Case No: HQ12X00189
Neutral Citation Number: [2013] EWHC 2952 (QB)
IN THE HIGH COURT OF JUSTICE
QUEEN'S BENCH DIVISION

Royal Courts of Justice
Strand, London, WC2A 2LL

Date: 04/10/2013

Before :

THE HONOURABLE MRS JUSTICE SWIFT DBE
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Between :

	Mrs Dorothy Clara Florence Matthews (Widow & Executrix of Reginald Anthony Matthews, Deceased)	Claimant	
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	(1)	HERBERT COLLINS t/a HERBERT COLLINS & SONS
(2)	PHILIP COLLINS t/a HERBERT COLLINS & SONS
(3)	URRY STRUCTURES LIMITED
(4)	JA TOLSON t/a TWB CONSTRUCTION
(5)	TOLSON WOOD BEACH (BUILDERS) LIMITED
(6)	DAVID WYNDHAM MORGAN t/a MORGANS OF USK
(7)	MRS NANCY MORGAN t/a MORGANS OF USK	Defendants	
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Mr Jeremy Roussak (instructed by JMW Solicitors, Manchester) for the claimant 
Mr David Platt QC (instructed by Berryman Lace Mawer LLP, Solicitors, London) for the defendants 

Hearing dates: 30 July 2013
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Judgment
The Honourable Mrs Justice Swift DBE : 
The application 
1.	The seven defendants to this claim apply to strike out the claimant’s statement of case as an abuse of process pursuant to CPR 3.4(2)(b).  The defendants’ application was supported by a witness statement from Ms Raveena Mehta, solicitor for the sixth and seventh defendants who, for the purpose of this application, is acting on behalf of all the defendants.  There was also a witness statement from Mr Andrew Lilley, solicitor for the claimant, in opposition to the application, together with what appears to be an earlier draft of the same statement.  On 30 July 2013, I heard oral submissions on the application from Mr Jeremy Roussak for the claimant and Mr David Platt QC for the defendants.  Counsel had also provided written submissions in advance of the hearing.  I reserved judgment which I now give.
The claim
2.	The claimant brings the claim as the widow and executrix of the late Mr Reginald Anthony Matthews (“the deceased”) under the provisions of the Law Reform (Miscellaneous Provisions) Act 1934 and for her own benefit as the deceased’s dependant under the provisions of the Fatal Accidents Act 1976 (as amended).  The claimant alleges that, throughout the deceased’s periods of employment as a steel erector/cladder with the seven defendants, which periods of employment fell between 1973 and 1980/81, he was exposed to and inhaled asbestos dust caused by cutting, mitring and drilling asbestos cement sheets and asbestos boards.  It is alleged that, as a result of his exposure to asbestos dust, the deceased developed the type of diffuse interstitial pulmonary fibrosis which, when caused by asbestos exposure, is known as ‘asbestosis’.  It is alleged that his asbestos exposure also resulted in the development of lung cancer which caused his death.
3.	The defendants deny liability and causation.  They accept that the deceased developed diffuse interstitial pulmonary fibrosis but they deny that any asbestos exposure which may have occurred during the deceased’s employment with them caused or contributed to the development of that condition.  They contend that it is probable that his pulmonary fibrosis was in fact idiopathic pulmonary fibrosis (IPF), i.e. pulmonary fibrosis the cause of which is unknown.  The most common sub-type of IPF is usual interstitial pneumonia (UIP).  The defendants also deny that the deceased’s lung cancer was caused by asbestos exposure.  They contend that the most likely cause of his lung cancer was cigarette smoking.  
The deceased’s medical history
4.	The deceased suffered some shortness of breath during the mid-2000s.  His symptoms increased in 2007 and he developed a persistent cough.  He underwent various medical investigations, including chest x-rays and a CT scan which revealed pleural thickening, together with probable evidence of interstitial pulmonary fibrosis.  At that stage, the fibrosis was considered by the doctors treating the deceased as likely to be UIP.  The pleural thickening was attributed to previous asbestos exposure.  There were also some emphysematous changes and it was noted that the deceased had smoked 20 cigarettes a day for 40 years or so before giving up smoking in about 1995.
5.	By November 2008, the deceased had developed chest and back pain, together with increased shortness of breath.  He was admitted to hospital.  A CT scan resulted in a diagnosis of probable lung cancer with underlying interstitial disease.  He was discharged from hospital, but re-admitted in late December 2008.  Investigations by bronchoscopy and biopsies suggested the presence of squamous cell carcinoma but were insufficient to confirm the diagnosis.  The deceased became oxygen-dependent.  His condition deteriorated quickly and he died in hospital on 21 January 2009.  At that stage, there had still been no diagnosis of asbestosis.
The Post Mortem findings
6.	A post mortem examination was performed on 23 January 2009 by Dr Hayes, consultant pathologist, on the instructions of the Coroner of Herefordshire.  A report of the examination was prepared and is dated 3 February 2009.  This revealed:
i)	Some generalised adhesions and thickening of the pleura;
ii)	A “honeycomb pattern” of pulmonary fibrosis affecting the sub-pleural lung tissue in the lower lobe on the left;
iii)	On the right, a large hilar tumour involving the adjacent lymph nodes; and
iv)	Evidence of secondary malignancy involving the right adrenal gland.
7.	Histological examination of samples of lung tissue was carried out by Dr Hayes who reported as follows:
“HISTOLOGY: Microscopy confirms the presence of established sub-pleural pulmonary fibrosis with distended air pockets, smooth muscle hypertrophy and ‘bronchiolisation’ of distal air spaces; the tumour is an extensively necrotic and widely infiltrative squamous carcinoma which is poorly differentiated and in places anaplastic.  Asbestosis fibres are readily demonstrable.
INTERPRETATION: This gentleman has died against a background of pulmonary fibrosis and lung cancer; the presence of asbestosis fibres implies a causal relationship certainly with former, and quite possibly with the latter.”
8.	Dr Hayes’ opinion was that the direct cause of the deceased’s death had been respiratory failure due to pulmonary fibrosis and lung cancer.  Under “other significant conditions contributing to death”, Dr Hayes identified “asbestos exposure”.  That information was subsequently recorded on the deceased’s death certificate.
The Inquest
9.	An Inquest into the deceased’s death took place on 20 July 2009 before the Deputy Coroner for Herefordshire, Mr Wooderson.  I have been provided with a transcript of those proceedings prepared by Ms Mehta.
10.	Dr Hayes gave oral evidence describing his findings on post-mortem examination.  He referred to his interpretation of those findings:
“… my interpretation was this gentleman has died against a background of pulmonary fibrosis and lung cancer and that the presence of asbestos fibres provided a causal relationship solely with the pulmonary fibrosis and very possibly with the lung cancer.”
Dr Hayes was asked by the Deputy Coroner to confirm that the asbestos fibres were “very much linked” to the pulmonary fibrosis and very possibly to the lung cancer, to which he replied:
“Yes … and I think also with the thickening of the pleura that was also evident.”
11.	Dr Hayes went on to refer to what he described as the “very strong link” between the inhalation of asbestos fibres and the three disease processes found on post-mortem examination, i.e. pleural thickening, pulmonary fibrosis and lung cancer.  He went on:
“I found asbestos fibres very easily on the microscope examination and people are familiar with the idea that if you were to open out the lungs … each small piece of tissue that I examined was about the size of a 50 pence piece so you could sort of extrapolate from that into the lungs as a whole if you find lots of fibres in one of those small pieces of tissue then exposure is likely to have been considerable and as I say, there is a well known and established link between asbestos exposure in those conditions.”
12.	Dr Hayes was then asked (by an advocate acting for one or other of the defendants) whether, on a microscopic examination of the lung tissue, there were any characteristic features which would point to a diagnosis of either UIP or asbestosis.  Dr Hayes replied that, since the fibrosis was “quite end stage” by the time of his examination, the changes were “fairly non specific”.  He suggested that the presence of a large number of asbestos fibres would tend to imply a relationship between asbestos exposure and the fibrosis.  He acknowledged that it was possible to have two disease processes (i.e. asbestosis and UIP) together, but said that that would be “less likely”.
13.	The Inquest was told that the deceased had been represented by solicitors during his lifetime in connection with his asbestos exposure and had completed an Asbestos Related Industrial Disease Questionnaire on 24 June 2008.  The completed Questionnaire included a history of his various employments, including his employment with the defendants.  In that Questionnaire, he had said:
“I started work in the construction industry with a company and the cladding used on the majority of buildings was asbestos and there was never any mention of protective gear from anyone and we all assumed we were quite safe.  Each company I worked for was the same and one of my jobs was to mitre the asbestos sheets which we did in the early days with a hand saw which soon changed to an electric circular saw, then an angle grinder with an abrasive disc.  The dust would billow around and there were times when you would have thought I worked in a flour mill and would finish with a coughing fit.”  
14.	The Inquest also heard that the deceased had told those treating him in hospital that he had been exposed to asbestos for about 12 years, mainly whilst working as a steel erector and roofer, when he recalled encountering asbestos dust caused by the manual handling and cutting of asbestos sheets.
15.	Dr Phillips, the consultant physician who was responsible for the deceased’s care from the time of his admission to hospital in November 2008 until his death, gave oral evidence to the Inquest.  As to the causation of the deceased’s fibrosis, he said:
“… he also in addition to that had pulmonary fibrosis – that is scarring of the fine lung tissue.  In the terms of the causes of lung fibrosis they are multiple but after investigation there seemed to be two primary likely diagnoses [of] his lung fibrosis - that of asbestosis or what is called idiopathic fibrosis.  The two are very difficult to tell apart …. Bearing in mind his exposure and the latency period the clinical appearance and the presence of asbestos bodies on post mortem I would conclude it is more likely than not that [it] was in fact asbestosis… 
I think it is more likely than not that asbestos led to the development of pulmonary fibrosis and the fact he developed lung cancer which again is a recognised complication of asbestos exposure and I think it is highly likely that asbestos is a highly contributing factor towards that.”
16.	Dr Phillips had previously referred to the possible part played by smoking:
“… lung cancer is nearly always smoking related, 98% of cases are related to smoking and having said that asbestos is also a well known cause of lung cancer by itself causing lung cancer.  It is also well recognised that the combination is notable so the risks of a smoker developing asbestosis and lung cancer go up fourfold.”
17.	The Deputy Coroner recorded a verdict that the deceased had died of an industrial disease and the death certificate duly recorded his verdict, “Died of industrial disease of pulmonary fibrosis”.
The histological samples
18.	Persons exposed to asbestos inhale asbestos fibres which are then deposited in the tissue of the lungs.  Some of those asbestos fibres become coated with iron.  The coated fibres are known as asbestos “bodies” and can be seen when the tissue is examined by means of light microscopy.  Asbestos fibres are not generally evident on light microscopy and can be detected only by the more sophisticated process of analysis by means of electron microscopy.  The efficiency with which coating of asbestos fibres occurs varies from individual to individual.  Some individuals have a poor coating mechanism, as a result of which the number of asbestos bodies present in their lung tissue does not properly reflect the extent of their previous asbestos exposure.  In the case of those individuals, a more accurate method of assessing their previous asbestos exposure is by means of electron microscopy.  Electron microscopy can also be used to identify the type of asbestos fibres present, i.e. whether the fibres are of crocidolite (blue asbestos), amosite (brown asbestos) or chrysotile (white asbestos).  Asbestos of the amphibole types (which include crocidolite and amosite) are in general more likely to cause fibrosis than the non-amphibole types such as chrysotile.  However, persons exposed only to chrysotile can develop asbestosis.  
19.	Only one centre in the UK, University Hospital at Cardiff (also known as the Llandough Hospital), is equipped to carry out the analysis of asbestos content in lung tissue by means of electron microscopy.
20.	The histological examination conducted by Dr Hayes would have been performed by means of light microscopy.  In his evidence, Dr Hayes referred to finding asbestos fibres in the samples of the deceased’s lung tissue which he examined.  Since, as I have already observed, asbestos fibres are not generally evident on light microscopy, it is virtually certain that, in his post mortem report and his oral evidence to the Inquest, Dr Hayes was in fact referring to asbestos bodies.  It is clear from Dr Phillips’ oral evidence to the Inquest (see paragraph 15 of this judgment) that he assumed that Dr Hayes had been describing asbestos bodies, not asbestos fibres.   
21.	Samples of tissue had been taken from the deceased’s lungs in order for Dr Hayes to carry out his histological examination.  The post mortem report refers to nine “blocks”, which I take to be a description of the samples of lung tissue which had been taken for examination.  There is no reference to the tissue samples in the transcript of the Inquest proceedings.  However, the claimant’s evidence was that, at some stage, the Deputy Coroner had suggested that the samples should be retained after the Inquest and she confirmed to him that she was happy to consent to his suggestion.
After the Inquest
22.	On the advice of the doctors treating him for his lung condition, the deceased consulted JMW Solicitors LLP (JMW) in May 2008.  In June 2008, the deceased completed the Questionnaire to which I have already referred and in August 2008 JMW obtained details of the deceased’s employment history from HMRC.  At that stage, the deceased’s pleural thickening did not appear to be producing symptoms so it was not considered that there was any basis on which to commence proceedings.  The matter was therefore allowed to lapse.  In early 2009, however, following the deceased’s death, JMW were instructed by the claimant and thereafter JMW corresponded with the Coroner’s Office about the forthcoming Inquest.  JMW did not represent the claimant at the Inquest but they subsequently requested a CD containing a recording of the proceedings. 
23.	JMW then made efforts to trace the deceased’s former employers and/or their insurers. This was a long process.  They located the first and second defendants in 2010 and sent a letter of claim to them in December 2010.  At that stage, JMW had not managed to trace any of the other defendants and they were unable to do so until several months later.  In July 2010, JMW also obtained a witness statement from Mr Cyril Jennings (who was employed with the deceased by a company called Payne Bros. between about 1968 and 1971 on work said to have been similar to that undertaken by the claimant for the defendants).  JMW also obtained a witness statement from the deceased’s brother, Mr Brian Matthews, who worked alongside the deceased throughout his periods of employment with all seven defendants. 
The events of November 2010
24.	The claimant’s account of the events of November 2010 came initially from her Replies to a Request for Further Information made on 1 August 2012 by the sixth and seventh defendants under CPR Part 18.  The claimant stated that, in about November 2010, she had received a letter from the Coroner’s Office, asking what should be done with the samples of the deceased’s lung tissue that were being held by the Coroner.  I have seen a copy of that letter which was dated 2 November 2010 and written by the Coroner’s Officer, Ms Maggie Oliver, to the claimant.  Ms Oliver wrote:
“I do apologise but it is necessary that now the Inquest has been concluded that I am directed as to how you wish the histology to be dealt with.
I have enclosed a family instruction sheet and would be grateful if you would return it direct in the enclosed envelope.
If I do not hear from you within 3 months of the date of this letter I will assume that you require the histology to be disposed of and will instruct the hospital to do so in accordance with their procedure.
If you require any further clarification in relation to this letter please do not hesitate to contact me direct.”
25.	The claimant said that she did not know what to do so she telephoned the Coroner’s Office and asked the member of staff to whom she spoke what was usually done.  She was told that samples were not normally retained.  The claimant therefore agreed that the samples should be destroyed.  Subsequently, she completed the form which had been enclosed with the letter, giving the requisite authority for disposal of the samples.
26.	The claimant explained that, since these events had taken place more than 15 months after the Inquest, she had assumed that, by that time, the Coroner would have obtained whatever information he needed from the samples.  She did not appreciate that destruction of the samples might have any impact on her claim against the defendants.  In particular, she did not realise that the proposed defendants to the claim might want to carry out their own histological examination of the tissue samples.  She did not therefore see any need to seek the advice of her solicitors as to whether she should agree to disposal of the samples. The member of the Coroner’s staff to whom she spoke did not suggest that she should do so.
27.	In her later witness statement, the claimant gave a slightly different version of the circumstances of the telephone discussion, suggesting that a telephone call (not the letter of 2 November 2010) was the first communication she had received on the topic.  She said that, in November 2010, she knew that JMW had been in contact with the Coroner’s Office and that the Coroner was aware that she might be making a claim.
After November 2010
28.	After November 2010, JMW continued to investigate the claim on the claimant’s behalf, unaware that the tissue samples had been destroyed.  Proceedings were issued in January 2012 and served in May 2012, together with Reports from the experts instructed on the claimant’s behalf, Mr David Brady (consulting engineer) and Dr Martin Muers (consultant respiratory physician).
29.	By a letter dated 16 July 2012, Berrymans Lace Mawer LLP, solicitors representing the sixth and seventh defendants, requested access to the tissue samples.  JMW made enquiries of the Coroner’s Office and learned that the samples had been destroyed.  Having been informed of that, the sixth and seventh defendants made the Request for Further Information to which I have already referred and the claimant provided Replies explaining how the samples had come to be destroyed.  Lay witness evidence was exchanged in September 2012 and, in October 2012, the defendants served their expert evidence from Mr Robert Mitchell (consulting engineer) and Dr John Moore-Gillon (consultant physician).  The latter provided a Report dated 25 September 2012 together with a Supplementary Report dated 30 October 2012.
30.	On 11 February 2013, the defendants issued their application for strike out.
The deceased’s asbestos exposure
The lay evidence 
31.	The evidence of the deceased’s asbestos exposure comes from the Questionnaire completed by the deceased and the information he gave to his treating doctors during his lifetime, and from Mr Jennings and Mr Brian Matthews.  The first and second defendants have disclosed witness statements from Mr Philip Collins and Mr Keith Prosser.  The sixth and seventh defendants have disclosed witness statements from Mr Dave Sanger and Mr David Morgan.  All four of the defendants’ witnesses recall the deceased and are able, to a greater or lesser extent, to describe the work he did during his employment with the first, second, sixth and seventh defendants.  The third, fourth and fifth defendants are no longer in existence and have not disclosed any evidence.  
32.	During his periods of employment with the defendants (and with Payne Bros.), the claimant was employed as a member of a gang which erected large farm buildings.  Each building had a steel framework and all the lay witnesses agree that the deceased and other members of the gang used corrugated cement sheets containing chrysotile (known as “Big Six” sheets) in order to construct the roofs and guttering of the buildings.  The asbestos cement sheets had to be cut or mitred, using a hand saw or cutting disc fixed to a hand held electric cutter (an angle grinder), and drill.  This work was done outside.  The evidence of Mr Brian Matthews is that the cutting of asbestos sheets and cladding would create “clouds of dust” to the extent that the men performing the work would become covered in dust “like snowmen”.  The defendants’ witnesses agree that the cutting work had to be done but say that it was generally possible for the person carrying out the cutting to position himself so as to avoid the worst of the dust.  The defendants’ witnesses also suggest that a much smaller proportion of the deceased’s working time would have been spent cutting asbestos cement sheets than is described by Mr Brian Matthews.
33.	There appears to be a dispute between the lay witnesses for the claimant and the defendants as to whether (in addition to being used for constructing the roofs) asbestos material was also used as cladding for the walls of the farm buildings.  In his witness statement, Mr Brian Matthews refers briefly to the use of “asbestos cladding”.  In his Report, Mr Brady referred to telephone discussions he had had with Mr Brian Matthews which suggested that the deceased and Mr Brian Matthews had been involved in cutting and fixing “Asbestolux” insulating board (as well as “Big Six” corrugated asbestos sheets), which was used as external cladding for the buildings being erected.  Mr Brady seems to have understood that the “Asbestolux” board was used to form the walls of the buildings being constructed.  However, the defendants’ witnesses are adamant that the wall cladding did not contain asbestos but was made of steel, wool or a combination of both.  They do not mention the use of “Asbestolux” boards.   
The expert evidence 
34.	Mr Brady’s evidence is that asbestos cement products such as “Big Six” or “Asbestolux” roofing sheets usually contained between 15% and 30% chrysotile.  Mr Mitchell says that “Big Six” asbestos roofing sheets could on occasion contain 10-15% chrysotile, but “typically” contained only about 9%-12%.  
35.	As for “Asbestolux” boards (if they were used), Mr Brady said that they contained around 50% amosite.  Mr Mitchell’s evidence is that Asbestolux board typically contained 15-25% amosite, or a mixture of amosite and chrysotile, in calcium silicate. 
36.	Based on the evidence of Mr Brian Matthews (but not the evidence of the defendants’ lay witnesses, which was not available when he reported), Mr Brady concluded that the deceased spent on average approximately three hours a day cutting asbestos sheets and boards.  He estimated that the deceased had been exposed to “at least 20 fibres/ml and more like 60 fibres/ml” over an exposure period of three years in total.  That, he said, equated to a total cumulative exposure of between 60 and 180 fibre ml years.  
37.	At the time Mr Mitchell prepared his Report, he had seen Mr Brady’s Report, together with all the lay witness evidence.  Mr Mitchell indicated that he agreed with Mr Brady that the deceased may well at times have been exposed to asbestos concentrations of between 20 and 65 fibres/ml.  However, he considered that Mr Brady had “grossly overestimated” the deceased’s overall asbestos exposure.  Mr Brady had based his period of three years’ exposure on a daily exposure of three hours’ exposure a day which did not, Mr Mitchell said, reflect the overall effect of the witness evidence.  Mr Mitchell calculated the deceased’s total exposure period as between 0.11 and 0.13 years.  As to his total cumulative exposure, he estimated it as between 1.71 fibre ml years and 7.87 fibre ml years.
The medical evidence
The Helsinki criteria
38.	In 1977, a convention of experts in the field of asbestos exposure agreed on a number of criteria for the diagnosis of asbestosis which have subsequently been widely used and are generally recognised as authoritative.  They produced a Report (known as the 1997 Consensus Report) and a set of criteria (the Helsinki criteria). The Helsinki criteria established that the ‘threshold’ total cumulative dose of asbestos likely to be associated with the development of clinical signs of asbestosis is 25 fibre ml years. 
Dr Muers and Dr Moore-Gillon
39.	The medical experts examined other evidence which might tend to confirm or refute the diagnosis of asbestosis.  Having reviewed the medical history, Dr Muers expressed the opinion that the deceased’s interstitial fibrosis had been present at least since 2004 and had gradually worsened between then and the deceased’s death in 2009.  He observed that UIP is “quite an aggressive disease” which tends to progress rapidly.  Consequently, the history of the disease was more typical of asbestosis.  He noted also the finding of plentiful asbestos bodies in lung tissue on post mortem examination.  Taking those features in conjunction with Mr Brady’s estimate of the deceased’s total cumulative asbestos exposure, he considered it reasonable to conclude that the deceased had suffered from asbestosis.  
40.	When dealing with the causation of the deceased’s lung cancer, Dr Muers noted that it has been accepted for many years that there is a strong association between the development of asbestosis and an excess risk of lung cancer.  The risk of developing lung cancer is increased by a factor of about five in cases of well-established pulmonary asbestosis.  He concluded that, on a balance of probabilities, the deceased’s lung cancer could also be attributed to his previous occupational asbestos exposure. 
41.	In his initial Report, Dr Moore-Gillon noted that, in about 50% of cases of diffuse interstitial pulmonary fibrosis, no cause is identified.  However, he observed that the presence of asbestos bodies (he also assumed they were asbestos bodies, not fibres) in lung tissue seen at the post mortem examination of the deceased was evidence of asbestos exposure.  Dr Moore-Gillon went on to refer to the requirements for the histological diagnosis of asbestosis contained in the Helsinki criteria.  Those requirements are (i) the identification of diffuse interstitial fibrosis in well inflated lung tissue remote from a lung cancer or other mass lesion; and (ii) the presence of either two or more asbestos bodies in tissue with a section area of one square centimetre or a count of uncoated asbestos fibres that falls into the range recorded for asbestosis by the same laboratory.  The criterion of a finding of two or more asbestos bodies per square centimetre refers to histological examination of lung tissue under light microscopy.  Dr Moore-Gillon pointed out that Dr Hayes had not expressed his findings in terms of asbestos fibres (as he termed them) per square centimetre of tissue.  Instead, he described finding them “very easily” and the fibres being “readily demonstrable”.  Dr Moore-Gillon then observed that, given the importance, of the matter, it was “a very great pity” that the samples were no longer available for examination. 
42.	At the time he wrote his first Report, Dr Moore-Gillon had seen all the lay witness evidence and the claimant’s expert engineering evidence.  At that stage, he considered that the description of the deceased’s working practices, taken in conjunction with the (albeit imprecise) description of the pathological findings, were on balance sufficient for a diagnosis of asbestosis.  Furthermore, he expressed the view that, if the deceased had been subject to sufficient asbestos exposure to cause him to develop asbestosis, it would be reasonable to conclude also that the same asbestos exposure had caused or materially contributed to his lung cancer and therefore to his death.  
43.	Having seen the evidence of Mr Mitchell, however, Dr Moore-Gillon’s view changed somewhat.  His final position was that, if the deceased’s cumulative asbestos exposure were found by the Court to have been in excess of 25 fibre ml years, then on balance he would accept that the deceased’s interstitial pulmonary fibrosis was asbestosis.  In that event he would also attribute his lung cancer on balance to asbestos exposure.  If by contrast the Court were to find that the deceased’s asbestos exposure was below 25 fibre ml years, then he would conclude that on balance the deceased had had IPF and that his lung cancer could not be attributed on the balance of probabilities to asbestos exposure. 
Dr Gibbs
44.	Dr Muers made no reference in his Report to the fact that the tissue samples were not available for histological examination.  I have referred to Dr Moore-Gillon’s comment that it was a “very great pity” that they were not still available.  
45.	The defendants commissioned further medical evidence dealing with the potential value to the claim of the histological evidence.  They obtained a Report from Dr Allen Gibbs, consultant histologist, formerly of the Llandough Hospital, who has considerable experience of the examination and mineral fibre analysis of lung tissue by both light and electron microscopy.  Dr Gibbs was asked to comment generally on the reliability and cogency of the use of electron microscopic fibre analysis of lung tissues to assess an individual’s cumulative dose of asbestos and to determine the cause of an individual’s lung cancer.  It is to be noted that he was not asked to address the issue of causation of asbestosis.  I have assumed that his comments would be equally applicable to that issue.  
46.	Dr Gibbs identified the four potential types of evidence that can assist in assessing the total cumulative asbestos dose to which an individual has been exposed.  Those four types of evidence are (i) lay witness evidence (which Dr Gibbs referred to somewhat pejoratively as “anecdotal” evidence); (ii) expert engineering evidence; (iii) the results of examination of lung tissue samples by light microscopy; and (iv) mineral fibre analysis of lung tissue using electron microscopy.  
47.	Dr Gibbs referred to the potential weaknesses of both lay and expert engineering evidence.  He observed that the reliability of the former is dependent on the accuracy of the witness’s recollection.  That recollection may be adversely affected by the effects of time or by a tendency (whether conscious or unconscious) to fit the account of asbestos exposure to the disease suffered by the claimant/deceased.  As to expert engineering evidence, he said that engineers’ estimates of cumulative exposure often vary widely because of the different (and frequently inaccurate) data on which those estimates are based.  
48.	Dr Gibbs went on to observe that examination of samples of lung tissue under light microscopy can provide useful objective information about asbestos exposure.  If the Helsinki criteria requirement of two asbestos bodies per square centimetre of lung tissue is met, the lung cancer/asbestosis can be attributed (at least partly) to asbestos exposure.  He described the statement by Dr Hayes in his post mortem report that asbestos fibres were “readily demonstrable” as “very imprecise”.  He pointed out that it was impossible to know from that statement whether the number of asbestos bodies was below or above the Helsinki criteria requirement for the diagnosis of asbestosis/lung cancer.  
49.	Dr Gibbs went on to say that, if the Helsinki criteria requirement of two asbestos bodies per square centimetre of lung tissue is not met, that does not necessarily mean that causation cannot be established since the individual in question may have a poor coating mechanism (see paragraph 18 of this judgment), resulting in a disproportionately low count of asbestos bodies.  Thus, if the Helsinki criteria requirement of two asbestos bodies per square centimetre of lung tissue not is met, mineral fibre analysis by means of electron microscopy is usually recommended.  
50.	Dr Gibbs said that mineral fibre analysis using electron microscopy is the most sensitive and specific method for identifying and quantifying asbestos fibres in lung tissue.  It has the benefit of being a wholly objective method which does not rely on any assumptions.  However, the weakness of electron microscopy is that it may significantly under-estimate an individual’s asbestos exposure.  This is because of the effects of clearance of asbestos fibres from the lungs.  Clearance of asbestos fibres is known to take place over time and, since analysis under electron microscopy will inevitably be undertaken many years after the relevant asbestos exposure, the results of the analysis must be adjusted to take account of the substantial amount of clearance of asbestos fibres that will have taken place in the intervening period.  The rate at which clearance takes place varies as between the different types of asbestos.  Dr Gibbs said that the clearance rates for amosite and crocidolite are known, so that it is possible to adjust the results of analysis by electron microscopy to take account of clearance of those types of asbestos.  However, since the rate at which chrysotile is cleared from the lungs is relatively rapid, electron microscopic analysis cannot provide a realistic estimate of the extent of an individual’s previous dose of that type of asbestos. 
51.	Dr Gibbs also pointed out that there can be some variation in the distribution of asbestos fibres within the tissue of the lungs, which can result in variations in the results of electron microscopic analysis as between samples of tissue.  In order to ensure reliability of results, therefore, it is best to analyse multiple pooled samples from the lung tissues taken on post mortem examination.  
52.	Dr Gibbs concluded that the assessment of the deceased’s lifetime exposure to asbestos was severely hampered by the lack of lung tissue samples for evaluation by light microscopy and electron microscopy.   
The law
53.	The defendant’s application to strike out is made pursuant to CPR 3.4 (2)(b) which provides:
“(2) The court may strike out a statement of case if it appears to the court – 
…
(b) that the statement of case is an abuse of the court’s process or is otherwise likely to obstruct the just disposal of the proceedings;”
54.	The defendants submit that the conduct of the claimant and/or of her solicitors, JMW, which resulted in the destruction of the tissue samples, was unreasonable and blameworthy such as to amount to an abuse of process.  They further argue that the destruction of the samples of lung tissue, thereby depriving them of the opportunity of subjecting those samples to further histological examination, gives rise to a real risk of injustice arising, such that a fair trial is no longer possible.  Consequently, they say, the appropriate sanction is strike out of the claimant’s statement of case.  
55.	In making this submission on behalf of the defendants, Mr Platt relied on the test set out by Chadwick LJ in Arrow Nominees Inc v Blackledge and others [2000] CP Reports 59 at paragraph 54:
“ … where a litigant's conduct puts the fairness of the trial in jeopardy, where it is such that any judgment in favour of the litigant would have to be regarded as unsafe, or where it amounts to such an abuse of the process of the court as to render further proceedings unsatisfactory and to prevent the court from doing justice, the court is entitled - indeed, I would hold bound - to refuse to allow that litigant to take further part in the proceedings and (where appropriate) to determine the proceedings against him.  The reason, as it seems to me, is that it is no part of the court's function to proceed to trial if to do so would give rise to a substantial risk of injustice.  The function of the court is to do justice between the parties; not to allow its process to be used as a means of achieving injustice.  A litigant who has demonstrated that he is determined to pursue proceedings with the object of preventing a fair trial has forfeited his right to take part in a trial.  His object is inimical to the process which he purports to invoke.”
56.	It is clear from Arrow Nominees and also from the case of Logicrose v Southend United FC (1988) Times LR 5th March 1988 that the threshold for striking out a case under CPR 3.4 (2)(b) is high and that the type of conduct which has been regarded as rendering the statement of case an abuse of process has in general been seriously improper. 
57.	This is not the first case in which the destruction of tissue samples has resulted in an application to strike out pursuant to CPR 3.4(2)(b).   
58.	In Celia Maureen Weaver and another v Contract Services Division Limited, an unreported decision of the Senior Master dated 3 September 2009, the deceased had commenced proceedings in his lifetime and the claimants (who were the deceased’s daughters) took over those proceedings. They claimed that, as a result of asbestos exposure whilst working for the defendant, the deceased had contracted asbestosis which caused his death.  As in the present case, the issue was whether or not the deceased’s pulmonary fibrosis had been caused by his asbestos exposure. 
59.	A post mortem examination, including histology, was carried out by Dr Hayes (i.e. the same pathologist as in the present case).  On microscopic examination of lung tissue, he found “occasional asbestos bodies”.  He concluded that the cause of death was end stage respiratory failure caused by pulmonary fibrosis and asbestos exposure.  After the post mortem examination, one of the claimants signed a letter, requesting that the tissue samples taken by Dr Hayes should be retained for further examination.  
60.	In January 2009, one of the claimants telephoned the solicitor acting for herself and her sister and asked whether, in view of the distress being caused to the family by the retention of the tissue samples, the samples could now be destroyed.  The solicitor responded that he was satisfied with the medical evidence that had been obtained on the claimants’ behalf and therefore he did not need the tissue samples.  He did not consult the defendant’s solicitors about the matter.  The claimant telephoned the Office of the Coroner of Herefordshire and asked for the lung tissue samples to be destroyed.  She was advised that this could be done provided that her solicitor confirmed that the samples were not required for the purposes of the claim.  She rang her solicitor again to confirm this.  The solicitor reiterated that he did not need the samples for the purpose of the claimants’ claim and therefore had no objection to their disposal.  He went on to explain to her that the defendant might object to destruction but that, as far as he was concerned, it was “a family issue”.  He agreed to provide confirmation of his advice in writing for the Coroner.  At a subsequent hearing in the claim, directions were made in respect of the histological evidence despite the fact that the claimants’ solicitor well knew that the relevant samples had been destroyed.
61.	Not surprisingly, the Senior Master was very critical of the conduct of the claimants’ solicitors in Weaver.  He described the events that had occurred as “astonishing” and the solicitor’s advice that, whilst the defendant might object to disposal of the tissue samples, it was nevertheless “a family issue”, as “breathtaking”.  He considered that there was no doubt that the claimants’ conduct in destroying the tissue samples was “worthy of sanction”.  He said that the question was what nature of sanction should be imposed and, in particular, whether strike out of the claim was proportionate and necessary on the basis that there was a substantial risk that there could not be a fair trial.  He went on to review the issues and evidence in the case and to conclude that, in the circumstances, a fair trial would not be possible.  He therefore acceded to the defendant’s application for strike out.
62.	The case of Irene May Currie v Rio Tinto Plc and others, a decision of Master Eastman dated 6 October 2010, was a claim for asbestosis.  The deceased had commenced the claim in his lifetime and, after his death, it was taken over by his widow.  The defendants’ case was that the correct diagnosis was IPF, not asbestosis.  The deceased had died in Australia, where post mortem examinations are not routinely carried out in cases of industrial disease.  The defendants requested the deceased’s family’s agreement to a private post mortem examination and, when the family refused, indicated their intention to apply to strike out the claim if consent was not forthcoming.  The refusal was maintained and the deceased was cremated.  The defendants duly applied for strike out.
63.	Having reviewed the circumstances of the claim, the Master concluded that the claimant’s action in denying the defendants the chance of obtaining histopathological evidence had caused a substantial risk that the court may not be able to deal with the case justly.  He therefore struck out the claim.
64.	The case of J Preston & Sons Ltd v Julie Hurst [2012] EWHC 870 (QB) was an appeal from a decision of the Senior Master not to strike out a claim for damages arising from the deceased’s death from lung cancer alleged to have been caused by asbestos exposure whilst he was working for the appellant.  The grounds of the application for strike out were various alleged failings on the part of the claimant’s solicitors.  One of those alleged failings was their omission to take any steps to ensure the preservation by the Coroner’s pathologist of lung tissue samples.  A diagnosis of asbestosis had been made during the deceased’s lifetime and there was a well documented history of asbestos exposure.  In the report of his post mortem examination, the pathologist reported that there was histopathological evidence of lung cancer, but did not address the issue of whether there was evidence of asbestosis.  He did not retain any histopathological samples.  The appellant’s solicitors had not been informed of the deceased’s death until some time after it occurred and had had no opportunity to take any steps to ensure that samples of lung tissue were taken and retained for examination.
65.	In determining the appeal, Cranston J considered that the Senior Master had been correct to focus on the omissions of the pathologist.  Like the Senior Master, Cranston J, did not consider that the claimant’s solicitor could be faulted for failing to anticipate that the pathologist would not retain appropriate lung tissue samples.  Cranston J also agreed with the Senior Master that none of the complaints raised by the appellant could prejudice a fair trial because of the clear diagnosis of asbestosis made in the deceased’s lifetime.  
The parties’ submissions  
The defendants
66.	Mr Platt relied on the fact that the claimant had been told at the Inquest that the Coroner intended to retain the samples of lung tissue.  He said that it must have been clear to her from the evidence given at the Inquest that the samples were important and that they constituted evidence that could potentially be of significance to her claim.  That claim was being conducted by JMW on her behalf and she should have referred the letter from Ms Oliver to JMW for advice.  It was not reasonable for her to accept without question the informal ‘advice’ given by a member of staff in the Coroner’s Office about what was ‘usually done’ in the circumstances.  Mr Platt argued that the claimant’s conduct was plainly culpable.
67.	Mr Platt also criticised the conduct of JMW.  He pointed out that the duty of a solicitor to advise a lay client of the need to preserve documents is well established and is now the subject of a specific provision of the CPR (at CPR PD 31B).  The relevant paragraph provides that the duty arises “as soon as litigation is contemplated”.  Mr Platt submitted that real evidence relevant to a contemplated claim (such as the samples of lung tissue) is analogous to disclosable documents and gives rise to a similar duty on the part of a solicitor to warn a client of the need to preserve it.  He submitted that the retention of tissue samples in asbestos claims is particularly important because the results of histological examination of such samples often constitute the only objective evidence available.  He argued that any firm of solicitors experienced in conducting asbestos claims should have been aware of the importance of preserving tissue samples.  The failure on the part of JMW to inform the claimant of the need for her to ensure that the tissue samples were retained was, he contended, highly culpable and amounted to gross negligence on their part.
68.	Mr Platt submitted that histopathological examination of the samples of lung tissue would clearly have been of value in this case, for the reasons set out by Dr Gibbs.  He referred also to the judgments in Weaver and Currie, in which the importance of histopathological examination was emphasised.  Such examination in this case would, he said, have revealed whether or not the requirements of the Helsinki criteria for the diagnosis of asbestosis (see paragraph 41 of this judgment) were fulfilled.  As it is, Dr Hayes’ evidence about the presence of asbestos fibres (or bodies) had not been expressed by reference to the Helsinki criteria.  Mr Platt also pointed out that the mere presence of asbestos fibres in the lungs is not sufficient to establish asbestosis since the lungs of individuals living in an urban environment with no occupational asbestos exposure will contain large quantities of asbestos fibres.  It is for that reason that the Helsinki criteria require that the count of asbestos fibres on electron microscopy examination should fall into the range recorded for asbestosis by the relevant laboratory.  That range is designed to exclude asbestos fibres resulting from purely environmental exposure.
69.	Mr Platt did not accept that the histopathological evidence would be irrelevant because of the effects of clearance.  He pointed out that neither Dr Moore-Gillon nor Dr Gibbs appeared to consider that it would be irrelevant.  He argued also that there is no evidence that asbestos bodies are cleared in the same way as asbestos fibres.  
70.	Mr Platt referred also to the fact that it was alleged by the claimant that the deceased had been exposed to amosite dust from “Asbestolux” insulation board.  Exposure to amosite was denied by the defendants.  He said that, if electron microscopy had been possible, it would have revealed whether or not amosite fibres were present in the deceased’s lung tissue.  If no amosite fibres were found, that fact would have shed doubt on the assertion that the deceased had been exposed to amosite dust.  On the other hand, if high levels of amosite had been found, this might have suggested that amosite exposure had occurred during a period of employment other than those with the defendants.
71.	Mr Platt argued that, without the histopathological evidence, the Court hearing the claimant’s claim would be left with widely diverging lay and witness evidence.  The claimant’s lay evidence comes mainly from Mr Brian Matthews who, as the deceased’s brother, has an obvious motive to exaggerate the extent of the deceased’s asbestos exposure.  Mr Platt observed that, it was on the basis of Mr Brian Matthews’ evidence that Mr Brady had reached his conclusion that the deceased’s cumulative asbestos exposure would have been between 60 and 180 fibre ml years and therefore over the threshold for cumulative asbestos exposure of 25 fibre ml years.  Thus, in effect, Mr Brian Matthews’ evidence could be determinative of the claim. Mr Platt argued that it would be unsatisfactory and unfair for the outcome of the case to be dependent solely on the trial judge’s assessment of the lay evidence when other evidence could have been available which might have assisted the defendants’ case.
72.	Mr Platt suggested that, up to the time of the deceased’s death, the medical evidence was highly equivocal, with the treating doctors appearing to favour a diagnosis of IPF.  This appeared to be because the deceased’s fibrosis had the ‘honeycomb’ appearance typical of IPF.  He suggested that the speed of progression of the fibrosis also supported a diagnosis of IPF.  He submitted that histological examination would have been highly valuable in determining which diagnosis – IPF or asbestosis – was the more probable.  
73.	Mr Platt argued that the absence of the histological evidence deprived the defendants of the opportunity of adducing objective evidence in support of their case.  As it is, the outcome of the evidential disputes is uncertain and the defendants are robbed of the ability that they would otherwise have had to properly assess the prospects of successfully resisting the claim and of making an informed choice whether to settle the claim or to fight it robustly.
The claimant
74.	For the claimant, Mr Roussak argued that the criticisms of her conduct were unfair and unfounded.  She had no knowledge about medicine or the law.  Having received Ms Oliver’s letter, she did not merely ignore it, but telephoned the Coroner’s Office for clarification as the letter had invited her to do.  It was, Mr Roussak contended, entirely reasonable for her to agree to follow what was represented to her as the ‘usual practice’ and it was unfair to criticise her for not having consulted her solicitors. 
75.	Mr Roussak submitted also that it was a counsel of perfection to criticise JMW for not having warned the claimant in advance that, if she was asked whether the tissue samples should be retained, she should insist that this was done.  In his witness statement, Mr Lilley had explained that, having been in contact with the Coroner before and after the Inquest, he had not anticipated that the Coroner would take any action in relation to the tissue samples without reference to JMW.  Mr Lilley had observed that, if the Coroner’s Office had contacted JMW to discuss disposal of the samples – or had suggested to the claimant that she should consult her solicitors before making a decision about disposal – the problem would have been avoided.
76.	Mr Roussak submitted that, in any event, despite the destruction of the tissue samples, it was still possible for there to be a fair trial.  The deceased gave a brief account of his exposure in the Questionnaire he completed and there will also be live evidence from his brother who worked alongside him.  The defendants are in a position to call several witnesses to describe the deceased’s working conditions.  The evidential position is very different from that in Weaver, for example, where the defendant had no means of challenging the claimant’s evidence.  In this case, it will be for the judge to assess the lay witness evidence and, in the light of that assessment, to evaluate the evidence of the engineers.  The doctors are agreed on the threshold cumulative exposure of 25 fibre ml years.  If the judge finds that that threshold has been reached, causation of both asbestosis and lung cancer will be established.
77.	Mr Roussak questioned whether examination of the tissue samples would in fact have been of any value.  He submitted that there was no evidence about the condition of the blocks of tissue that had been retained after the Inquest.  It was therefore impossible to know whether potentially helpful evidence had really been lost.  He submitted that, in any event, on Dr Gibbs’ evidence, the effect of clearance of chrysotile fibres would have rendered the results of electron microscopy unreliable.  There is, he said, no evidence as to whether chrysotile bodies are subject to clearance in the same way as chrysotile fibres. He suggested that Dr Gibbs did not appear to differentiate between the two.
78.	Mr Roussak submitted that, in the circumstances of this case, strike out – which would have the effect of depriving the claimant of consideration of her claim on the merits – would be a draconian remedy.  He argued that to strike out the claim on the basis of the destruction of evidence which would not necessarily have been of any value in determining the outcome would be wholly disproportionate.  It would also be unnecessary since a fair trial remains possible.
Discussion and conclusions  
79.	I do not consider that the defendants’ criticisms of the claimant in this case are justified.  She had lost her husband quite suddenly in January 2009.  It is clear from the transcript of the Inquest proceedings that, six months after the deceased’s death in July 2009, she was still confused about what had caused his death and distressed at what she said had been the lack of information given to the family whilst he was in hospital.  Whilst she plainly remembers that the retention of tissue samples was mentioned on the day of the Inquest, it appears to me most unlikely that she would have appreciated why it might be necessary to preserve the samples and what part they might play in any future claim she might make in respect of the deceased’s death.  Although JMW were involved in investigating a possible claim at the time of the Inquest, they did not represent her at the proceedings so would not have been in a position to explain matters to her at the time. 
80.	When the claimant received Ms Oliver’s letter, she was uncertain what she should do and accepted the invitation contained in the letter to seek clarification from the Coroner’s Office.  She knew of no reason why she should not follow the ‘usual practice’ and authorise the disposal of the tissue samples.  It seems from her Response to the defendants’ Request for Further Information that she believed that, at the time of the Inquest, the Coroner wanted the tissue samples preserved for some purpose of his own.  Not unreasonably, she believed that, more that 12 months after the Inquest, the Coroner would have obtained whatever information he needed from the samples.
81.	I see no reason to believe that the claimant would have connected the preservation of the samples with her claim at all.  In those circumstances, it would not have occurred to her to consult her solicitors about what she should do.  I regard the suggestion that she should have recognised that the tissue samples were or might be required for the purposes of her claim as wholly unrealistic.  In my view she cannot be criticised for her actions.   
82.	With hindsight, it is of course easy to say that JMW should have made clear to the Coroner’s Office and/or the claimant that the tissue samples should be preserved unless and until they advised otherwise.  However, I do not consider that, before these events, they could be criticised for failing to anticipate the situation that arose here.  The Coroner’s Office was aware of their involvement in the case.  The Inquest had resulted in a verdict of death due to industrial disease.  The post mortem report referred to asbestos exposure.  I do not regard it as unreasonable for JMW to have assumed that the Coroner’s Office would not dispose of the tissue samples without seeking their prior agreement or advising the claimant to do so.
83.	It was suggested that a knowledge of what had happened in Weaver (a case which although unreported, is nevertheless well known to solicitors specialising in asbestos claims) should have alerted JMW to the potential problem in this case, particularly since Weaver involved the same pathologist and Coroner’s Office as this case.  I do not accept that that would necessarily be so.  The circumstances of Weaver were very different from those in the present case.  In an event, it is noteworthy that, in Weaver, the Coroner’s Office advised the claimant that she must obtain her solicitor’s confirmation in writing before authorising disposal of the samples.  It seems to me that, if JMW were aware of Weaver before November 2010, it might in fact have served to reassure them that, in a case of industrial disease where a solicitor was involved, a Coroner would not dispose of tissue samples on the authority of a lay client alone.  
84.	I do not consider either that the analogy with CPR PD 31B assists the defendants.  First, there is no equivalent provision in the CPR relating to real evidence.  In any event, there is a wealth of difference between documents relating to issues being litigated which are in the possession or control of a litigant and histological samples which are being held by a judicial officer.
85.	In the circumstances, I do not consider that there has been any culpable behaviour on the part of the claimant or her solicitors, let alone the type of behaviour that could properly be characterised as an abuse of process.  The circumstances of this case are completely different from those in either Weaver or Currie and the behaviour of the claimant and her solicitors far removed from the deliberate pursuit of proceedings with the object of preventing a fair trial described by Chadwick LJ in Arrow Nominees Inc.
86.	It seems to me that the histopathological evidence could have been of value in two respects.  First, if it had been apparent on examination under light microscopy that the Helsinki criteria requirement of two asbestos bodies per square centimetre of lung tissue was met, the diagnosis of asbestosis and the causation of the deceased’s lung cancer would have been clearly established.  Second, electron microscopy, if undertaken, should have established whether or not there had been any significant exposure to amosite and may thereby have assisted the Court in determining whether Mr Brian Matthews is correct in saying that the deceased was involved with cutting “Asbestolux” boards (as well as “Big Six” sheets).  The presence or absence of amosite would not, however, necessarily have been decisive to the outcome of the claim since it is possible for both asbestosis and lung cancer to be caused by chrysotile fibres alone.  
87.	Other than in the respects identified above, it does not seem to be me that the histopathological evidence would have been of assistance in this case.  If, on examination by light microscopy, the Helsinki criteria requirement of two asbestos bodies per square centimetre of lung tissue had not been met, this would not have been decisive since it may be that the deceased had a poor asbestos coating mechanism.  A low count of chrysotile fibres on analysis by electron microscopy would not have been determinative because of the effects of clearance described by Dr Gibbs.  Thus, so far as the presence of chrysotile fibres is concerned, electron microscopy is likely to have been inconclusive. 
88.	These observations are made on the basis that the lung tissue samples, if preserved, would have been suitable for analysis.  It is impossible to be certain about this but I can see no reason why this should not have been the case.  Furthermore, since it appears from the post mortem report that nine blocks of tissue were retained for histological examination, it seems likely that there would have been sufficient samples to meet the requirements set out by Dr Gibbs. 
89.	What other evidence would be available to the Court in the absence of histopathological evidence?  There is the evidence of Mr Brian Matthews who worked alongside the deceased during his employment with all the defendants and, before that, with Payne Bros.  Mr Jennings also worked with the deceased for Payne Bros.  Also available – somewhat unusually in a case of exposure more than 30 years ago – are four witnesses for the defendants who appear to have a good memory of the deceased and the work that he and they performed.  The judge hearing the case would have the opportunity to see and assess all those witnesses.  In carrying out that assessment, he/she would no doubt have very much in mind the need to consider in respect of each witness the extent, if any, to which that witness might be seeking to understate or exaggerate the extent of the deceased’s asbestos exposure.  
90.	Having made his/her assessment of the lay witness and other evidence, the judge would then have the benefit of the expert witnesses’ assistance in converting his/her findings into an estimate of the deceased’s total cumulative asbestos exposure and would have the opportunity, insofar as may be necessary, of determining which of those expert witnesses he/she considered the more reliable.  
91.	The judge would also have the evidence about the medical features which might tend to point to a diagnosis of either asbestosis or IPF: the evidence about the progression of the deceased’s fibrosis, for example, and its “honeycomb” appearance.  There is also the evidence about the “readily demonstrable” asbestos bodies found on post mortem examination.  Whilst Dr Hayes did not express his findings in terms of the Helsinki criteria, it appears from his evidence at the Inquest that he regarded the incidence of asbestos bodies (which he described as “fibres”) in the deceased’s lungs as indicative of occupational – rather than environmental – asbestos exposure.  All these pieces of evidence would form part of the decision making process and would enable the judge to reach a satisfactory conclusion as to the issue of causation.  
92.	In all the circumstances, I am satisfied that, despite the destruction of the samples of lung tissue, it is perfectly possible for a fair trial of the claimant’s claim to take place and I do not consider that it would be just, necessary or proportionate to deprive the claimant of the opportunity to have her claim heard.  
93.	The defendants’ application is therefore dismissed. 
Postscript 
94.	In an attempt to avoid a recurrence of the circumstances that arose in this case, I propose to send a copy of this judgment to the Chief Coroner with a request that he considers advising all Coroners that, in cases where there has been a verdict that a contributory cause of death was industrial disease, any communication to the deceased’s family about the disposal of histological samples should contain advice that, if a claim in respect of the deceased’s death is pending, they should consult their solicitor before giving authority for disposal.  
95.	In the light of what has happened in this case, it would be good practice also for solicitors instructed by claimants in fatal asbestos claims to advise both their clients and the relevant Coroner’s Office that disposal of histological samples should not be undertaken without confirmation from those solicitors that the samples are not required for the purposes of the claim.