis and that a formal fibre
analysis would be very helpful in resolving this important point and also Dr
Burnett's point about fibre types and asbestos body formation. In his report of
7 September 2004 Dr Thomas stated:
"The histopathological
features present in this case do not allow the distinction between one cause of
pulmonary fibrosis and another. The sections examined show end stage pulmonary
fibrosis that is predominantly basally and subpleurally distributed and could
equally be due to CFA or asbestosis. The relative absence of tissue bodies in
tissue sections and the low asbestos fibre count reported by Dr Gibbs do not
support a diagnosis of asbestosis."
[62] Dr
Thomas's conclusion was that, although the deceased had been occupationally
exposed to asbestos during his working life, the pathological features in the
case favoured a cause of pulmonary fibrosis other than asbestos. Dr Burnett
thought that Dr Thomas's report of 30 May 2003 was closest to his own
report. Both of them now agreed that there were asbestos bodies in the lung. He
himself had originally used H & E sections, but when asked to review to
make an assessment of asbestos bodies he used Perl stained sections and found
several asbestos bodies which he photographed. It was more likely that asbestos
bodies would be found using Perl stained sections as an iron method was used to
identify asbestos bodies. Dr Thomas had said he stained for iron, which meant
he was using Perl staining. In classical asbestosis in the 1970s and 1980s you
would have expected to find a lot more asbestos bodies than this: the fibre and
body counts in these cases were high, much higher than you would expect to see
in a patient who survived for 25 years. The deceased's asbestosis took 25 years
to kill him and was therefore likely not to have been as severe or aggressive
as it would have been had he died in the 1980s, for example. Asbestosis
proceeded at different rates in different individuals: severity and rate of
progression were individual points and there was a huge variation. Almost all
the literature, both pathological and clinical, on asbestosis was derived from
patients all of whom were dead by the early 1980s. What we were seeing now were
the patients who had survived. In typical full-blown asbestosis you normally
saw a lot more asbestos bodies. Some people with bilateral pleural plaques did
not have any asbestos bodies at all as they had got rid of all of them. What
was being argued about in the present case was whether there were enough fibres
to indicate sufficient exposure to cause asbestos. Asbestos bodies were almost
all amphibole, which degraded much slower than serpentine. If you saw asbestos
bodies in the lungs at all that was a significantly raised number. He did not
think you could do a back calculation, he knew of no literature on
back-counting and he thought that there were too many huge variables involved.
His impression was that in cases where you can readily make a diagnosis of
asbestosis there were more bodies than he saw in this case, which is why he
said in his first report that the bodies were sparse. Even the number he found
meant that there had been a very significant exposure to asbestos, especially
after 30 years. The material used by Roggli and Pratt was classical asbestosis
material because it was derived from deaths in the 1970s and 1980s: all of
their conclusions were based on asbestosis as it was back then, not as it is
now. If the deceased had had a biopsy in, say, 1980, it would have been very
interesting to have seen how many asbestos bodies he had in his lungs then. He
accepted in most general terms the statement in the paper by Parkes (7/19 of
process, page 521) that over the past two to three decades the latent
period between the commencement of significant occupational exposure to
asbestos and the first clinical evidence of asbestosis was likely to be well in
excess of 15 years, that exceptions might occur following unusually heavy
exposure but they had been rare since the 1960s and that DIPF (diffuse
interstitial pulmonary fibrosis) that first became apparent 15 to 20 years
after exposure ceased was unlikely to be asbestosis. You could have pulmonary
fibrosis for quite a long time without having any symptoms. DIPF that first
became apparent 15 to 20 years after exposure ceased was unlikely to be
asbestosis, but it depended on what was meant by "manifest", whether it
referred to symptoms or radiological evidence. The ultimate conclusion from
Parkes' paper would be that asbestosis does not exist any more.
[63] Dr
Burnett stated that he would still expect there to be elevated amphibole fibre
counts where there had been exposure to asbestos, even decades afterwards. It
was quite legitimate in a case such as this to carry out not only an asbestos
body count, but also a fibre count, which allowed you to determine what kind of
fibres were in the lung tissue. To carry out a fibre count you took some lung
tissue (which in this case was reclaimed from the paraffin block) and you
incinerated it and were left with the mineral content, in which you counted the
fibres and "do some fancy mathematics and that gives you the answer". The
mineral content could be examined with a light microscope or an electron
microscope. In the paper which he co-authored (6/17 of process), and which was
published in the journal entitled "Medicine, Science and the Law", two methods
of fibre counting were described, both of which used a light microscope. The
type of microscope used was irrelevant. An electron microscope could identify
the actual fibre type, but the count was going to be just as wrong as with a
light microscope. Any sampling error would be just as great using an electron microscope:
there was no fundamental or theoretical reason to suppose that an electron
microscopical count would be more accurate than a light microscopical count. In
a case where there is doubt whether there are sufficient asbestos bodies to
constitute asbestosis it would clearly be advantageous to carry out a fibre
count if you were sure you were going to get accurate fibre counts, but his
difficulty was that fibre counts were not reliable. The whole reason for his
published paper was that he had over the years been increasingly unhappy with
fibre counts because they did not seem to correlate with anything. He accepted
that in this case, where there appeared to be doubt about the number of
asbestos bodies, that it was sensible and appropriate to obtain a fibre count.
On being shown the letter of 13 February 2004 (7/7 of process) from the
Environmental Lung Disease Research
Group in Penarth, Wales stating that the deceased's lung tissue disclosed 1.21
million amphibole fibres per gram dry lung, slightly above background (1
million fibres per gram dry lung being upper level for background) and well
below that associated with asbestosis (in which the combined amphibole levels
are generally in excess of 50 million fibres per gram dry lung), indicating
that the most likely diagnosis of the fibrosis was CFA and not asbestosis, Dr
Burnett stated that his position was that this result was irreconcilable with
the fact that he found asbestos bodies in the lung. He had come across the
author of the letter, Dr Allen Gibbs. The asbestos fibre count suggested that
the deceased was just outside the normal range of exposure, and that was
inconsistent with the fact that not only he but also even Dr Thomas found
asbestos bodies. Dr Gibbs was a well known respiratory pathologist but he had
provided only the fibre count: he had had no other involvement in the case.
Most deceased patients with asbestos-related pleural plaques did not have
asbestos bodies in their lungs. The number of asbestos bodies he found was
probably at the lower end of Roggli and Pratt's paper, if not below. Dr Gibbs'
fibre count was likely to be wrong because it did not link at all to the number
of asbestos bodies found. If Dr Gibbs were correct you would not find any
asbestos bodies at all. There was a huge body of literature that suggested that
if you saw asbestos bodies you were dealing with significantly elevated
asbestos levels. He had spent an hour looking at the three sections in which he
found asbestos bodies.
[64] With
regard to the post mortem report, he personally had not examined the fibrosis,
but he could not tell if it was three years old or 30 years old: it could be
less than three years old for all he knew. Fibrosis in the lung reached an end
stage within about a year, but there were other features here (metaplasia and
displasia) which suggested it had been there for a longer rather than a shorter
period, perhaps about 20 years. He still maintained that you could not
histologically distinguish between CFA and asbestosis, but there were nuances
which pointed you in different directions. In general, classic textbook terms
CFA progressed more rapidly than asbestosis. At the time of his report he had
not seen the medical records and was not aware of anything to do with the
deceased's clinical condition. The post mortem findings did not suggest a huge
amount of ischaemic heart disease and if it had been significant he would have
expected the pathologist to have entered it on the death certificate as a
significant condition present but not directly contributing to death.
[65] When it
was suggested to Dr Burnett that the presence of alveolitis was more consistent
with CFA he responded that this was "opening a big can of worms" as there were
different ways to use the word alveolitis. It would have occurred shortly prior
to death because of acid aspiration: it was not due to CFA or to asbestosis. He
did not think that Dr Wightman was entitled to interpret ground glass shadowing
in the lungs as alveolitis. His understanding was that you could not diagnose
alveolitis on a CT scan. He did not know how Dr Wightman was using the word
alveolitis. If the alveolitis that he (Dr Burnett) saw was present on chest
x-ray two years before death the deceased would not have survived for two
years. The word "alveolitis" within CFA was used in a somewhat different way
from the way he had used it in his report. To his mind alveolitis was a
histological diagnosis. Even the pathologist handling the lungs at the autopsy
would not try to make a diagnosis of alveolitis, so how it could be made on an
x-ray or CT scan he was not sure.
[66] In
re-examination Dr Burnett said he did not feel justified in making a separate
diagnosis of pleural fibrosis. In general terms one very useful way of telling
CFA and asbestosis apart was the presence of pleural disease, which meant
pleural plaques and visceral pleural fibrosis. The presence of pleural disease
was usually associated with asbestosis and not with CFA. What was being argued
by the defenders was that the deceased had benign pleural disease due to
asbestos exposure and then went on to get CFA. So far as Dr Thomas's search for
asbestos bodies was concerned, you could not look for asbestos bodies properly
on 28 sections in one hour: it was not possible.
(ii) Dr Jeremy Thomas
[67] Dr
Jeremy Thomas, a witness led by the defenders, had been a consultant
pathologist at the Western General Hospital, Edinburgh since 1988 and Head of the
Department of Pathology there since 1999. He had a special interest in the
pathology of the lung. He had produced two reports, 7/6 of process dated 4 February 2003 and 7/28 of process dated 7
September 2004. He had considered the post mortem report (6/2 of process)
and Dr Burnett's report (6/5 of process).
[68] Dr
Thomas agreed with the autopsy findings that the lungs showed evidence of
diffuse firm fibrosis. The presence of vegetable matter in the lungs was
evidence of aspiration pneumonia. The post mortem report did not provide
evidence of infection but there would almost certainly have been infection in
an agonal lung. He had received 18 unspecified blocks and taken one H & E
stained section from each block and prepared iron stained sections for the 14
blocks of pulmonary origin. An H & E section was not an ideal section with
which to view asbestos bodies. In a case of asbestos he would initially look
for evidence of diffuse pulmonary fibrosis (which was clearly evident here) and
would expect to find asbestos bodies easily. One or two per section was
identified as the lower level in the literature: see the Roggli and Pratt
paper, an original and substantial paper. It was very difficult to achieve
publication in this area and both the authors and the journal were highly
regarded. A more recent publication regarded two asbestos bodies per section as
too stringent a requirement and stated that one was more appropriate: Pathology
of Occupational Lung Disease (7/21 of process). In February 2003 he had looked
at all 28 sections for about an hour and he then looked at them again in May
2003 for about one and a half hours on a Sunday afternoon. He had spent the
bulk of his time looking at the iron-stained sections. In his first examination
he identified one possible asbestos body in 28 sections and in his second
examination one definite asbestos body. After extensive examination he
concluded that asbestos bodies were extremely difficult to find and that in
these circumstances asbestosis was an unlikely diagnosis. A threshold of
asbestos exposure was required to produce asbestosis. There was a substantial
gap between normal individuals exposed to asbestos in the atmosphere and those
with asbestosis - 15 to 1 in fibre loads. He did not think that lack of
exposure from the 1970s mattered as pathogenic fibres (that is, fibres which
cause disease) were much less likely to be cleared.
[69] On
being referred to Dr Burnett's first report (6/5 of process) Dr Thomas stated
that he believed that Dr Burnett and he were saying the same thing here, that
asbestos bodies were sparse. He was satisfied that asbestos bodies 1, 2 and 3
identified by Dr Burnett were in fact asbestos bodies but was not certain about
asbestos body 4. He would not count it and would call it a possible asbestos
body. There was a well recognised variability in the presence of asbestos
bodies from one tissue to the next, hence the requirement to examine all tissue
sections to get a balanced view of what was going on. The accepted
recommendation for examination of tissue bodies for asbestos bodies was that
tissue sections should be stained and examined in accordance with normal
professional practice. He would regard 20 to 30 minutes per section as
abnormal professional practice. He would want to know the thickness of the
sections and the number of the bodies found. He would recommend a fibre count
particularly at the lower levels.
[70] On
being referred to Dr Gibbs' report (7/7 of process) Dr Thomas explained that
the Environmental Lung Disease Research Group in Penarth, South Glamorgan was the leading industrial
disease lung laboratory in the country, if not the world, and was staffed by
the leading experts in the field. It had received a lot of material from the
mines in South Wales and had developed into an asbestosis laboratory. The
findings of Dr Gibbs in his report appeared entirely consistent with the
asbestos body counts. He (Dr Thomas) had predicted, in view of the difficulty
which he had in finding asbestos bodies, that the fibre load would be low. A
figure of 5 million fibres on a "back count" of 25 years would not cause him to
change his view as 5 million was above background level but well outside the
range for asbestosis. Pleural plaques could materialise at low levels of
exposure.
[71] In
cross-examination Dr Thomas said that he knew Dr Burnett and as a senior
registrar had trained in his department in the Western Infirmary in Glasgow. One or two asbestos bodies
on each section in this case would not be consistent with the result of the
fibre count. It was easier to see asbestos bodies on iron-stained sections than
on H & E sections. He and Dr Burnett had been working at the same
magnification levels (x 200) with a field of view 1 mm in diameter. The section
was like a Swiss cheese: a lot did not contain any material. The focus on each
field had to be adjusted to view the entire field at a thickness of 4-5 microns.
[72] Under
reference to page 5 of his own report, Dr Thomas explained that it was very
likely that the aspiration pneumonia was generalised. Vegetable matter was
present in only two sections. He did not believe that Dr Burnett and he
disagreed on this point. They were not differing on the number of sections
where there was active alveolitis. Dr Burnett referred to two patterns of
pneumonia - aspiration pneumonia (including alveolitis) and retention pneumonia
but did not specify how much vegetable matter he had identified. It was
possible there was an asbestos body on block F. On review he had found a
definite body on a separate block. One could stare at the same field for a very
long period of time and one could look at a higher level of magnification. He
would not be surprised that one of the photographs of the asbestos sections had
come from block F. He gave a reference to the blocks by marking them with a
letter but did not know whether Dr Burnett had used the same lettering system
to mark his slides. He had not examined Dr Burnett's sections. Only the blocks
(not the sections) were sent to Penarth. He did not know how Dr Gibbs would
have selected the block. His expectations were based on normal professional
practice. It was much more difficult to say something was not there than to say
that it was. He had examined with the specific purpose of looking for asbestos
bodies. If one or two asbestos bodies had been present in each tissue section
or in the majority of tissue sections he would have accepted the diagnosis of
asbestosis. He did not think one could extrapolate from the first two sections.
He was sure Dr Burnett would not cut a thicker than average section.
[73] In
response to questions from me Dr Thomas stated that Dr Gibbs' fibre count could
stand with four asbestos bodies as they were identified in a proportion of the
sections after an unusually protracted period of examination of those sections:
the two were not at all necessarily inconsistent. He believed it was incorrect
to say that if Dr Gibbs' fibre count was correct you would not find any
asbestos bodies. In the case of the normal population exposed to background
levels of asbestos only you could find one asbestos body per 100 tissue
sections under normal examination. He had 28 sections from the deceased's
lungs to examine. The deceased had an above average exposure to asbestos. To
find one asbestos body in 28 sections was not surprising. He would not expect a
higher fibre count than Dr Gibbs found. The finding of asbestos bodies was a
crude indicator of the level of exposure. He thought that the deceased had had
a low level of exposure. He based his conclusion about the deceased's level of
exposure on Dr Gibbs' fibre count, not on the occupational history.
[74] In
re-examination Dr Thomas said that there was some variation in the widths of
the sections between bodies. It was important to give the context (that is, the
internationally accepted standard) when commenting on the number of bodies
found.
(iii) Dr Allen Gibbs
[75] Dr
Allen Gibbs (57), a witness for the defenders, was Consultant Pathologist to
the South Glamorgan Health Authority and Honorary Clinical Teacher to the
University of Wales College of Medicine since 1985. He explained that he
carried out clinical pathology involving surgical biopsies and autopsies every
day. His curriculum vitae (7/25 of process) set out 132 publications to which
he had been a party, of which half were concerned with asbestos-related
disease. He sometimes received cases from European pathologists for a second
opinion and from European laboratories for fibre counting.
[76] His
report on the fibre count of the lung tissue of the deceased was 7/7 of
process, dated 13 February 2004. It reads as follows:
"Re: James McHardy WRIGHT (Deceased)
Mineral fibre analysis has
been carried out on lung tissue retrieved from one of the paraffin wax blocks.
It discloses the presence of amosite, crocidolite, chrysotile and tremolite
asbestos. The combined amphibole (amosite + crocidolite + tremolite) level of
1.21 million fibres per gram dry lung is increased slightly above background
(upper level for background - 1 million fibres per gram dry lung). However, the
results are well below those associated with asbestosis in which the combined
amphibole levels are generally in excess of 50 million fibres per gram dry
lung. The results indicate that the most likely diagnosis of this fibrosis is
that of cryptogenic fibrosing alveolitis and against a diagnosis of
asbestosis."
[77] Dr
Gibbs explained how a fibre count was carried out. He looked at the tissue and
took a section to see if it contained good lung tissue representative of the
general pattern. He always checked the fibre count with the pathology. In this
case he had to de-wax the block and digest it in strong alkali, leaving him
with the mineral particles (dust) of which he then put a sample on a grid which
went into the electron microscope as it was more powerful than the light
microscope. It was possible to see the bodies in the light microscope, but not
the naked fibres. He then counted the fibres per square on the grid and
calculated according to the mass of tissue. He identified by physical
parameters and chemistry what kind of fibre it was. Amosite came from brown
asbestos and crocidolite from blue asbestos. These were amphibole fibres used
commercially for asbestos products. Chrysotile fibres came from white asbestos
and belonged to the serpentine family. The lung handled amphiboles in a
different way from serpentine. Other minerals were not thought to be related to
lung fibres. There was a low chrysotile level which was ignored as it cleared
within weeks or months of exposure. Other material got into the lung tissue and
stayed there. The half life of amosite was 20 years and the half life of
crocidolite was 8 years. In severe cases of asbestosis (such as the present
case was alleged to be) there were very high figures for amphibole fibres - in
excess of 50 million. He did not think the fact that another block might be
twice as high or half as high was significant in this case. If a back count
were done to 1975, giving a figure of 5 million fibres, that would not alter
his conclusion. If everything were pushed to the limit a figure of around 10
million fibres would be reached and that also would not alter his opinion in
any way.
[78] On
being referred to Dr Burnett's two reports (6/5 and 6/7 of process) Dr Gibbs
stated that he did not regard them as inconsistent with his fibre count. Dr Burnett
did not find many asbestos bodies. He spent a long time looking for them and
they were low in number, so his findings were not inconsistent with the fibre
count. The fibre count was above background level and consistent with the
finding of occasional asbestos bodies. It was also consistent with finding none
or an average of less than one per histological section. Asbestos bodies formed
a very low proportion of the total asbestos count. Several different factors
influenced the coating of fibres - the length of the fibre, the fibre type (a
higher proportion of amosite than crocidolite formed a coating) and the amount
of iron kicking around in the lung. A lot of things influenced how many bodies
you saw, but not the number of fibres. The size distribution of fibres would
influence the proportion which would get coated. An asbestos body count was
fine when there were a lot of bodies there. The electron microscope did not
miss fibres, as the light microscope did.
[79] On
being referred to Dr Thomas's report (7/28 of process) Dr Gibbs opined that 28
sections from the lung were a lot to examine and the low number of asbestos
bodies was consistent with his finding on electron microscopy. He thought it
was reasonable to spend one and a half hours looking at 28 sections.
[80] On
being referred to Dr Burnett's photographs of what Dr Burnett said were
asbestos bodies (6/18, 6/19 and 6/20 of process) Dr Gibbs said he was 98% sure
that three of the items were asbestos bodies but not about the fourth one
"which looked like a carrot". One could not be absolutely sure unless an
examination under an electron microscope were carried out. He thought Dr Thomas
had looked at different sections from Dr Burnett. He did not know if the
thickness of the sections was the same: most laboratories cut the sections at
4-5 microns, sometimes others cut them at 10 or 20. He did not think the
variability between the number of sections would be unusual. In classical
asbestosis cases you found asbestos bodies in seconds, clumps all over the
slide, and a substantial number of bodies in a couple of minutes. The fibre
count would be 100 million or greater, sometimes billions. If there were 13
sections he himself would look at all 13 sections because you did not know if
the sections you had examined were representative. He thought one asbestos body
per section was not sufficient for a diagnosis of asbestosis and that is why he
would do an electron microscope count.
[81] On
being referred to the article "Interobserver Variability in Analysis of
Asbestos Fibres and Asbestos Bodies in Human Lung Tissue" (6/17 of process) by
Roberts et al (including Dr Burnett) Dr Gibbs said that this indicated that
three people had looked at the same section and had not said how many bodies
they had found. They had not compared like with like. There was also a problem
with the actual techniques used. The Gold technique had been superseded for 30
years. Very few cases had been evaluated. His own laboratory had been doing
fibre counts for 20 years, not sporadically. He had examined the histology
in this case. He had found an occasional asbestos body and did not differ
significantly from Dr Thomas. He disagreed with the statement by Dr Burnett in
paragraph 3 of his letter of 29 April 2002 (6/6 of process) that "the
presence of any asbestos bodies on
histological examination implies a very significantly raised asbestos fibre
count". A lot of people would disagree with the statement by Dr Burnett in
paragraph 4 that "asbestosis is generally accepted to be mainly due to
serpentine asbestos (crysotile) whereas asbestos bodies are almost invariably formed
from amphibole asbestos fibres".
[82] Dr
Gibbs was referred to 7/23 of process, his letter of 17
August 2004 commenting on Dr Boyd's supplementary report. In that letter
he summarised three elements which in his opinion pointed strongly to a diagnosis
of CFA. These were as follows:
1. The progression of the
pulmonary fibrosis was relatively rapid with a typical time course for CFA.
2. Light microscopy showed very
few asbestos bodies - the usual criteria for a light microscopic diagnosis of
asbestosis being 2 asbestos bodies per cm2 - a standard section usually
measures approximately 3 cm2 - in this case there was an average of 1 per
section.
3. The asbestos fibre count by
TEM showed only a slightly elevated level of asbestos consistent with the
findings by light microscopy with (sic) very
few asbestos bodies.
[83] He
explained that there was no pathological difference between CFA and asbestosis
except the asbestos fibre load. He was not surprised at the finding of pleural
plaques and pleural thickening because the background exposure amply explained
the pleural changes. One had to differentiate the pleura from the parenchyma
(substance of the lung). The rapid progression of the disease pointed to CFA.
If (as here) there was a long period after the last exposure the asbestosis was
usually mild and slowly progressive. He thought that a long latent period after
exposure followed by a rapidly progressing disease was much more consistent
with CFA than with asbestosis. A period of two years from the onset of disease
until death was typical of CFA but extremely unusual for asbestosis. If
exposure began in 1947 he would think that asbestosis in the 1990s was
unlikely. The higher the exposure, the earlier the development of asbestosis
was likely to be. He did not think he had seen severe cases 20 years after
exposure. The fibre count in this case was consistent with intermittent
exposure. He thought that cases of intermittent exposure were often difficult
to quantify but the fibre count helped to assess intermittent exposure.
[84] The
cross-examination of Dr Gibbs began with Mr Marshall referring Dr Gibbs to
the 17 blocks in 6/21 of process. Dr Gibbs explained that he used one block and
destroyed it to do the count. His practice was to look at all the blocks and to
select a representative one (or two) to do the fibre count. His sections were
4-5 microns thick and stained by H & E. He
preferred H & E stains because he could see the cores of the bodies easier
than with iron staining: seeing the cores of the bodies was critical because of
the possibility of pseudo asbestos bodies. The block which he had selected in
this case was a good sample of lung which looked representative of the whole.
He scanned the sections for asbestos bodies, basically to check with the fibre count.
His instructions had been to provide an electron microscopic fibre count, not a
histological report. The practice was that a technician de-waxed the block and
then it was digested in alkali. The area of stub going into the microscope was
small. Professor Pooley and Mr Griffiths did the mineralogical part of the
work.
[85] Dr
Gibbs was then referred to the 1996 article "Analysis and interpretation of
inorganic mineral particles in 'lung' tissues" (7/17 of process), of which he
was an author along with Professor Pooley. He described it as setting out the
reasons for analysing mineral particles and the techniques which should be
used. He was referred to the following passage at p 327 under the heading
"Sampling and Tissue Availability":
"Several investigators have
shown that there is variation of results from the same lung when multiple
separate small samples are analysed because there is an uneven distribution of
fibres within the lung, just as examination of lungs for fibrosis shows
variation from area to area. Churg and Wood examined multiple 1 ml samples of
lung from each of nine subjects and found a mean in case ratio of maximum to
minimum fibre concentration of 7.5 for amosite and crocidolite, 3.8 for
chrysotile and 4.0 for non-asbestos fibres."
[86] He
explained that these were samples smaller than the average block. The more
tissue examined the more accurate the result was going to be. He did not take
thickened pleura for analysis as the number of fibres in it was much lower than
in the lung substance. At p 329 of the article it was stated that it was the
authors' practice to count and type 100-200 fibres of all sizes per
investigation. In this case he had counted 90 fibres, which he did not think
was inappropriate for the histology. He probably made a comment "sparse
asbestos bodies". If the asbestos bodies were below one per section you had to
correlate that with the electron microscopic fibre count. He would be happy to
call an average of six asbestos bodies per section asbestosis. At p 331 he had
written the following:
"Non-exposed controls
uncommonly show combined amphibole levels of more than two million fibres per g
whereas most cases of mesothelioma and asbestos-related diffuse pleural
fibrosis exceed this but frequently do not reach the levels associated with
asbestosis which, for the earliest microscopic grade, exceeds 50 million
amphibole fibres/g."
[87] What
mattered as to whether someone got a lung problem was the dose and size
distribution of fibres. You could see all the fibres with the electron
microscope and therefore were not dealing with something that was a guess. The
fibre count was a reflector of the retained cumulative exposure, which was the
main determinant of an asbestos-related disease. If there had been a high count
(50 million +) 20 years ago, one would expect that the patient would be at
higher risk. Breathlessness over 15 years due to lung fibrosis would make
a difference.
[88] Dr
Gibbs was then referred to the article in the European Respiratory Journal
entitled "Guidelines for mineral fibre analyses in biological samples: report
of the ERS Working Group" by De Vuyst et
al (7/18 of process) of which he was a co-author, and wherein it was stated at page 1419
of that there were marked variations (up to 10-fold) in the concentration of
asbestos fibres from the same lung, that the largest distances over which such
variations occurred were not yet well defined and that the "ideal" LT Sample
for fibre analysis consisted of three pieces of 1-2 cm3, one from the apex of
the upper lobe, one from the apex of the lower lobe and one from the base of
the lower lobe pooled together. He explained that it was not possible to have
the "ideal" sample in this case as only blocks of retained tissue were
available. The other blocks in this case could have been analysed if it was
deemed necessary. He agreed that a fibre count is not the be-all and end-all of
a diagnosis. At page 1424 the article stated:
"The differential diagnosis
between asbestosis and other diffuse lung fibrosis is the only situation where
asbestos bodies or fibre analysis may help in making a medical diagnosis and
affect the choice of therapy. In many countries the epidemic of asbestosis is
gradually shifting to older age categories and milder diseases. Meanwhile, the
incidence of idiopathic pulmonary fibrosis seems to be increasing. It is to be
expected that problems in the differential diagnosis will become more
frequent."
He explained that every decade there had been a
reduction in asbestos exposure. He still saw cases of insulators who had been
exposed to asbestos in the 1940s and 1950s.
[89] On
being referred to page 8 of Dr Thomas's report (7/28 of process) where it was
stated that it had been estimated that in the normal population one would have
to examine 100 iron-stained tissue sections to identify a single asbestos body
he opined that one in 100 or 200 was reasonable for the normal population. When
he had stated on page 2 of his report of 17
August 2004 that all the histopathologists involved in this case
commented on the low number or absence of asbestos bodies he was referring to
Dr Burnett, Dr Thomas and himself. If he had seen a substantial number of
asbestos bodies he would have asked permission to destroy another block. If
there had been a material divergence between the number of asbestos bodies and
the number of fibres he would have repeated the fibre count and asked to see
other sections. He would be happy to call two bodies/cm2 asbestosis. Below that
figure he would get a fibre count done. On being referred to the photographs
(6/ 18, 19 and 20 of process) he stated that he could not see the core of the
alleged asbestos body in the photograph 6/20 of process either because of the
angle or because it was not an asbestos body. He did not think it was necessarily
true that he would have found more asbestos bodies on iron stained sections. He
agreed with the statement on page 426 in chapter 14 of Parkes,
Occupational Lung Disorders (3rd Ed, 1994) (7/16 of process) that
although dissolution of amphibole fibres is not apparent some clearance
probably continues in the long term at a slow rate. You could have individuals
with heavy exposure who did not get asbestosis, but you would expect the
susceptibility to be operative during the period of exposure, not 25 years with
nothing and then fibrosis leading to death within two years (W R Parkes, op cit, chapter 15, 7/19 of process, page 510).
Looking at his own report and the article by himself and Professor Pooley (7/17
of process), he stated that their repeated examinations did not show a mean
variation of 7.5, as mentioned in the article. With reference to his letter of 17 August 2004, he read Dr Boyd in his report as saying there was no
appearance of CFA. The histological appearances of CFA and asbestosis were
indistinguishable apart from the asbestos bodies or fibre count. With this
degree of asbestos exposure it was not surprising to find some pleural change.
There was no obvious cause for CFA but he thought you had to get past the "no
obvious cause". He would expect gross
overload situations to be reflected by particles in the lung. The most likely
cause of pleural plaques here was exposure to asbestos.
[90] In
re-examination Dr Gibbs stated that in his home area 10% of people at autopsy
had pleural plaques. A figure of 40% in the Clydeside area would not surprise
him. CFA was a diagnosis of exclusion and the most common cause of lung
fibrosis in the elderly. It could be increasing due to the ageing
population. He agreed with the following
sentence in 7/19 of process, page 510: "Thus, workers with significant
past exposure to asbestos who do not develop asbestosis may, nevertheless, be
open to pulmonary fibrosis from some other cause". With regard to the statement
quoted above from p 1419 of the report of the ERS Working Group (7/18 of
process), things had moved on since then (1998) in terms of his own studies. He
thought the variation factor of 7 (7/17 of process) was unlikely to be above 2.
If 9 million fibres were found, he thought one would have found more asbestos
bodies. In a case of severe asbestosis the number of fibres found was sometimes
in the hundreds of millions or exceeded billions.
Whether the
deceased contracted asbestosis
[91] The
question whether the deceased contracted asbestosis falls to be answered from a
consideration of all the evidence fully set out above, and not from any part of
it considered in isolation. As this is an action brought by the deceased's
widow in her capacity as executrix only, it is not necessary for her to
establish that asbestosis was the cause of his death.
[92] It is
clear that the deceased was employed as a boiler man by Templetons at various
factory premises in Glasgow from 1957 to 1974. During
that period he was exposed to asbestos to some extent, but, not, I think, to a
great extent and probably not, on the basis of the evidence of Mr Howie, to as
great an extent as he was when serving in the Royal Navy and Merchant Navy
between 1943 and 1956. The degree of exposure to asbestos over the course of
his working life was sufficient to cause him to have pleural plaques. It was
submitted on behalf of the pursuer that asbestos dust was given off into the
atmosphere of the boiler rooms in Templetons in which the deceased worked as a
result of operations carried out by him and others during annual maintenance,
while other periodic maintenance was carried out and during the carrying out of
his ordinary duties and that the level of exposure was substantial-moderate to
heavy during the annual and periodic maintenance and light to moderate during
the daily duties. I do not accept those descriptions of the degree of exposure
to asbestos dust to which the deceased was subject. Mr Howie considered that
the concentration of asbestos dust would have been low on a daily basis (and
the degree of exposure therefore correspondingly low). Dr Crompton described
the deceased's exposure as "low grade exposure over many years". Dr Boyd, in
what I considered to be a good description, described the deceased's exposure
while working for Templetons as "constant but low grade exposure to asbestos
dust". Such descriptions are in keeping with the number of asbestos bodies
found and the asbestos fibre count. Dr Burnett conceded that the number of
asbestos bodies which he identified after even protracted searching was quite
low and that he would have expected to have seen more of them in what he
considered to be asbestosis of such severity. Dr Thomas thought that the
finding of asbestos bodies was a crude indicator of the level of exposure and
it was his opinion that the deceased had had low exposure based on the fibre
count, not the occupational history. Dr Gibbs' fibre count revealed exposure
slightly above background. Having considered all this evidence, I am content to
adopt as my finding of the degree of exposure of the deceased to asbestos dust
while working for Templetons between 1957 and 1974 Dr Boyd's expression,
"constant but low grade exposure".
[93] On the
question of diagnosis, I am not satisfied that the deceased contracted
asbestosis. Indeed, I accept the view of Dr Crompton that there are only two
possible diagnoses in this case, asbestosis or CFA, and I can go further and
state that the evidence satisfies me that what the deceased suffered from was
CFA. It is easy to see why the view was initially taken that he did suffer from
asbestosis. The deceased himself was told when in hospital in November 1998
that he had asbestosis. It is clear from Dr Vernon's letters of 14 July 1999 to the GP and the solicitors that he thought that the
deceased was suffering from asbestosis on the basis of the information then
available to him, consisting of an occupational history of asbestos exposure,
the presence of pleural plaques and pulmonary fibrosis. When, after the death
of the deceased, Dr Burnett added to that information his finding of asbestos
bodies, he similarly reached the conclusion that the deceased had suffered from
asbestosis. Dr Boyd reached a similar conclusion, principally on the basis
that the finding of the asbestos bodies by Dr Burnett weighed very firmly in
favour of asbestosis. In my opinion all three of these doctors erred in the
diagnosis which they reached because they did not consider the full picture,
which I am now able to consider in light of all the evidence led. It is only
being fair to Dr Burnett to record, as I have already done, that he did enter a
caveat to his findings by stating that the number of asbestos bodies which he
identified after even protracted searching was quite low and that he would have
expected to have seen more of them in what he considered to be asbestos of such
severity. In summary my reasons for holding that a diagnosis of asbestosis has
not been established and that a diagnosis of CFA has been established are
contained in the evidence of Dr Crompton, whom I considered to be an excellent
witness. He was thorough and objective in his consideration of all the
available evidence and it was my impression that he was highly authoritative in
all that he said. In more detail my reasons for reaching my conclusion are as
follows.
[94] First
of all, the rapid progression of the deceased's pulmonary disease was atypical
of asbestosis and consistent with CFA. His pulmonary fibrosis was first
diagnosed following his acute admission to hospital on 22 October 1998. He obviously must have had it for some time before
then for it to have progressed to that degree of severity. As his chest was
recorded as having been clear on 18 December
1995
the onset of pulmonary fibrosis must have occurred at some point after that
date and before 22 October 1998. His decline after 22 October 1998 was rapid and he died on 20
April 2000. The progression from first diagnosis of pulmonary fibrosis to death was
therefore over a period of 18 months. As Dr Crompton put it in his report of 10 April 2002 (7/5 of process): "Such a rapid disease progression
is much more in favour of CFA than asbestosis." He read the clinical history as
indicating death within five years from the onset of pulmonary fibrosis and
relied heavily on the rapid progression of the disease as tilting the balance
in favour of CFA. He would have expected asbestosis to have progressed slowly,
if there had been any progression, over 15 to 25 years. The only cases of rapidly progressing
asbestosis were where asbestosis occurred within a few years of massive
exposure and where one would expect to find numerous asbestos bodies and very
high amphibole fibre counts. Dr Boyd accepted that CFA developed rapidly
and that that was a feature for differential diagnosis. Both he and Dr Crompton
were clear that, contrary to the line being adopted on behalf of the pursuer in
the course of the evidence, there was nothing in the clinical history prior to 22 October 1998 to indicate a lung problem. In my view Dr Boyd was
unable to provide a reasonable explanation for the rapid progress of the lung
disease consistent with a diagnosis of asbestosis. He did not offer any such
explanation in either of his two reports, and all he could say in his oral
evidence was that "the interesting thing is how rapidly it's progressed". He conceded that he had never come across a
case of asbestosis where there had been an interval of 20 to 25 years from the
last exposure to asbestos and an interval of 18 months from diagnosis of pulmonary
fibrosis till death. Dr Moran expressed the firm opinion that the rapidity of
the progression of the disease in this case was "completely incompatible with
asbestosis". Dr Gibbs, who is not a clinician but a pathologist highly
experienced in the field of lung disease and well qualified to express an
opinion on the point, was clear that the rapid progression of the disease
pointed to CFA. According to him, where there was a long period since the last
exposure the asbestosis was usually mild and slowly progressive. A long latent
period after exposure and a rapidly progressing disease was much more
consistent with CFA. As he put it in his letter of 17
August 2004 (7/23 of process): "A period of two years from presentation
to death is typical of CFA and extremely unusual for asbestosis." In light of
the evidence on this point from Drs Crompton, Moran and Gibbs, which was
unchallenged and uncontradicted and which I have no hesitation in accepting, I
am satisfied that the rapid progression of the disease in this case was
atypical of, and completely incompatible with, asbestosis, but consistent with
CFA.
[95] Secondly,
the number of asbestos bodies and asbestos fibres found on pathological
examination is inconsistent with asbestosis and consistent with CFA. So far as
the number of asbestos bodies is concerned, Dr Burnett conceded that the number
of asbestos bodies identified after even protracted searching was quite low and
that he would have expected to see more in asbestosis of such severity. Dr Thomas
was satisfied that asbestos bodies 1, 2 and 3 identified by Dr Burnett were in
fact asbestos bodies, but was not certain about asbestos body 4, which he would
have regarded as a possible asbestos body. There is therefore agreement between
Dr Burnett and Dr Thomas to the extent of the finding of three asbestos
bodies by Dr Burnett, and acceptance by Dr Thomas that there was a
possible fourth asbestos body. Dr Thomas regarded the finding of asbestos
bodies as a crude indicator of the level of exposure and therefore relied upon
Dr Gibbs' fibre count for his conclusion that the deceased had had a low level
of exposure to asbestos. Dr Burnett was avowedly antagonistic to the carrying
out of an asbestos fibre count, a process which in his opinion was not very
reliable as asbestos fibres and asbestos bodies were different and only a small
proportion of fibres from blue or brown asbestos ever became asbestos bodies.
He went so far as to state that if asbestos bodies were seen there was no need
for fibre counting as the presence of asbestos bodies meant that the person had
been occupationally exposed to asbestos. Faced with the result of Dr Gibbs'
fibre count showing an exposure level just at the upper limit or just outside
the upper limit of normal, he was ultimately driven to express the view that Dr
Gibbs' fibre count was wrong. I do not find any sound basis for Dr Burnett's
aversion to the process of fibre counting or for his view that in this case Dr
Gibbs' fibre count was wrong. Prior to Dr Gibbs carrying out his fibre count Dr
Thomas made a correct prediction when he stated in his report of 30 May 2003:
"... I would anticipate that a
fibre analysis of his lung tissue would demonstrate a level above background.
It is my view however that the tissue burden is likely to be well below that
normally seen in cases of asbestosis..."
Although Dr Moran is a clinician, and not a
pathologist, I accept his view that Dr Gibbs is the world expert in this
field and the evidence in his report of 13 August 2004 (7/31 of process) that
Dr Gibbs' finding of an asbestos fibre count approximately 1/50th of
that to be expected in a case of asbestosis leaves no room for doubt and
excludes the diagnosis of asbestosis. I
also accept Dr Gibbs' evidence in his report of 13 February 2004 (7/7 of
process) that his results indicate that the most likely diagnosis of this
fibrosis is CFA and are against a diagnosis of asbestosis. I find no conflict
between the results of the asbestos body counts carried out by Drs Burnett and
Thomas on the one hand and the results of the fibre count carried out by Dr
Gibbs on the other hand. I can find no reliable evidence which would
contradict, or even undermine to any extent, the results of Dr Gibbs' fibre
count. I accept the view expressed by Dr Thomas that Dr Gibbs' findings are
entirely consistent with the asbestos body counts. Dr Gibbs himself was of the
view that there was no inconsistency between his asbestos fibre count and the
asbestos body counts.
[96] Thirdly,
in my opinion the radiological evidence is consistent with CFA and inconsistent
with asbestosis. I accept the evidence of Dr Wightman that the deceased's
interstitial fibrosis showed certain radiological features that support the
strong clinical and pathological evidence for CFA rather than asbestosis. Dr
Sproule found moderately severe pulmonary fibrosis in both lungs. He thought
that the presence of benign pleural plaques was suggestive of asbestosis but
accepted that it was not possible on CT scanning alone to ascertain the
aetiology of pulmonary fibrosis with any certainty and that the appearance
could therefore be due to CFA with coincidental pleural plaques due to previous
asbestos exposure. On specific examination of the CT scan he found ground glass
shadowing and early honeycomb formation and stated that the prominent ground
glass opacity suggested an element of active alveolitis. He accepted that only
the pleural plaques pointed in the direction of asbestosis rather than CFA and
also that active alveolitis was more common in CFA than in asbestosis (70%
rather than 50%). It was the opinion of Dr Wightman that two radiological
features favoured CFA over asbestosis as the cause of the interstitial
fibrosis: first, the ground glass appearance, rare in asbestosis and common in
CFA which signified active alveolitis confirmed by the histology of the post
mortem lung carried out by Dr Thomas and, secondly, the honeycomb shadowing
which, while commonly present in the late stages of asbestosis, was usually
accompanied by prominent parenchymal bands, but was in this case accompanied
only by sparse bands, a feature more in keeping with CFA. Dr Wightman explained
that the ground glass appearance showed inflammation of the walls of the
alveoli, causing alveolitis, a definite and unequivocal change which was a
strong pointer in favour of CFA. While Dr Sproule accepted that the parenchymal
bands in this case were "not pronounced", he thought the absence of bands would
be more suggestive of CFA.
[97] I am of
the view that the evidence of Dr Wightman on the significance of the
radiological appearances of the lungs falls to be accepted, not only because I
did not understand it to be seriously challenged in its own right, but also
because it is consistent with the general clinical picture. Dr Crompton was of
the view that the ground glass appearance favoured CFA and stated that he had
never seen alveolitis in a case of asbestosis (the literature suggesting it was
uncommon). Dr Boyd (6/16 of process, para 10) accepted that what he termed
ground glass opacification was more common in CFA than in asbestosis and Dr Moran
(7/30 of process) was of the view that the appearances on the CT scan films,
including the possible component of alveolitis, were entirely consistent with a
diagnosis of CFA which he and others had made on the basis of the clinical
history and the pathological findings.
[98] Accordingly,
for these reasons I am in agreement with the conclusion of Dr Crompton in
his report of 10 September 2004 (7/29 of process) that "on the balance of
probabilities ... the clinical, radiographic and pathological evidence makes a
diagnosis of CFA in a man who has coincidental asbestos-related pleural plaques
very much more likely than asbestosis". I find not only that the pulmonary
fibrosis from which the deceased suffered was not asbestosis, but also that it
was CFA.
Liability
[99] Although
my above finding results in the failure of the pursuer's asbestosis case it is
appropriate that I should proceed to consider, assuming that the deceased had
contracted asbestosis, whether, on the evidence, the case on liability has been
established. The pursuer has four separate cases of liability, which are
pleaded in condescendences 5 to 8. These cases are as follows: (1) negligence
at common law; (2) breach of sections 4, 43 and 47 of the Factories Act 1937
("the 1937 Act"), re-enacted as sections 4, 59 and 63 of the Factories Act 1961
("the 1961 Act"); (3) in respect of exposure after 31 March 1960, breach of
section 5 of the Factories Act 1959 ("the 1959 Act"), re-enacted as section 29
of the 1961 Act; and (4) in respect of exposure after 14 May 1970, breach of
regulation 5(1)(a) of the Asbestos Regulations 1969.
(i) Negligence
[100] So far
as the case based on negligence is concerned, the averments are follows. It was the duty of the defenders to take
reasonable care to protect the deceased against the risk of suffering injury or
disease caused by the inhalation of dust containing asbestos, which they knew
carried with it a material risk of injury or disease to the lungs. They knew or
ought to have known that considerable quantities of asbestos dust were given
off into the atmosphere by the work carried out by the deceased and by others
in close proximity to whom he required to work and that in such circumstances
damage as happened to the deceased was likely to result. It was the duty of the
defenders to take reasonable care (a) to warn the deceased of the nature and
extent of the risk to his health caused by the inhalation of asbestos dust; (b)
to separate off, so far as reasonably practicable, workplaces from which
asbestos dust was created from each other and from places at which asbestos
dust was not created in order the better to control the spread of such dust in
the workplace; (c) not to cause or permit the deceased to work in the vicinity
of other workers so as to increase the risk and extent of inhalation of
asbestos; (d) to provide and maintain sufficient, proper and efficient
ventilation of his workplace in order to supply the deceased with fresh air and
to remove asbestos dust from his breathing zone; (e) to provide and maintain
and instruct and enforce the use of efficient and suitable masks or respirators
for use by the deceased when carrying out his work or when working in proximity
to others with asbestos; (f) to instruct, maintain and enforce a system whereby
floors, benches, ledges and other internal surfaces were regularly damped down
to prevent dust arising therefrom, and were damped down before cleaning; (g) to
provide the deceased with suitable and adequate protective clothing and to
instruct and enforce its use; (h) to provide the deceased with adequate
accommodation for his working clothes and for his non-working clothes and to
maintain a system for cleaning his working clothes so as to avoid or minimise
the risk of inhaling asbestos dust from them; (i) to provide bathing or shower
facilities and to advise the deceased to wash after each shift. (An averment of
a duty to take reasonable care to maintain and instruct and enforce the use of
a sufficient number of suitable and efficient exhaust appliances to extract
asbestos dust from the air at source before it escaped into the atmosphere of
the workplace was departed from).
[101] It was
submitted on behalf of the pursuer that none of the above precautions had been
taken and that this failure, married to the evidence of knowledge of the danger
of asbestos, caused the defenders to be in breach of their common law duty of
care to the deceased. On the question of the state of knowledge of employers
reference was made to the decision of Lord Cameron of Lochbroom in Rennie v Upper Clyde Shipbuilders Ltd (20 May 1993, unreported) in which
his Lordship concluded at page 15 that by at least 1938 any reasonable shipyard
employer would have been well aware of the harmful nature of asbestos dust
itself and the risk of injury arising from its inhalation. That statement, it
was said, fortified the submission on the state of knowledge of the defenders
in this case. For the defenders it was
submitted that it was necessary to relate the degree of exposure to the
standards of the day and ask whether, applying those standards, the defenders
should have done anything. There were no averments, nor was there any evidence,
that the average exposure levels in the defenders' premises exceeded the
standards of the day. There was no evidence that the degree of exposure in
terms of weight and duration gave rise to a foreseeable risk of significant
harm. The exercise undertaken by the pursuer in Boyle v Laidlaw &
Fairgrieve Ltd 1989 SLT 139 had not been followed through by the pursuer in
this case. In that case, which dealt with exposure to wool dust, not
categorised as hazardous in itself, Lord Morison held that "likely to be
injurious" fell to be tested by the state of the employers' actual or imputed
knowledge. The court should resist the temptation to apply modern standards and
today's risk-averse culture to another age: Roe
v Ministry of Health [1954] 2 QB 66.
[102] I have
set out above in detail the evidence relating to the degree of asbestos
exposure to which the deceased was subjected while in the employment of
Templetons. That evidence comes from the deceased's own statement and from the
pursuer, Mr Affleck and Mr Howie. As previously mentioned, Mr Howie considered
that the concentration of asbestos dust in Templetons' premises where the deceased
worked would have been low on a daily basis and the degree of exposure
therefore correspondingly low. I have also set out the evidence relating to the
asbestos body and fibre counts (respectively "quite low" and "slightly above
background"), which is relevant when considering the question of negligence,
and my conclusion that during his period of employment with Templetons the
deceased was subjected to constant but low grade exposure. I therefore accept the submission for the
defenders that there was no evidence that the degree of exposure in terms of
weight and duration gave rise to a foreseeable risk of significant harm to the
deceased (and, in particular, to the risk of contracting asbestosis). I
therefore conclude that it has not been established that Templetons negligently
exposed the deceased to the risk of harm from asbestos dust.
(ii) Sections 4, 43 and 47
of the 1937 Act, re-enacted as sections 4, 59 and 53 of the 1961 Act
[103] These
provisions provided as follows:
"4. Effective and suitable
provision shall be made for securing and maintaining by the circulation of
fresh air in each workroom the adequate ventilation of the room, and for
rendering harmless, so far as practicable, all fumes, dust and other impurities
that may be injurious to health generated in the course of any process or work
carried on in the factory.
43/59. There shall be
provided and maintained for the use of employed persons adequate and suitable
accommodation for clothing not worn during working hours.
47/63. In every factory in
which in connection with any process carried on there is given off any dust or
fumes or other impurity of such character and to such an extent as likely to be
injurious or offensive to the persons employed or any substantial quantity of dust
of any kind all practicable measures shall be taken to protect the persons
employed against inhalation of the dust or fumes or other impurity and to
prevent its accumulating in any workroom, and, in particular, where the nature
of the process makes it practicable, exhaust appliances shall be provided and
maintained as near as possible to the point of origin of the dust or fumes or
other impurity, so as to prevent its entering the air of any workroom."
[104] So far
as section 4 is concerned, the submission for the pursuer was that there were
two possible interpretations of that provision. The first was that it could be
separated into two distinct parts giving rise to separate duties, and the
second was that it gave rise to only one duty as the second part required to be
read as qualifying the first part. The first possible interpretation had so far
not found favour with any court. In Ebbs v James Whitson & Co Ltd [1952] 2 QB
877 Hodson LJ at page 886 expressed the opinion that there was "no duty
imposed by this particular section apart from the duty of ventilation". At
pages 884-5 Denning LJ said:
"In my opinion section 4
cannot be taken literally. It is directed to ventilation, and the governing
words are 'by the circulation of fresh air', which must be read as governing
both the first and second parts of the section. This view is supported by
subsection (2), and also by the fact that any other view would render section 4
inconsistent with section 47, which deals with dust that is 'likely to be
injurious to health'. It would be very strange if a person injured by dust, who
could not succeed under section 47, because the dust was not 'likely to be
injurious', could nevertheless recover under section 4 on the ground that it
'may be injurious'. In my opinion, therefore, section 4 must be read as
confined to defects of ventilation and it does not extend to description of
protection in other respects."
Singleton LJ at pages 882-3 was to the like effect.
[105] It was
submitted that the decision in Ebbs was
wrong: although it had been followed in subsequent cases it had not been
subjected to particularly close scrutiny. The duty in section 4 to make
effective and suitable provision for rendering harmless, so far as practicable,
all fumes, dust and other impurities that may be injurious to health generated
in the course of any process or work carried on in the factory was not confined
to ventilation: there was a comma before the words "and for rendering". In Graham
v Co-operative Wholesale Society Ltd [1957]
1 All ER 654 Devlin J said at pages 659-660:
"The contention of counsel
for the defendants concentrated on the more general aspect of section 4(1).
Counsel submitted that it was a subsection dealing with adequate ventilation in
the ordinary sense of the term, that is, securing adequate ventilation by the
circulation of fresh air as that was ordinarily understood, by vents and
windows and doors and so on, and that the subsection was not dealing with the
provision of exhaust appliances for the removing of a particular impurity. He
fortified that submission by reference to section 47 of the Act of 1937,
where exhaust appliances are specifically dealt with. In the last part of section 47(1)
it is provided that:
'..... where the nature of the
process makes it practicable, exhaust appliances shall be provided and
maintained, as near as possible to the point of origin of the dust or fume or
other impurity, so as to prevent it entering the air of any workroom.'
That, said counsel, is a
provision which is specifically dealing with the sort of situation for which
these extractors were provided, and the obligation is based on section 47.
Counsel for the plaintiff also relied on section 47, which I shall have to
consider next, but at the moment I am dealing with section 4(1), and
counsel for the defendants submitted that the proper construction of
section 4(1) is that it should not be held to apply to matters which are
covered by section 47.
In my judgment that
submission is right, and section 4(1) should not be treated as requiring
the provision of exhaust appliances. In Ebbs
v James Whitson & Co Ltd,
while the Court of Appeal did not expressly say that, I think that the
reasoning which they adopted on the construction of section 4(1)
inevitably leads to that conclusion, for the basis of the submission of counsel
for the defendants (and it was also, I think, the basis of the reasoning in the
Court of Appeal) is that, if section 4(1) were available, it would impose
a duty so much more stringent than that imposed by section 47 that there
would be no room for section 47. It is true that it may be said that section 47
applies to a substantial quantity of dust, whether it is likely to be injurious
or not; but taking, for the purpose of comparison of the two sections, a small
quantity of dust, then section 47(1) requires that a small quantity of
dust which is 'likely to be injurious' should be removed by exhaust appliances,
but section 4, on the reading which the plaintiff desires to give to it,
would already have provided that a small quantity of dust which 'may be
injurious' would have to be removed by exhaust appliances; and the obligation
to remove something which 'may be injurious' is much more stringent than the
obligation to remove that which is 'likely to be injurious'. That is a
reasoning specifically adopted in the Court of Appeal in Ebbs v James Whitson & Co
Ltd, and it applies equally on the point which I am considering.
Another point is that,
whereas the obligation under section 47(1) to provide exhaust appliances
arises only where the nature of the process makes it practicable to do so,
there is an unrestricted obligation under the first part of section 4(1),
and an obligation 'so far as practicable' under the second part of section 4(1).
Whichever be the relevant part of section 4(1), the term 'where the nature
of the process makes it practicable' in section 47(1) is a more favourable
limitation from the employer's point of view than anything that is contained in
section 4(1). That, therefore, again means that section 47(1) would
be unnecessary if section 4(1) were given the wider meaning of application
to exhaust appliances. The only scope that would be left for section 47(1)
would be in relation to substantial quantities of dust that were not likely to
be injurious, and even then, as I have said, the provision in relation to
exhaust appliances would be a narrower one than that which is to be found in section 4(1)
on the wider reading.
For these reasons, not
merely because I respectfully adopt the nature of the reasoning of the Court of
Appeal in Ebbs v James Whitson & Co Ltd, but also because, on the larger aspect
of endeavouring to put a proper construction to section 4 in its place in
the Factories Act 1937 as a whole, I am satisfied that that on its proper
construction section 4(1) refers only to adequate ventilation for ordinary
purposes by the circulation of fresh air and does not include any requirement
which would mean that exhaust appliances would have to be provided to remove
dust from the point of egress so as to prevent it entering the air. Section 4
is dealing with the circulation of fresh air which gets rid of impurities which
come into the air, whereas section 47 is dealing with methods of
prevention, of stopping the impurities from ever getting into circulation at
all."
[106] In Brophy v J C Bradfield & Co Ltd [1955] 3 All ER 286 the deceased was a
lorry driver employed by the defendants in whose factory premises there was a
boiler room containing a coke furnace and boiler which provided hot water for
central heating. He accidentally killed himself by interfering with the furnace
which had operated without accident for 25 years and which he had no right to
touch. The Court of Appeal held that the boiler room was not a workroom within
the meaning of section 4(1) of the 1937 Act. At page 289G Singleton LJ
stated:
"On the facts it does not
appear to me that the boiler room was a workroom within the meaning of s 4(1)
of the Act or that the fumes were 'generated in the course of any process or
work carried on in the factory'. This was a boiler used for heating the
factory. Moreover, in the absence of any evidence it cannot be said that
effective and suitable provision had not been made having regard to the fact
that the boiler had existed for some twenty-five years in the same place with
such ventilation as there was from above and through the flue without anybody
ever having noticed anything wrong so far as the evidence shows..... I do not
think that s 4(1) of the Act applies to this case."
[107] The
submission for the pursuer was that the decision in Brophy could be distinguished because (a) the boiler room in that
case was not the place where the deceased worked, and (b) in Templetons the
boilers were used to generate not only heat but also power for the manufacturing
process.
[108] The
submission for the defenders on section 4 was that section 4(1) related to
adequate ventilation for ordinary purposes (Graham),
that a boiler room supporting a factory (as in the present case) was not a
"workroom" in the ordinary sense (Brophy)
and that there was no evidence that any breach of section 4 was likely to
have materially contributed to the
deceased's condition.
[109] In my
opinion the construction placed on section 4 by the Court of Appeal in Ebbs and Devlin J in Graham is correct and I am therefore not
prepared to depart from it and adopt the construction proposed on behalf of the
pursuer. I do not accept the submission that the decision in Ebbs, although followed in subsequent
cases, has not been subjected to particularly close scrutiny. The terms of the
subsection were subjected to very close scrutiny by Devlin J in Graham and he came to the same
conclusion as the Court of Appeal in Ebbs.
I find the reasoning of Devlin J highly persuasive, indeed faultless. I therefore
hold that the duty imposed by section 4 is a duty restricted to ventilation.
Moreover, I am not satisfied that any boiler room in the defenders' factories
in which the deceased worked constituted a "workroom" within the meaning of
section 4 (Brophy). In its ordinary
sense the word "workroom" means, in my opinion, a room where the dedicated
manufacturing work of the factory is carried on. In this case there is no
evidence that the manufacturing work of the factory was carried on in a boiler
room.
[110] The only
evidence about ventilation came from Mr Affleck and it was vague in nature. It
consisted of the following question and answer:
"What would the conditions
be like generally speaking in the boiler room of one of these factories? -
Pretty grim, they were all old factories and apart from coal dust they'd ash,
it was pretty poor ventilation and broken asbestos quite considerable amounts.
But at that time the asbestos danger was ignorance, we didn't know anything
about it."
[111] No
precise evidence was led about the systems of ventilation, if any, which were
operated in the boiler rooms of Templetons' factories during the relevant
period and in these circumstances I find myself unable to make any finding
about whether there was a breach of section 4.
[112] So far
as section 43 of the 1937 Act and section 59 of the 1961 Act are concerned, no
evidence was led about the accommodation or lack of it for clothing not worn
during working hours and no submissions were made about these provisions. In
these circumstances I cannot hold that there was any contravention of these
provisions. In any event, even if there had been, there was no evidence to
suggest that the condition of the clothing not worn by the deceased during
working hours caused or contributed to his lung condition.
[113] So far
as section 47 of the 1937 Act and section 63 of the 1961 Act are concerned, the
submission for the defenders was that insulation work in a boiler room was not
"in connection with any process carried on" in the factory. In Brophy at page 290B Singleton LJ,
following upon the passage cited above and a reference to section 47 of
the 1937 Act, said:
"That section again deals
with workrooms and with processes carried on in a factory. For the reason I
have given with regard to s 4(1), I do not think that s 47(1) applies to the
facts of this case."
[114] In Banks v Woodhall Duckham Ltd [1996] CLYB 2990 the plaintiff was a pipe
fitter in a steelworks who claimed damages for bilateral diffuse pleural
thickening caused by exposure to asbestos dust. The Court of Appeal held that
section 47 of the 1937 Act was not applicable to his case because the work of
lagging pipes was not a process carried on in the factory: the factory's
process was the manufacture of steel.
[115] I agree
with the decisions in the above two cases and I do not think that sections 47
of the 1937 Act and 63 of the 1961 Act apply to the facts of this case. It
seems to me that these sections were intended to deal with dust or fumes given
off in a workroom in a factory in the course of the carrying out of the
manufacturing process. As the deceased worked in a boiler room which was not a
workroom and the dust and fumes were not given off in the course of a process
carried on in the factory in my opinion the sections have no application to the
facts of this case.
(iii) Section 29 of the 1961
Act (previously section 5 of the 1959 Act)
[116] These
provisions were in force as from 31 March 1960. Section 29(1) of the 1961
Act, which re-enacted section 5(1) of the 1959 Act, provided as follows:
"There shall, so far as is
reasonably practicable, be provided and maintained safe means of access to
every place at which any person has at any time to work, and every such place
shall, so far as is reasonably practicable, be made and kept safe for any
person working there."
[117] In
condescendence 7 it is averred that "the defenders failed to comply therewith
in respect that the deceased was exposed to noxious dust therein". The
submission for the pursuer was that there was no doubt that the boiler room of
each of the defenders' factories was a place at which the deceased had to work,
the conditions in each boiler room were the same, with the exception of that in
the Dixons Blazes factory, and the defenders were in breach of section 29.
Reference was made to Mains v Uniroyal Englebert Tyres Ltd 1991 SC
158, in which it was held by the Inner House that, apart from the defence of
reasonable practicability, the obligation on an employer under section 29(1)
was to make and keep the place of work safe from dangers regardless of whether
or not they were foreseeable. The submission for the defenders was that it was
questionable whether the duty to provide a safe place of work was applicable to
what concerned activities rather than the specific location. It was not
reasonably practicable to take precautions where exposures were only
intermittent and quite possibly indirect. The hazard warning in the 1956 report
by HM Inspector of Factories was essentially directed to employers of
full-time asbestos workers. In Yates v Rockwell Graphic Systems Ltd [1988] ICR
8 the plaintiff contracted dermatitis as a result of his hands having come into
contact with heavily contaminated coolant for 25% of the period of his
employment in the defendants' light machine shop. Steyn J, as he then was,
stated at pages 14G to 15C as follows:
"In the present context the
first question is whether section 29 can apply to the conditions of work to
which the plaintiff was exposed. It is, of course, clear that 'place' within
the meaning of section 29 does not simply mean the floor space within a
factory. One has to have regard to the permanently installed machinery and the
regular activities carried on in the factory in order to decide whether the
place is safe. Having regard to the fact that the plaintiff was exposed in his
daily routine, as to 25 per cent of his working time, to contaminated coolant,
which involves an enhanced risk of dermatitis, it is as a matter of common
sense difficult to see why such a case should fall outside the scope of section
29. The submission was, as I understand it, that it falls outside the scope of
section 29 because the plaintiff is only exposed to the enhanced risk for 25
per cent of his working life. The plaintiff cited a number of authorities and
so did the defendants. Helpful as these authorities are, I am content to decide
the matter on the basis of the natural and ordinary meaning of the words in
section 29, read in a common sense way and against the background of the
obvious legislative purpose. After all, it is difficult to say that a seat of
work is safe if, as to 25 per cent of his working time, it exposes the employee
to a serious risk of contracting an unpleasant disease. In any event the
statute was passed for the benefit of workmen and I unhesitatingly choose the
interpretation which serves to promote the purpose of that statute. I rule that
section 29 can apply in the present case."
[118] It was
submitted on behalf of the defenders that it was questionable whether section
29 could apply where the activity giving rise to exposure had been carried out
for, say 5% of the employee's time. The question had to be asked, for how long
was the deceased exposed to asbestos dust? "Guilty" dust was excess dust which
would have been prevented and had to have made a material contribution to the
illness. There was a lack of evidence on this point as there was no relevant
evidence from any of the medical witnesses or Mr Howie.
[119] In my
opinion there is no good reason why section 29 should not be applicable to the
facts of this case. Adopting the approach to that section of Steyn J in Yates, with which I agree, I think that
a place of work is not made and kept safe for any person working there when it
contains a quantity of asbestos dust which is likely to be injurious to the
health of any such person. Having said that, I accept the submission for the
defenders that there is a lack of evidence in this case as to whether the
quantities of asbestos dust in the boiler rooms of Templetons' factories were
likely to be injurious to the health of persons working there. I refer to my
finding above that the deceased was subject to constant but low grade exposure
exposure to asbestos while working for Templetons. Moreover, I am not
satisfied, for the same reasons as in relation to the common law case, that any
exposure would have made a material contribution to asbestosis, had he suffered
from it.
(iv) The Asbestos
Regulations 1969
[120] These
regulations came into operation on 14 May
1970.
They therefore applied only to the last four years of the deceased's employment
with Templetons, for approximately 18 months of which he worked at the Dixons
Blazes factory. Regulation 7(1) provided:
" .... No process to which
these Regulations apply shall be carried on .... unless equipment is provided,
maintained and used which produces an exhaust draught which prevents the entry
into the air of any workplace of asbestos dust."
[121] It was
conceded on behalf of the defenders that these regulations applied during the
relevant period but maintained that the question of "reasonable practicability"
could be decided on inferences from the evidence without recourse to onus of
proof being on the defenders (Jenkins v Allied Ironfounders 1970 SC (HL) 37 per
Lord Hodson at page 43) and that there was no evidence that any breach was
material to the deceased's condition in terms of overall exposure.
[122] As the
entry of asbestos dust into the air of the workplace was not prevented by
Templetons during the relevant period, and nothing in the evidence points to it
not having been reasonably practicable for equipment to have been provided,
maintained and used which produced an exhaust draught which prevented such
entry, Templetons were in breach of Regulation 7(1) during the relevant period.
On the other hand, had I been satisfied that the deceased had contracted
asbestosis, I would not have been satisfied on the evidence that his low grade
exposure to asbestos dust during his period of his employment with Templetons
had made a material contribution to his condition.
Damages
(i) Quantum
[123] By joint
minute (no 44 of process) it was agreed that, in the event that I were to find
in favour of the Pursuer, damages were agreed at £80,000 inclusive of interest,
subject to any apportionment the court may determine on a time/exposure basis
to reflect the defenders' contribution
to the deceased's disease, with interest from the date of decree until payment
on the relevant apportionment of the principal sum of £57,500 only.
(ii) Apportionment
[124] The
submission for the defenders that, if the pursuer were successful, their
liability should be apportioned on a time / exposure basis was based on the
decision of the Court of Appeal in Holtby
v Brigham & Cowan (Hull) Ltd [2000] 3 All ER 421. Identifying the question in issue at the outset of his judgment
at para 1, page 423 b-c Stuart-Smith LJ stated:
"This case raises a point of
general importance which, surprisingly, does not appear to have been considered
previously by this court. The question is this: where a claimant suffers
injury, in this case asbestosis, as a result of an exposure to a noxious
substance by two or more persons, is the defendant who is one of those persons
whose tortuous act has made a material contribution to the injury liable in
respect of the whole resulting disability, subject only to such rights as he
only has against tortfeasors? Or, is he liable only to the extent that he has
contributed to the disability?"
The judge at first instance held that the latter was
the correct answer and the Court of Appeal dismissed the appeal against his
decision. The judge accepted the evidence of a medical witness that it was
cumulative exposure which caused asbestosis and aggravated it, and that if the
claimant had sustained exposure to asbestos dust only whilst working for the
defendants his condition would probably have been less. He then went on to say:
"The defendants are liable
only for the damage which they have caused, but the quantification of that
factor is difficult. Whilst there is no mathematical division to be made in
medical terms, for the purpose of assessment I have felt bound to apply a
discount factor and I have done so in the amount of 25%."
[125] In the
Court of Appeal counsel for the claimant (Mr May) relied on passages from three
decisions of the House of Lords, namely, Bonnington
Castings Ltd v Wardlaw [1956] AC 613 per Lord Reid at page 620; McGhee
v National Coal Board [1972] 3 All ER 1008 per Lord Salmon at page 1017;
and Wilsher v Essex Area Health Authority [1988] AC 1074 at page 1090, as
well as the unreported decision of Longmore J in Milner v Humphreys &
Glasgow Ltd (24 November 1998) and the decision of the United States Court
of Appeal Fifth Circuit in Borel v Fibreboard Paper Products Corp (1973) 49
F 2d 1076. In Milner Longmore J said:
"Many diseases depend on
cumulative exposure; many diseases may have more than one cause; some causes
may be tortuous in origin and some may be non-tortious. It may be difficult to
separate the two. Where, as in Thompson v
Smith Shiprepairers (North Shields) Ltd [1984] QB 405, the operations of a
single employer or the same operations of two consecutive employers may have
been tortious only after a certain date justice may require and the facts may
permit an apportionment to be made so that the tortious employer is not held
liable for the consequences of non-tortious conduct of himself or the conduct,
tortious or otherwise, of another. Such cases do, however, present quite
serious factual difficulties and the law has been concerned to ensure that a
meritorious plaintiff does not fail for want of proof.
Mr May for the plaintiff
submitted that where there are concurrent causes of an industrial disease and a
plaintiff can show that a defendant's breach of duty has materially contributed
to the disease, he can recover for the consequences of that disease (see Bonnington Castings Ltd v Wardlaw [1956] AC 613). He then submitted that the same principle should apply to sequential
causes of industrial disease.
I do not think that this
argument can be accepted in the broad form in which it was put. As Mustill J
pointed out (Thompson's case [1984]
QB 405 at 441), the Bonnington principle
is but a variant of the principle that, where an injury is indivisible, any
tortfeasor whose act has been a proximate cause must compensate for the whole
injury, leaving the tortfeasor to sort out with other possible tortfeasors any
other appropriate claim for contribution (see Dingle v Associated
Newspapers Ltd [1961] 2 QB 188 per Devlin LJ). Where there are causes
concurrent in time, the likelihood is that a resulting injury will be
indivisible; but where causes are sequential in time, it is not likely that an
injury will be truly indivisible especially if .... the injury is a disease which
can get worse with cumulative exposure. The Bonnington
case can, nevertheless, assist the plaintiff to this extent: the principle,
as formulated by Mustill J, is that where it is proved that a wrongful act has
made a material contribution to the plaintiff's injury, the law regards this as
sufficient discharge of the plaintiff's burden of proof on causation to render
the defendant liable for the injury in full. That does not mean that no
question of apportionment can ever arise but it does, in my judgment, mean that,
unless the defendant pleads and proves facts which justify apportionment, the
plaintiff can recover in full."
[126] In the
American case of Borel Wisdom J
summarised as follows the effect of an earlier decision when giving the
judgment of the court:
"Where several defendants
are each shown to have caused some harm, the burden of proof (or burden of
going forward) shifts to each defendant to show what portion of the harm he
caused. If the defendants are unable to show any reasonable basis for division,
they are jointly and severally liable for the total damages." (See (1973) 493 F
2d 1076 at 1095.)
[127] At para
20, pages 428h-429c in Holtby Stuart
Smith LJ dealt with the submissions on behalf of the claimant as follows:
"I do not accept Mr May's
submissions. In my judgment, as the passages cited from the three House of
Lords' decisions show, the onus of proving causation is on the claimant; it
does not shift to the defendant. He will be entitled to succeed if he can prove
that the defendant's tortious conduct made a material contribution to his
disability. But strictly speaking the defendant is liable only to the extent of
that contribution. However, if the point is never raised or argued by the
defendant, the claimant will succeed in full as in the Bonnington case and McGhee's
case. I agree with Judge Altman that strictly speaking the defendant does not
need to plead that others were responsible in part. But at the same time I
certainly think that it is desirable and preferable that this should be done.
Certainly the matter must be raised and dealt with in evidence, otherwise the
defendant is at risk that he will be held liable for everything. In reality I
do not think that these cases should be determined on onus of proof. The
question should be whether at the end of the day and on a consideration of all the evidence the claimant has proved that
the defendants are responsible for the whole or a quantifiable part of his
disability. The question of quantification may be difficult and the court only
has to do the best it can using its common sense, as Lord Salmon said in the
passage cited. Cases of this sort, where the disease manifests itself many
years after the exposure, present great problems, because much of the detail is
inevitably lost. ..... But in my view the court must do the best it can to
achieve justice, not only to the claimant, but to the defendant, and among
defendants."
[128] The
Court of Appeal in Holtby adopted and
applied the earlier decision of Mustill J in Thompson v Smiths Shiprepairers
(North Shields) Ltd [1984] QB 405, in which the plaintiffs had been engaged
in the ship repair industry where they had been exposed to excessive noise over
extended periods of their employment which had resulted in deafness. All
excessive noise had contributed to their disability, but the defendant
employers were not guilty of negligence until 1963, by which time considerable
damage had been done, though it was not recognisable. There was also the
problem of successive employers. Mustill J rejected arguments on behalf of the
plaintiffs similar to those raised by Mr May for the claimant in Holtby and said at pages 443-444:
"The defendants as well as
the plaintiffs are entitled to a just result. If we know (and we do know, for
by the end of the case it was no longer seriously in dispute) that a
substantial part of the impairment took place before the defendants were in
breach, why in fairness should they be made to pay for it? The fact that
precise quantification is impossible should not alter the position. ... Thus,
whatever the position might be if the court were to find itself unable to make
any findings at all on the issue of causation and was accordingly being faced
with a choice between awarding for the defendants in full, or for the plaintiff
in full, or on some wholly arbitrary basis such as an award of 50%, I see no
reason why the present impossibility of making a precise apportionment of
impairment and disability in terms of time should in justice lead to the result
that the defendants are adjudged liable to pay in full, when it is known that
only part of the damage was their fault. What justice does demand, to my mind,
is that the court should make the best estimate which it can, in the light of
the evidence, making the fullest allowances in favour of the plaintiffs for the
uncertainties known to be involved in any apportionment. In the end,
notwithstanding all the care lavished on it by the scientists and by counsel, I
believe that this has to be regarded as a jury question, and I propose to treat
it as such."
[129] Mummery
LJ formally concurred with Stuart-Smith LJ, but Clarke LJ (now the Master of
the Rolls), while holding that, on the facts found, the judge's conclusion was
justified, disagreed with Stuart-Smith LJ on the question of burden of proof.
At paras 30-37, pages 431e-433h, he said:
"30. The point on which I
regret that I am unable to agree with Stuart-Smith LJ relates to burden of
proof. In short, I prefer the view which has been expressed by Longmore J in
the passage which has been quoted from his judgment in Milner v Humphreys &
Glasgow Ltd. My reasons are shortly as follows.
31. The burden of proving
that the defendants' negligence or breach of duty caused the relevant injury or
condition is on the claimant (see Bonnington
Castings v Wardlaw [1956] AC 613,
Nicholson v Atlas Steel Foundry and Engineering Co Ltd [1957] 1 All ER 776, McGhee v National Coal Board [1972] 3 All ER 1008 and Wilsher v Essex Area Health
Authority [1988] AC 1074). The claimant discharges that burden by proving
that the defendants' negligence or breach of duty made a material contribution
to his injury or condition. Thus, for example, in Wilsher's case Lord Bridge of Harwich described the decision in the
Bonnington case in this way:
'Their Lordships concluded,
however, from the evidence, that the inhalation of dust to which the pursuer
was exposed by the defenders' breach of statutory duty had made a material
contribution to his pneumoconiosis which was sufficient to discharge the onus
on the pursuer of proving that his damage was caused by the defenders' tort.
([1988] AC 1074 at 1086.)'
He added that the next year,
in Nicholson's case, the House of
Lords held, in another case of pneumoconiosis, that the employers were liable
for the employee's disease arising from the inhalation of dust from two
sources, one 'innocent' and the other 'guilty', on facts virtually
indistinguishable from those in the Bonnington
case.
32. It is, I think, at least
arguable on the basis of those decisions that in a case of this kind, where the
claimant proves that two employers have made a material contribution to his
condition, he is entitled to judgment in full against each, leaving them to
contest issues of contribution between them. That would certainly be the case
where the injury was truly indivisible, so that each made a material
contribution to the same damage, as in a case of damage caused by, say, a
collision. However, in this class of case, as Longmore J observed, the injury
or disease is not truly indivisible, but is contributed to by sequential
exposure to asbestos which aggravates the condition. (His lordship then quoted
what Mustill J had said in Thompson at
p 443 and stated that in his opinion that approach applied to the facts of the Holtby case.)
33. Assuming that to be
correct, the question is whether, once the claimant has proved that the
defendants' breach made a material contribution to his condition, he is
entitled to judgment unless the defendants prove that a definable part of his
condition was caused either by 'innocent' asbestos or by 'guilty' asbestos
caused by others, as Longmore J thought, or whether, once the point has been
raised by the defendants, the claimant is not entitled to anything unless he
proves what part of his disease was caused by the defendants.
34. It seems to me that
Longmore J's view is more consistent with the approach in the cases. If the
position were that the claimant cannot, as a matter of law, recover anything
more than the contribution which the defendant has tortiously made to his
disease, it does seem to me to be surprising that none of their Lordships
mentioned the point in either the Bonnington
case or in Nicholson's case. That
seems to me to be so even though (as appears to have been the case) the point
was not raised by counsel. Moreover, Mustill J's approach in Thompson's case also seems to me to be
consistent with the conclusion that the burden of proof in this regard (whether
classified as the legal burden or the evidential burden) is on the defendant.
(His Lordship then quoted what Mustill J said in Thompson at [1984] QB 405 at 443-444.) It seems to me that it would
not be appropriate to make 'the fullest allowances in favour of the plaintiffs'
if the burden of establishing the apportionment were on them and not on the defendants.
35. I do not share the view
that justice demands that the burden on this question should be on the
claimant. It seems to me that once the claimant has shown that the defendants'
breach of duty has made a material contribution to his disease, justice
requires that he should be entitled to recover in full from those defendants
unless they show the extent to which some other factor, whether it be
'innocent' dust or tortious dust caused by others, also contributed. It follows
that I regard the part of the judgment of the Fifth Circuit of the United
States Court of Appeals in Borel v Fibreboard Paper Products Corp (1973)
493 F 2d 1076 at 1095 as expressing a just result and not an unjust result.
36. Just as the burden is on
a negligent defendant to prove contributory negligence, so the burden should be
on a negligent defendant who has contributed to the claimant's disease to show
that others have also contributed and to what extent. I do not think it matters
in this regard whether such a burden is classified as a legal burden of proof
or an evidential burden, the result will be the same and, in either event, in
my opinion defendants must plead the point if they wish to rely on it.
37. I should add, by way of
postscript, that, although I have expressed a different view from that
expressed by Stuart-Smith LJ, I entirely agree with him that in reality these
cases should not be determined by onus of proof. That seems to me to be so
whatever the correct view of where the burden of proof lies. That is because,
as Mustill J put it in Thompson's case:
'The fact that precise quantification is impossible should not alter the
position. The whole exercise of assessing damages is shot through with
imprecision.' (See [1984] QB 405 at 433.) The assessments of questions of this
kind are essentially jury questions which have to be determined on a broad
basis, so that it will only be in the rarest of cases that recourse need be had
to the burden of proof. Moreover, this is not such a case on the facts. I agree
that the appeal should be dismissed."
[130] The
question of apportionment has been raised in the pleadings in the present case.
In answer 9 at p 27E the defenders aver:
"Esto the deceased
did suffer from asbestosis (which is denied), it is explained and averred that
the severity of such disease is dose exposure related."
Plea-in-law 4 for the defenders is in the following
terms:
"Esto the deceased
died of (sic) asbestosis for which
these defenders are responsible (which is denied), any damages awarded should
be on a several basis reflecting the degree of contribution by these defenders
to said condition."
[131] It was
submitted for the defenders that in a disease such as asbestosis there was a
dose / response relationship, on the medical evidence the loss was divisible
and the defenders' contribution could not have caused all the symptoms. As the
deceased had spent 16 years working for Templetons and 13 years working in the
Navy, the defenders were liable only to the extent of 55%. The question was,
what damage was caused by the defenders' negligence? The present case was no
different from Holtby, where the
disease was quantifiable by reference to dose. In Allen v British Rail
Engineering [2001] ICR 942, a case of vibratory white finger, Schiemann LJ,
delivering the judgment of the Court of Appeal, having considered the cases on
this issue referred to above, said at para 20, p 952C-F:
"In our judgment the case
law as it now stands establishes five propositions of which the first is
concerned with liability and the others with quantifying damages. (i) The
employee will establish liability if he can prove that the employer's tortious
conduct made a material contribution to the employee's disability. (ii) There
can be cases where the state of the evidence is such that it is just to
recognise each of two separate tortfeasors as have caused the whole of the
damage of which the claimant complains; for instance, where a passenger is
killed as a result of a head-on collision between two cars, each of which was
negligently driven and in one of which he was sitting. (iii) However in
principle the amount of the employer's liability will be limited to the extent
of the contribution which his tortious conduct made to the employee's
disability. (iv) The court must do the best it can on the evidence to make the
apportionment and should not be astute to deny the claimant relief on the basis
that he cannot establish with demonstrable accuracy precisely what proportion
of his injury is attributable to the defendant's tortious conduct. (v) The
amount of evidence which should be called to enable a judge to make a just
apportionment must be proportionate to the amount at stake and the
uncertainties which are inherent in making any award of damages for personal
injury."
[132] In Simmons v British Steel PLC [2004] SC (HL) 94 Lord Rodger of Earlsferry,
dealing with a submission by the defenders that the Wardlaw principle did not apply to the facts of that case, said at
para 58, p 113:
"The usual rule applies, and
in the absence of any basis for identifying and apportioning the respective
roles played by the various factors in the development of the pursuer's
condition, the pursuer is entitled to recover damages for all of his injuries."
[133] In Woodland v Advocate General for Scotland (24 March
2004,
unreported) a plea to the competency of a joint and several conclusion against
three defenders in a vibration white finger case was taken. The submission for
the defenders was that vibration white finger, like asbestosis, was a
cumulative disease which was dose or time related, that the pursuer's case
alleged three separate, unconnected delicts, that there was no averred basis
upon which any of the defenders should be made responsible for the acts and
omissions of the others and a joint and several conclusion was therefore
incompetent. It was stated that in asbestosis cases there was a growing
practice of pleading separate conclusions against each defender as harm was
divisible on the basis of time exposure and it was not equitable to hold each defender
responsible for the consequences of the whole period of exposure. At para 14
Temporary Judge Reid QC held that the decision in Holtby, in which the trial had taken place, did not affect the
position at procedure roll stage. He referred to the judgments in Holtby, and, after summarising the
judgment of Clarke LJ, said:
"I agree with and adopt
these views, which seem just, sensible and in accordance with principle and
practice in Scotland. In particular, they seem
to me to be consistent with Scottish House of Lords authority, namely, Wardlaw v Bonnington Castings 1956
SC(HL) 26 and McGhee v National Coal Board 1973 SC(HL) 37 at
55, 57 and 62."
At para 20 he stated:
"A defender is only liable
for the consequences of his own actions; therefore one must consider what
damage was caused or materially contributed to by the defender's negligence (Balfour v William Beardmore & Co Ltd 1956 SLT 205 at 216). Where an
injury is caused by two (or more) factors operating cumulatively, one (or more)
of which factors is a breach of duty by a defender and one (or more) is not, or
is a breach by another, in such a way that it is impossible to ascertain the
proportion in which the factors were effective in producing the injury or which
factor was decisive, the law does not require a pursuer to prove the impossible
but holds that he is entitled to damages for the injury if he proves, on a
balance of probabilities, that the breach or breaches of duty materially
contributed to causing the injury; if such factors so operate cumulatively, it
is not material whether they do so concurrently or successively (see McGhee v National Coal Board 1973 SC(HL) 37 per Lord Simon of
Glaisdale at page 57). If it is possible, it remains open to a defender,
having made appropriate averments in his pleadings, to establish, if he can,
the limited extent or proportion of the loss which was the consequence of his
own actions and thus to restrict his liability. Thus in Balfour one of the other pursuers had been exposed to dust in the
steel industry for some 16 years before entering the employment of the
defender. The medical evidence was that within three years thereafter he had
contracted pneumoconiosis (214-5); it was held that the defender materially
contributed to the pursuer's injury and was liable for the whole of the
pursuer's loss."
[134] The
facts in Balfour v William Beardmore & Co Ltd 1956 SLT
205 are briefly summarised by Temporary Judge Reid in the above excerpt from
his opinion, but in the report the court also dealt with the case of another
pursuer by the name of James Begg, who had contracted pneumoconiosis
before he entered the defenders' employment. It was held that his condition had
been aggravated by two years exposure to dust in the defenders' employment,
materially contributed to by the defenders' negligence in failing to issue him
with a respirator. At page 216 Lord Strachan
said:
"The assessment of damages
in this case raises an important question of principle as to whether the
defenders are liable for the full amount of the pursuer's loss and injury or
only for a proportion thereof corresponding to the proportion of the
aggravation which is attributable to their negligence. Counsel for the pursuer
argued that the defenders were liable for the full amount in respect that their
negligence had caused the pursuer's disability, having converted a man who was
fit for work as a steel dresser into a man unfit for anything but light work.
In any event, it was argued, the defenders' negligence had materially
contributed to the pursuer's disability and they were therefore liable for the
whole consequences. It was maintained that if the actings of previous employers
were to be taken into account at all, there are only two alternatives. Either
those previous employers were negligent, in which case the previous employers
and the defenders are joint wrongdoers and each is liable in solidum; or the previous actings were innocent, in which case
they have no bearing on the matter. In my opinion that is not a true statement
of the position. I cannot possibly hold in this case that any of the previous
employers were negligent, and therefore no question of joint wrongdoers can
arise. If, on the other hand, the previous employers were not negligent, that
would not in my opinion solve the question which I have to decide. The question
is, what damage was caused by the defenders' negligence? The true view I think
is this. The immediate reason why the pursuer was transferred to light work was
because his disease had been detected by radiological examination, and not
because his employment with the defenders had caused him to contract the
disease. The defenders were not responsible for the pursuer contracting
pneumoconiosis. He had the disease when he was first employed by them, but it
had not been detected because no one had x-rayed him. The defenders, in an
effort to do the best for their workers, detected the disease by a mass x-ray
examination. It would be strange indeed if their efforts for the safety of the
pursuer should render them liable for the consequences of 29 years
exposure to dust in the employment of others over which they had no control.
The defenders are liable only for the consequences of their own actions and in
the peculiar circumstances that means, in my opinion, that they are liable only
for the results of the aggravation which their own negligence has caused. Upon
the medical negligence it is possible to determine the extent of that
aggravation. In these circumstances, the correct method of proceeding is, in my
view, to assess the full amount of the damage caused by the pursuer's disease
and to find the defenders liable for such proportion thereof as corresponds to
the proportion of aggravation which their negligence has caused. I do not think
that any other view would do justice."
His Lordship then went on to determine the extent of
the aggravation caused by the defenders' negligence at seven and a half per
cent.
[135] The
submission for the pursuer in the present case was that the decision in Holtby was not correct and should not be
followed. The question which arose was whether it was ever appropriate to
apportion damages once a pursuer had established that the defender had made a
material contribution to his injury or illness. If the defender had materially
contributed to the injury or illness he was liable for the whole loss. It made
no difference whether it was an injury or an illness. If Holtby were correct there would be no need for section 3 of the Law
Reform (Miscellaneous Provisions) (Scotland) Act 1940 ("the 1940 Act"),
which deals with contribution among joint wrongdoers. Where more than one
wrongdoer has made a material contribution to a single injury or illness, those
wrongdoers were jointly and severally liable for the whole loss. Section 3 of
the 1940 Act had been enacted precisely to permit such wrongdoers to seek
relief from each other in such circumstances. The decision of Lord Strachan in Balfour was in favour of the pursuer in
the present case and against Holtby.
In any event there was no support in the evidence for the contention that a
measurable proportion of the deceased's condition had been caused by exposure
in Templetons: the evidence established only that a material contribution to
his condition had been made by Templetons. It was not known how much exposure a
particular individual had to undergo before developing the illness: it was
known only that there had been exposure and that the illness had resulted.
[136] In my
opinion the question which has to be resolved is whether it is competent to
apportion damages in a case where a pursuer has established that a single
defender has made a material contribution to his injury or illness when there
has been no finding of joint and several liability against that defender and
another party who has also made a material contribution to the injury or
illness. I think that the starting point for consideration of this question
must be the decisions of the House of Lords (which are binding upon me) in the
Scottish cases of Wardlaw v Bonnington Castings 1956 SC (HL) 26, Nicholson v Atlas Steel
Foundry and Engineering Co 1957 SC (HL) 44 and McGhee v National Coal Board 1973 SC (HL) 37. In Wardlaw the pursuer's
case against the defenders was that in breach of statutory duty they had
allowed silica dust to escape into the air from swing grinders, causing him to
contract pneumoconiosis. He was also exposed to silica dust from pneumatic
hammers, not due to any breach of duty by the defenders. At pages 31-33 Lord
Reid said:
"In my judgment, the employee must in all
cases prove his case by the ordinary standard of proof in civil actions; he
must make it appear at least that on a balance of probabilities the breach of
duty caused or materially contributed to his injury. ....
The medical evidence was
that pneumoconiosis is caused by a gradual accumulation in the lungs of minute
particles of silica inhaled over a period of years. That means, I think, that
the disease is caused by the whole of the noxious material inhaled and, if that
material comes from two sources, it cannot be wholly attributed to material
from one source or another. ..... I cannot agree that the question is which was
the most (sic) probable source of the
respondent's disease, the dust from the pneumatic hammers or the dust from the
swing grinders. It appears to me that the source of the disease was dust from
both sources, and the real question is whether the dust from the swing grinders
materially contributed to the disease. What is a material contribution must be
a question of degree. A contribution which comes within the exception de minimis non curat lex is not
material, but I think that any contribution which does not fall within that
exception must be material. I do not see how there can be something too large
to come within the de minimis principle
but yet too small to be material. ....
In my opinion, it is proved
not only that the swing grinders may well have contributed but that they did in
fact contribute a quota of silica dust which was not negligible to the
pursuer's lungs and did help to produce the disease. That is sufficient to
establish liability against the appellants, and I am therefore of opinion that
this appeal should be dismissed."
[137] Stuart-Smith
LJ remarked in Holtby (para 14, p
426e):
"What the House of Lords did
not consider in that case was the extent of the defendants' liability, because
it was never argued that the defendants were only liable to the extent of the
material contribution."
[138] That
statement does not accord with what Lord Rodger of Earlsferry (who dissented in
the result) said in Barker v Corus UK Ltd [2006] 2 AC 572 at page 602,
para 72 after referring to the latter part of the first paragraph which I
have cited above from Lord Reid:
"Bonnington Castings soon became established as the classic
authority for the proposition that, to succeed and recover damages in full
against a defendant, a plaintiff need do no more than prove that the
defendant's wrongful act materially contributed to his injury. Since anything
above de minimis will do, this means
that a claimant can succeed even though an injury would have occurred without
the defendant's act. The "but for" or sine
qua non test of causation gives way to this considerably more generous test
based on the defendant's contribution to the victim's injury."
[139] Nicholson followed and applied the
decision in Wardlaw. Viscount
Simonds, having reviewed the evidence, said at page 3:
"It follows that owing to
the default of the respondents the deceased was exposed to a greater degree of
risk than he should have been, and, though it is impossible even approximately
to quantify the particles which he must in any event have inhaled and those
which he inhaled but need not have, I cannot regard the excess as something so
negligible that the maxim "de minimis"
is applicable. Accordingly, following the decision in Wardlaw's case, I must hold the respondents liable."
[140] In McGhee the pursuer contracted dermatitis
from contact with brick dust in the course of his employment. The defenders
were negligent in not providing proper washing facilities, which would have
ameliorated the position, but the pursuer would still have been exposed to some
unavoidable dust. He was unable to prove that provision of washing facilities
would have prevented him contracting dermatitis. The House of Lords held that
the failure to provide washing facilities increased the risk of injury and that
the pursuer had therefore established that it made a material contribution to
his disease. At page 53 Lord Reid said:
"It has always been the law
that a pursuer succeeds if he can show that fault of the defender caused or
materially contributed to his injury. There may have been two separate causes
but it is enough if one of the causes arose from the fault of the defender. The
pursuer does not have to prove that this cause would of itself have been enough
to cause him injury."
At page 57 Lord Simon of Glaisdale said:
"Wardlaw v Bonnington Castings
and Nicholson v Atlas Steel Foundry & Engineering Co establish,
in my view, that where an injury is caused by two (or more) factors operating
cumulatively, one (or more) of which factors is a breach of duty and one (or
more) is not so, in such a way that it is impossible to ascertain the
proportion in which the factors were effective in producing the injury or which
factor was decisive, the law does not require a pursuer or plaintiff to prove
the impossible, but holds that he is entitled to damages for the injury if he
proves on a balance of probabilities that the breach or breaches of duty
contributed substantially to causing the injury. If such factors so operate
cumulatively, it is, in my judgment, immaterial whether they do so concurrently
or successively."
[141] Commenting
on the decision in McGhee at para 13,
p 427a-b in Holtby, Stuart-Smith LJ
said:
"Once again the question of
the extent of the defendant's (sic) liability
was not considered, since, like the defendants (sic) in the Bonnington case,
their case was that they were not liable at all."
It is, of course, quite correct to point out, as
Stuart-Smith LJ did in the passages cited above, that in neither Wardlaw nor McGhee did the House of Lords consider the extent of the defenders'
liability as it was never argued that they were liable only to the extent of
their material contribution. In my opinion that point was never argued either
because it was never even contemplated or because it was contemplated and
considered to be a bad point. In either event I do not think that was because
counsel for the defenders in the two cases were remiss in their duty. Counsel
for the defenders in Wardlaw later
became respectively Lord Avonside and Lord McDonald and counsel for the
defenders in McGhee later became
respectively Lord Mackay of Clashfern LC and Lord Hope of Craighead. It seems
to me that there is considerable force in the comment by Clarke LJ at para 34
of Holtby that, if the position were
that the claimant cannot, as a matter of law, recover anything more than the
contribution which the defendant has made tortiously to his disease, it does
seem surprising that none of their Lordships mentioned the point in either Wardlaw or Nicholson, even though, as appears to be the case, the point was
not raised by counsel. I think that these three decisions of the House of Lords
authoritatively establish that where a pursuer proves that a single defender
made a material contribution to his injury or illness, that defender is liable
in full to the pursuer for causing the injury, and not just to the extent of
his material contribution. It seems to me that the passage from Lord Reid
at page 53 in Wardlaw, which I
have quoted above, puts the matter beyond any doubt: in effect, making a
material contribution to an injury or illness is in law equivalent of causing
it, and accordingly full liability for the injury or illness follows. If the
defender wishes to seek a contribution from another party whom he considers
also to be liable, then it is for the defender to bring that party in to the
action as a third party or subsequently to raise a separate action against that
party for contribution under section 3(2) of the 1940 Act, but that is a matter
for the defender himself and of no relevance in a question between the pursuer
and defender. This was emphasised by Lord Scott of Foscote in Barker (supra) at p 598, para 60, where
he said:
"It is a well established
principle of the law of tort that if more than one tortfeasor causes the damage
of which complaint is made, and if it is not possible to attribute specific
parts of the damage to a specific tortfeasor or tortfeasors (sic) in exoneration, as to those parts
of the damage, of the other tortfeasors, the tortfeasors are jointly and
severally liable for the whole damage. A pedestrian on the pavement injured by
a collision between two cars both of whose drivers were driving negligently can
hold either driver liable for his or her injuries. The apportionment of
liability between the two negligent drivers is no concern of the victim."
[142] It seems
to me that that is so whether the injury or illness is divisible or not and
whether the wrongs are concurrent or consecutive. The principle which applies
is the same throughout. It is, of course, necessary to ask first of all what
injury or illness was caused by the defender. If there were entirely distinct
and separate injuries or illnesses, then, of course, the defender is liable
only for the injury or illness which he caused. If the defender made a material
contribution to causing the injury or illness in question, he is liable in full
for causing the injury or illness, but if he made only a material contribution
to aggravating or exacerbating the injury or illness in question, then he is
liable in full to the extent of the aggravation or exacerbation. This is
illustrated by the decision of Lord Strachan in the two separate actions
mentioned above with which he dealt in the Balfour
case: in the action at the instance of Balfour the defenders had made a
material contribution to causing the injury, whereas in the action at the
instance of Begg they had made a material contribution only to the aggravation
or exacerbation of the injury. It is further illustrated by the same
distinction which Lord Strachan drew between the claim by Balfour and the claim
by another pursuer, Crawford: see the discussion by Lord Rodger of Earlsferry
in Heaton v AXA Equity and Law [2002] 2 AC 329 at pages 351-353, paras 71-77.
[143] Moreover,
I think the point made on behalf of the pursuer that if the decision in Holtby were correct there would be no
need for section 3 of the 1940 Act is a sound one. Section 3 of the 1940 Act
provides as follows:
"(1) Where in any action of
damages in respect of loss or damage
arising from any wrongful acts or negligent acts or omissions two or more
persons are, in pursuance of the verdict of a jury or the judgment of a court
found jointly and severally liable in damages or expenses, they shall be liable
inter se to contribute to such
damages or expenses in such proportions as the jury or the court, as the case
may be, may deem just: Provided that nothing in this subsection shall affect
the right of the person to whom such damages or expenses have been awarded to
obtain a joint and several decree therefor against the persons so found liable.
(2) Where any person has
paid any damages or expenses in which he has been found liable in any such
action as aforesaid, he shall be entitled to recover from any other person who,
if sued, might also have been held liable in respect of the loss or damage on
which the action was founded, such contribution, if any, as the court may deem
just."
[144] It is
important to bear in mind why section 3(2) of the 1940 Act was enacted. The
common law initially was as stated in Bell, Principles at para 550:
"There is no contribution or relief among wrongdoers." That position was
altered by the House of Lords when it held that joint wrongdoers were liable inter se only on a pro rata basis, at least in cases involving non-deliberate injury.
In Palmer v Wick and Pultneytown Steam Shipping Co Ltd (1894) 21R (HL) 39 the
widow of a man who had been killed by the breaking down of the tackle used in
discharging a ship's cargo raised an action against the shipowner and the
stevedore who was using the tackle at the time of the accident for damages, the
fault alleged against the former being that his tackle was unfit for the work,
and that alleged against the latter being that he had recklessly overloaded the
tackle. The pursuer obtained decree against both the shipowner and the
stevedore, jointly and severally, for a sum of damages and expenses. Thereafter
she gave the shipowner a charge for the whole sum. He paid it and obtained from
her an assignation to the sum of damages and expenses, and to the decree. He
then raised an action against the stevedore for payment of half of that sum.
The stevedore pleaded in defence that the action was incompetent and
irrelevant, in respect that there was no contribution between wrongdoers. The
House of Lords held that the shipowner was entitled to recover half of the
damages and expenses from the stevedore because he was in right of the decree
against the latter, and that the (then) rule of law that there was no
contribution between wrongdoers was inapplicable. Lord Watson stated at page 47:
"There might be some
principle in a Court of law refusing to permit a suitor to aver and prove his
own crime or moral delinquency as the medium of recovering from one whom he
alleges to have been a co-delinquent. But the case is very different where the
injured party's claim of damage is liquidated by a joint and several decree
against all the delinquents. In that case - which is the present case - the sum
decreed is simply a civil debt, and the meaning which the law attaches to a
decree constituting a debt in these terms is that each debtor under the decree
is liable in solidum to the pursuer,
and that inter se each is liable only
pro rata, or, in other words, for an
equal share with the rest. In this case it is the appellant who seeks to escape
from the natural import of the decree by going behind it in order to establish
his own co-delinquency."
[145] In Glasgow Corporation v John Turnbull & Co
1932 SLT 457 an action was brought against the Corporation in respect of
the death of a person killed in a collision between two vehicles, one of which
was owned by the Corporation, and decree was granted against the Corporation, who
then raised an action against the owners of the other vehicle for one-half of
the principal sum, interest and expenses contained in the decree. The action
was held relevant by the Lord Ordinary and the Inner House, of consent, allowed
a proof before answer.
[146] In National Coal Board v Thomson 1959 SC 353 the pursuers, who
were liable for the driver of one of two vehicles involved in a collision which
resulted to injury to a passenger in one of them and had settled the claim at
the passenger's instance against them extra-judicially, brought an action of
relief against the owner of the other vehicle, averring that he was equally to
blame for the accident and sought to recover in relief one-half of the sum paid
in settlement. It was held by a majority of the Second Division, reversing Lord
Walker, that it was implicit in section 3 of the 1940 Act that a joint and
several decree, or some equivalent instrument constituting the debt, was an
essential pre-requisite to an action of relief. Commenting upon the decision in
Glasgow Corporation v John Turnbull & Co Lord
Justice-Clerk Thomson stated at page 363:
"This case, therefore, so
far as it went, established that where a joint delinquent had been pursued to
judgment, and had paid the whole sum awarded by a competent court after full
investigation, he could sue his fellow delinquent for a pro rata share, and the fellow delinquent's contention that he was
not a party to the proceedings was held to be of no avail. It would obviously
be unjust to limit contribution to the one case where the injured party elects
to sue all the co-delinquents."
His Lordship then went on at page 366 to quote
the terms of section 3(2) of the 1940 Act and continued:
"This means that in 1932,
had the Act then been operating, Glasgow Corporation would clearly have had a
relevant action against Turnbull, and might have recovered more (or less) than
50 per cent."
Later, at pages 371-3, his Lordship explained the
common law background, the effect of the decisions in Palmer and Glasgow Corporation
v John Turnbull & Co and also
the innovation effected by section 3 of the 1940 Act:
"Prior to 1940 there was no
means of apportioning, as between co-delinquents, the degree to which each had
contributed to cause the damage. If, therefore, one paid the sum found due to
the injured party under a decree against two co-delinquents, he was entitled to
recover from the other delinquent one-half of the sum he had paid. The present
action claims a similar right, and there can be no apportionment of the degree
to which the co-delinquents contributed to cause the injury. Such apportionment
was introduced by the Law Reform (Miscellaneous Provisions) (Scotland) Act 1940. Section 3 (1)
dealt with the case where, in an action of damages arising from wrongful acts
or negligent acts or omissions, two or more persons are found jointly and
severally liable in damages or expenses. It provided that, in such a case, they
shall be liable, inter se, to
contribute to the damages or expenses in such proportions as the tribunal may
deem just. Now, this is the case where it had already been settled in Palmer's case that the right of relief
should be accorded, but now it is dictated that the co-delinquents shall
contribute to the total sum of damages according to their shares of
responsibility for the injury, not pro
rata according to their number.
Section 3(2) dealt with the
case where a person has paid damages or expenses in which he has been found
liable in an action such as the above, he alone having been sued. This is the
instance where the case of Glasgow
Corporation v John Turnbull & Co
left it doubtful whether the right of relief between co-delinquents would be
accorded. The subsection resolves that doubt. It provides that such a person
shall be entitled to recover from any other person who, if sued, might also
have been held liable in respect of the loss or damage on which the action was
founded, such contribution, if any, as the court may deem just. Again, the
contribution is to be according to the proportions in which the faults of the
co-delinquents contributed to the injury, not pro rata according to their number.
Let us assume that, apart
from the statute of 1940, the common law would have afforded relief between
co-delinquents where only one of them had been sued by the injured party to
judgment. If the pursuers, instead of settling the injured party's claim at
their own hand, had been sued to judgment by him, and had then claimed relief
from the defender under the statute, there would have been an apportionment of
the blame and the loss between them. The defender would have had to pay a sum
proportionate to the extent to which he was to blame for the injury. But, if we
now sustain the pursuers' novel claim under the common law, there will be no
apportionment. It is true that the pursuers aver and plead that the accident
was caused to an equal extent by the fault of their servant and the fault of
the defender's servant, but their counsel would not clearly concede that they
must prove that averment or fail in their action. Indeed, under the common law
right of relief, which they rely on, they need not prove that averment. Under
that law, joint delinquents, whatever their respective degrees of fault, are
liable pro rata according to their
number.
Accordingly, if we grant to
the pursuers the common law right of relief, the defender will have to pay
one-half of the damage suffered by the injured man, even if his responsibility
for the accident was one-eighth and the pursuers' responsibility was
seven-eighths. Moreover, we shall have permitted them to bring about this
result in a case where, if they had not sought relief until the injured party
obtained a decree against them, section 3(2) of the Act of 1940 would have
dictated that the defender should pay no more than a sum proportionate to his
responsibility for the accident. The right of relief between wrongdoers is an
equitable right afforded by the common law. If we give the pursuers a right of
relief in the circumstances of the present case it would, in my opinion, be a
most inequitable result.
The pursuers, however,
contend that we must ignore the Act of 1940 in deciding this matter .........
In my opinion, when we are
deciding whether we should for the first time accord an equitable remedy in
novel circumstances, we must decide that matter in the circumstances existing
today, which means that we must take account of the presence on the statute
book of the statute of 1940. There was no right of relief, such as the pursuers
now claim, in our law prior to 1940, and equity demands that we should not now
accord such a right."
[147] It seems
to me that what I am being invited to do by the defenders in this action is to
carry out an exercise apportioning liability between the defenders and other
parties not convened in the action. Adopting the approach of Lord Justice-Clerk
Thomson, I think that there is no power in the court to carry out such an
exercise either at common law or under section 3 of the 1940 Act. I am
therefore of the opinion that, had I been satisfied that the deceased had
contracted asbestosis, it would be incompetent to apportion the defenders'
liability as they invited me to do and I decline to follow the approach taken
by the Court of Appeal in Holtby. I
am course, considering only the position in Scotland but I have no reason to
think that the position in England is any different in light of section 6 of
the Law Reform (Married Women and Tortfeasors) Act 1935, which essentially
effected the same reform to English law as the 1940 Act did to the law of Scotland.
The existing English law is now contained in the Civil Liability (Contribution)
Act 1978. Section 6(2) of the 1935 Act provided, and section 2(1) of the 1978
Act now provides, that in any proceedings for contribution "the amount of the
contribution recoverable from any person shall be such as may be found by the
court to be just and equitable having regard to the extent of that person's
responsibility for the damage". The question can be asked, if the court had a
non-statutory power to do what the Court of Appeal did in Holtby, why was there a need for these provisions?
[148] No
discussion of the question of apportionment of damages in this context would be
complete without reference to the recent decisions of the House of Lords in Fairchild v Glenhaven Funeral Services Ltd [2003] 1 AC 32 and Barker v Corus UK Ltd (supra). Fairchild
dealt with proof of causation in cases of mesothelioma, and, as Lord
Hoffman pointed out in Barker at p
579, para 1, "decided that a worker who had contracted mesothelioma after being
wrongfully exposed to significant quantities of asbestos dust at different
times by more than one employer or occupier of premises could sue any of them,
notwithstanding that he could not prove which exposure had caused the disease."
Barker was the sequel to Fairchild and raised two questions,
formulated by Lord Hoffman at p 580, para 2, as follows:
"First, what are the limits
of the (Fairchild) exception? .....
Secondly, what is the extent of liability? Is any defendant who is liable under
the exception deemed to have caused the disease? On orthodox principles, all
defendants who have actually caused the damage are jointly and severally
liable. Or is the damage caused by a defendant in a Fairchild case the creation of a risk that the claimant will contract
the disease? In that case, each defendant will be liable only for his aliquot
contribution to the total risk of the claimant contracting the disease - a risk
which is known to have materialised."
[149] Their
Lordships (Lord Rodger of Earlsferry dissenting) held that, under the exception
to the normal rules on liability in negligence, whereby any relevant employer
could be liable in relation to mesothelioma caused by wrongful exposure of an
employee to asbestos, liability was imposed where a defendant, by a breach of
duty, had materially increased the risk that the employee would contract
mesothelioma; that, in fairness, where more than one person was in breach of
duty and might have been responsible, liability should be attributed according
to the defendant's relative degree of contribution to the risk, probably
measured by the duration and intensity of the exposure involved, and that,
accordingly, the defendants' liability was several only. Lord Rodger of
Earlsferry (the only Scottish Lord of Appeal who was a member of the committee
which heard the appeal), in a forceful dissenting speech, disagreed with the
majority on the question of apportionment. Fairchild
was an exception to the rule on establishing liability in cases of
mesothelioma and Barker established a
further exception in such cases to the orthodox principle of joint and several
liability. Indeed, it re-affirmed the "orthodox principle" of joint and several
liability. I therefore do not think that Barker
is inconsistent with the view I have taken on apportionment of damages in
this case. In any event, the decision of the majority in Fairchild, being an English appeal, is not binding on me and I
prefer the view of Lord Rodger of Earlsferry on the question of apportionment.
I respectfully adopt his analysis of the law on apportionment.
[150] In the
event that I am wrong in my view on apportionment, I must consider what course
I would have adopted in light of the evidence. First, I accept the submission
for the pursuer that the evidence established only that a material contribution
to the deceased's condition had been made by Templetons, that there was no
support in the evidence for the contention that a measurable proportion of his
condition had been caused by exposure in Templetons, that it was not known how
much exposure a particular individual had to undergo before developing the
illness and that in this case all that
was known was that there had been exposure and the illness had resulted. I
would therefore have declined to make any apportionment at all of the
defenders' liability. Secondly, if I am wrong about that, I would have made an
apportionment of the defenders' liability at 55%, but only because that was the
figure conceded by them. The apportionment takes into account the deceased's
employment only in the Navy (Royal and Merchant) and with Templetons. It
ignores his period of 15 years working with Ciba-Geigy during which he was
exposed to asbestos dust. Had the defenders themselves not suggested an
apportionment of 55%, I would, adopting a broad approach, have made an
apportionment of 35%, taking into account the periods of exposure to asbestos
dust while he worked for other employers.
Pleural
Plaques
[151] In the
event that I was not satisfied that the deceased had contracted asbestosis I
was asked to make an award to the pursuer in respect of his having contracted
pleural plaques. A helpful explanation
of what pleural plaques are was given by Holland J in J Grieves & Ors v F T
Everard & Ors [2005] EWHC 88 (QB). At paras 4 and 5 he described
the pleura and pleural plaques as follows:
"5.The Pleura. The movement of the lung in the course of respiration
is facilitated by a slippery membrane covering, that is, the pleura. There are
two layers to the pleura: the parietal pleura which lines the inside of the rib
cage, and the visceral pleura which covers the lungs. Normally there is no gap
between these layers which are lubricated with pleural fluid. It is to be
emphasised that the pleura is separate from, and not part of, the lung. ....
6. Pleural Plaques. These are localised areas of pleural thickening
with well demarcated edges. They usually develop on the parietal pleura but
occasionally develop on the visceral pleura. They consist of bland fibrous
tissue. The pathogenisis remains uncertain but it is believed that the presence
of asbestos fibres leads to a prolonged low-grade inflammatory response
resulting in the release of chemical mediators, in turn leading to the laying
down of fibrous tissue. The following propositions can be ventured:
a. Pleural plaques are by far
the most common respiratory effect of asbestos inhalation.
b. They may occur after
occupational exposure at a lower level than is needed to cause asbestosis.
c. The frequency of occurrence
and the extent have a relationship with the amount inhaled and the duration of
exposure.
d. The presence of pleural
plaques does not normally occasion any symptoms. Very occasionally the patient
may be aware of an uncomfortable grating sensation on respiration.
e. Given the absence of
symptoms, the presence of pleural plaques is only established by way of chest
x-ray or CT scan - alternatively on post-mortem autopsy - often incidental to
some other investigation. When reading an x-ray it may not be easy to
distinguish between pleural plaques and pleural thickening.
f.
Pleural plaques are rarely detected during the first 20 years
following exposure to asbestos. However, exposure to asbestos does not
necessarily result in the development of plaques notwithstanding the passage of
20 or more years.
g. With time plaques may become
more extensive.
h. Plaques do not in themselves
lead to the other asbestos induced conditions, nor indeed are they a necessary
pre-condition for such; they do not increase the risk of lung cancer; they
differ from diffuse pleural thickening; and their pathology is entirely
distinct from that of mesothelioma. It is the exposure to asbestos that they
evidence, taken in conjunction with the probable life expectancy, which
accounts for the risks of further asbestos induced conditions ....."
[152] Two
separate questions arise out of the pursuer's request for an award in respect
of the deceased's pleural plaques.
(i) Is there a claim for
pleural plaques in the pleadings?
[153] There
is no conclusion claiming damages for pleural plaques, no plea-in-law relating
to pleural plaques and no averment that damages are sought for pleural plaques.
The only reference in the pleadings to pleural plaques is in condescendence 9,
where, in the description of the tests which the deceased underwent at the
Victoria Infirmary on or about 22 October 1998, the following averment appears
at page 24D:
"X-ray and CT scan films
disclosed changes consistent with previous asbestos exposure, namely, pleural
plaques and interstitial fibrosis secondary to asbestos exposure."
[154] The
submission for the pursuer was that she was entitled to an award in respect of
the deceased's pleural plaques on the basis of this averment. It was sufficient
to bring in a claim for pleural plaques. The deceased had been told that he had
"an asbestos related condition", and pleural plaques came under that umbrella.
He had initially applied for industrial injuries disablement benefit for
pleural plaques. The submission for the defenders was that this averment
amounted to no more than a reference to an evidential feature of asbestosis.
Pleural plaques, a condition distinct from asbestosis, had not been pleaded as
a separate head of damage. The plaques themselves were merely an indication of
asbestos exposure. There were no averments about the deceased's awareness of
having pleural plaques and the risk attached to them or of any anxiety on his
part arising out of his knowledge of having pleural plaques. There were no
averments of loss relating to pleural plaques, such as when they developed and
their effect upon the deceased. To assess damages for pleural plaques a judge
had to assess the risks of another condition developing, based on medical
reports providing such an assessment. If the pursuer had sought to lead
evidence of pleural plaques as a separate head of damage the defenders would
have taken objection, but no such evidence was sought to be led. The deceased in his statement (6/23 of
process) stated that while in hospital he was told he had asbestosis (which was
a misdiagnosis). It was a fudge to say that he was told he had "an asbestos
related condition". He made no mention in his statement of pleural
plaques.
[155] In my
judgment the submission for the defenders on this point is correct. It is not,
in my view, essential to have separate conclusions or pleas-in-law for an award
of damages for pleural plaques when such is sought (although separate
conclusions and pleas-in-law would undoubtedly put the matter beyond any
doubt), but there must at least be some indication in the pleadings that an
award of damages for pleural plaques is being sought. I think that there is no
such indication in this case and that it is correct to say that the only
reference to pleural plaques is as an evidential feature of asbestos exposure.
I do not consider this to be a mere technical pleading matter: it is a question
of giving fair notice to the defenders of what damages are being sought for.
Condescendence 9, in which the only mention of pleural plaques is made, begins
with the averment "In consequence of his exposure to asbestos the deceased
contracted asbestosis". It seems to me that that averment makes clear for what
condition the award of damages is sought. In addition to the pleading point, I
have to consider, in deciding whether there is a claim for pleural plaques, how
the proof was conducted. There was nothing in the evidence led which even
hinted at the fact that at the conclusion of the proof an award of damages for
pleural plaques, a condition quite distinct from asbestosis, would be sought.
Had the pursuer sought to lead such evidence there would have been an objection
by the defenders upon which I would have to have ruled. I do not see how the
pursuer could have been allowed to lead such evidence in the absence of proper
averments on record. I am therefore of the view that in this case no claim was
advanced in either the pleadings or the evidence for an award of damages for
pleural plaques and that, assuming such an award to be otherwise competent, it
is not open to me to consider making such an award.
(ii) Damages for pleural plaques
[156] The view
which I have just expressed is sufficient to deal with the issue of pleural
plaques, but, lest my view be incorrect, it is appropriate that I should
express my opinion on the question of damages for pleural plaques. There are
three separate aspects to this question. First, do pleural plaques sound in
damages at all? Secondly, if they do, in what circumstances? Thirdly, if an
award for pleural plaques is competent in this case, what is the appropriate
award of damages?
[157] I heard
extensive submissions on these three aspects of the question on two separate
occasions: first, after the decision of Holland J in J Grieves & Ors (supra) and, secondly, after the decision of
the Court of Appeal in Rothwell v Chemical & Insulating Co Ltd [2006] 4 All ER 1161. The decision of the Court of Appeal in Rothwell was appealed by the claimant to the House of Lords and the
hearing of the appeal took place in June of this year. I understand that
judgment will not be given by the House of Lords before October of this year.
The decision of their Lordships' House will definitively state the law on the
recoverability of damages for pleural plaques. In these circumstances I see no
useful purpose in my dealing at this stage with the submissions I heard on the
question and giving my own independent opinion. Apart from anything else, to do
so could possibly give rise to an unnecessary reclaiming motion from my
decision in light of the decision of the House of Lords. Accordingly, what I
propose to do is to reserve my opinion on this question and to issue a
supplementary opinion dealing with it once the decision of their Lordships'
House has been issued.
Decision
[158] For the
reasons set out above I shall sustain the second and third pleas-in-law for the
defenders and repel the first plea-in-law for the pursuer and assoilzie the
defenders.
