England and Wales High Court (Queen's Bench Division) Decisions

IN THE HIGH COURT OF JUSTICE
QUEEN'S BENCH DIVISION

		Royal Courts of Justice Strand, London, WC2A 2LL
		28/10/15

Mr Justice Hickinbottom :

Introduction

1. The Claimant was born on 20 December 1944. From leaving school in 1959 to the date of his early retirement in 1996, he had a wide variety of jobs, including work as an apprentice painter and decorator (1959-62), and work for the Defendant Council's predecessor, Cardiff Corporation, as a playing fields groundsman (1963-65), a boilerman at the Schools Meals Department, Clydesmuir Road, Tremorfa (which cooked and delivered meals for children at schools which did not have a kitchen) (1966-68) and a school caretaker (1971-73). As a boilerman at the School Meals Department, for about 18 months, he spent a good deal of time in a boilerhouse, which housed boilers with asbestos lagging in very poor condition which gave rise to asbestos dust. That was the only period during which the Claimant was exposed to asbestos. He retired at the age of 52, due to ill-health caused by kidney stones.
2. The Claimant now suffers from a number of medical conditions, including (i) a condition of the pleura caused by asbestos, and (ii) chronic obstructive pulmonary disease ("COPD") caused by smoking. As a result of those two conditions, he has an overall cardiorespiratory disability of about 50%, of which each condition has contributed about half.
3. In this action, the Claimant claims damages from the Defendant ("the Council") for the respiratory injuries he has suffered as a result of exposure to asbestos during the course of his employment which was itself a result of the Council's negligence and breach of statutory duty.
4. The Council accepts that it is not in a position to deny the Claimant's alleged asbestos exposure, nor does it dispute that such exposure was in breach of duty.
5. Proceedings were issued on 18 August 2014. In paragraph 5 of its Defence, the Council contends that the claim is statute-barred by operation of the Limitation Act 1980 because, prior to 18 August 2011, the Claimant knew that he suffered from a significant injury that was likely to have been caused as a consequence of asbestos exposure whilst he was employed by the Council. In paragraph 1 of his Reply, the Claimant expressly denied that he had acquired the relevant knowledge prior to 18 August 2011, and thus denied that the claim was statute-barred. He indicated that, if the date of knowledge was prior, he did not intend to apply for an extension of time pursuant to section 33 of the Limitation Act 1980. Although Mr Phillips for the Claimant before me attempted to pursue a section 33 application in the alternative, it had not been pleaded, was not raised at all until Mr Phillips' skeleton argument was served a few days before the hearing and, understandably, the Council had not lodged evidence in relation to that issue nor was Mr Turton for the Council prepared to argue such an application. I accordingly refused to extend the scope of this hearing.
6. The only issue before me is therefore whether the Claimant had the requisite knowledge only after August 2011.
7. At the trial, Matthew Phillips appeared for the Claimant, and Philip Turton for the Defendant. The Claimant gave evidence. His was the only live evidence; but I also had the benefit of written expert evidence from two expert consultant physicians, Dr D G Sinclair and Dr John Moore-Gillon, instructed on behalf of the Claimant and the Defendant respectively.

The Law

8. Section 11 of the Limitation Act 1980 applies a special time limit for the commencement of any action in respect of personal injuries, such as this. It provides, so far as relevant to this claim:

"(3) An action to which this section applies shall not be brought after the expiry of the period applicable in accordance with sub-section (4)….

(4) ... [T]he period applicable is three years from –

(a) the date on which the cause of action accrued; or

(b) the date of knowledge (if later) of the person injured."

9. Section 14 provides, again so far as relevant to this claim:

"(1) … [I]n section 11… references to a person's date of knowledge are references to the date in which he first had knowledge of the following facts –

(a) that the injury in question was significant; and

(b) that the injury was attributable in whole or in part to the act or omission which is alleged to constitute negligence… or breach of duty; and

(c) the identity of the defendant; …

(2) For the purposes of this section an injury is significant if the person whose date of knowledge is in question would reasonably have considered it sufficiently serious to justify his instituting proceedings for damages against a defendant who did not dispute liability and was able to satisfy a judgment."

10. In relation to these provisions, the following propositions were common ground before me, and are uncontroversial.

i) The effect of section 11(4)(a) and (b) is that, where proceedings are not commenced within three years of the cause of action arising, generally the claimant has the burden of proving that he did not have the requisite knowledge until a date within the three years preceding the date of issue of proceedings (Nash v Eli Lilly & Co [1993] 1 WLR 782 at page 793H, paragraph 6).

ii) "Knowledge" in the context of section 14 does not mean know for certain: it means know with sufficient confidence reasonably to justify embarking upon steps preliminary to the institution of proceedings against those whose act or omission has caused the significant injury concerned, such as submitting a claim to the proposed defendant, taking legal and other advice and collecting evidence (Halford v Brookes [1991] 1 WLR 428 at page 443, approved in Dobbie v Medway Health Authority [1994] 1 WLR 1234 at page 1240B; and Nash at page 793C-D, paragraph 3). Of course, even where a particular individual has that level of confidence, he may have perfectly good reasons for not pursuing a claim and may quite reasonably decide not take steps to do so (see A v Hoare [2008] UKHL 6; [2008] 2 WLR 311 at [38] per Lord Hoffmann); but whether or not steps are in fact taken does not affect the date of knowledge.

iii) The test for "significance" of injury is one of quantum alone, and does not invite consideration of the cause or nature of the injury (Dobbie at page 1241H). But, for an injury to be "significant" for these purposes, the quantum level is low: it has been said that the test comes close to the test of seriousness of an injury for which the courts could properly award damages and thus in respect of which a cause of action in negligence accrues (Cartledge v E Jopling & Sons Limited [1963] AC 758 at 781; Rothwell v Chemical & Insulating Company Limited [2006] EWCA Civ 27; [2006] ICR 1458 at [21]). That test is essentially an illustration of the principle "de minimis non curat lex". Thus, where an injury is any more than very minor, it will generally satisfy the test for "significance" in section 14(2).

iv) However, the House of Lords in Rothwell held that, where a breach of duty has given rise to physiological changes but the condition is symptomless, and does not presage or threaten a more serious condition, that will not satisfy the test for bringing a negligence action; nor will it, even if known, be sufficient to satisfy the knowledge test in section 14(2). The opinions were handed down in Rothwell on 26 January 2006. Prior to that, it was at least arguable that an asymptomatic condition which does not presage or threaten a more serious condition could nevertheless found a suit in negligence.

Asbestos-Related Conditions

11. It is well-established that exposure to asbestos dust or fibres carries with it the risk of a variety of medical conditions including, at their most serious, lung cancer and mesothelioma. Notably, for the purposes of this claim, such exposure may result in physiological changes to the pleura, a lubricated membrane which facilitates movement of the lung. Whilst being morphologically distinct, the pleura envelops the lungs and lines the walls of the chest cavity. It comprises two distinct layers of an essentially single membrane: the parietal pleura lines the inside of the rib cage, whilst the visceral pleura covers the lungs.
12. The way in which asbestos fibres arrive at the pleura (and, particularly, how they reach the parietal pleura) is not fully understood; but it is well-recognised that exposure to asbestos may cause pleural abnormalities. Two such diseases are described in the chapter on "Asbestos-related Diseases" contributed by Dr Robin Rudd, recognised as a particular expert in the area, in the textbook "Respiratory Medicine" (3rd edition) (2003), to which I was referred.
13. "Pleural plaques" are defined thus:

"Plaques are circumscribed areas of thickening of the parietal pleura of the chest wall, mediastinium and diaphragm. Occasionally they affect the visceral pleura…".

Plaques (it is said) are composed of fibrous tissue, and there is no treatment for them. They are not in themselves precursors of malignant change; but, because they reflect asbestos exposure, they are associated with an increased risk of other asbestos-related diseases, benign and malignant. With regard to clinical features, Dr Rudd says:

"Usually, pleural plaques are an incidental finding on the chest radiograph, whether this is performed for routine employment health screening or some other purpose.  In the unusual case where the plaques are very extensive and fused to form a cuirass-like structure, or where there are adhesions, they may give rise to shortness of breath on exertion.  Rarely, pleuritic pain occurs, probably caused by adhesions, and occasionally extensively calcified plaques may give rise to an uncomfortable grating sensation during breathing, which may be audible on auscultation."

14. The second condition is "diffuse pleural thickening", defined by Dr Rudd as:

"… pleural fibrosis that extends continuously over a variable proportion of the thoracic cavity without well-circumscribed margins.  It principally involves the visceral pleura, although this is often adherent to the parietal pleura."

 With regard to clinical features of this condition, he says:

"The principal symptom is shortness of breath on exertion.  There may have been a history of episodes of pleurisy in the past and there may also be pleuritic pain due to adhesions.  Occasionally, pain is a persistent feature and may be disabling.

On examination there is usually little to find…".

Once established, pleural thickening tends to progress, mainly in the first 15 years of onset. In most cases, no treatment is advised.

15. It can therefore be seen that there is some degree of overlap – or, perhaps more accurately, an uncertain diagnostic boundary – between these two conditions. The former usually affects the parietal pleura, but may affect the visceral pleura; the latter, vice versa. The former usually comprises well-defined thickened discs, but these may fuse to cover a substantial area; the latter is diffuse and extends continuously over an extensive area. The former is usually asymptomatic, but in a small percentage of cases it may be symptomatic; whilst the latter is usually symptomatic. Clinically, it seems to me that the distinction is of modest importance – because, as I understand it, there is no treatment for either condition.
16. Before I leave the definitions of asbestos-related conditions, I should briefly refer to "asbestosis". This was a term widely used to describe any and all asbestos-related diseases; but, as defined in 1979 by the Advisory Committee on Asbestos, "asbestosis" has a particular restricted meaning, namely "fibrosis of the lungs caused by asbestos dusts which may or may not be associated with fibrosis of the parietal or pulmonary layer of the pleura". By that definition, asbestosis is a condition distinct from pleural plaques and diffuse pleural thickening; but the term continued to be used in a more generalised way well after 1979.

The Claimant's Medical Condition

17. The Claimant appears to have complained of shortness of breath in 1994 and had two chest x-rays which identified some atelectasis (i.e. an area of less than fully inflated lung) and pleural fluid, which improved over the week between the two x-rays. No abnormality of the pleura was identified, and it is not suggested that this episode is of any significance in the context of this claim.
18. However, in 2000, the Claimant started to suffer from breathlessness and pain in his chest. He said that, at first, it was intermittent and not severe; but there came a point when he realised that, on exertion, he was more breathless than he ought to have been, and he began suffering from intermittent pain in his chest, usually when he was breathless. Although the breathlessness and pain has been progressive – over time, gradually worsening in terms of both frequency and severity – the type and nature of the symptoms have not altered since 2000.
19. In October 2000, the Claimant had a chest infection. However, once that had cleared, he attended his GP on 18 October 2000 complaining of breathlessness and "tight band round chest" on mild exertion. He was given an immediate x-ray in the doctor's surgery, which the notes record as follows:

"Chest: There is a large pulmonary mass present in the left mid zone. This mass has a rather irregular border and there appear to be spicules extending towards the pleural surface. There is also possibly a little loss of volume in the right upper lobe. Further evaluation of this lesion is required. A CT examination [i.e. an x-ray computed tomography, or 'CT scan'] is recommended in the first instance. The lungs elsewhere appear clear. The heart is a little enlarged."

The Claimant said that, at the time, he was told he had a lump in his lung together with what were described to him as "tiny Christmas tree-like" projections from the lump. The lump, he was told, would require further investigation.

20. By letter dated 10 November 2000, the Claimant was referred to Dr David Jones at Withybush Hospital, Haverfordwest. Dr Jones saw him at his clinic on 22 November 2000. He reported to the Claimant's GP by letter of 24 November 2000:

"Seen 22 11 00.  For the last 3-4 weeks he has had episodes of tightness on both sides of the front of his chest.  It will last for between half an hour and all day.  Not typically pleuritic.  No cough or phlegm.  Appetite and weight are fine.  He smokes 20 cigarettes a day (30 pack years).  In the past he worked as an industrial painter on large sites such as chemical works for 3 years soon after leaving school i.e. almost 40 years ago.  Thereafter he was a labourer on domestic building sites and a gardener.  He was a boilerman in the schools in Cardiff but was not exposed to asbestos other than probably as an industrial painter….

I had previously looked at the chest x-ray and thought it was suspicious of pleural plaques.  He had a CT scan which confirms a large area of pleural thickening in the left anterior chest and one small plaque posteriorly on the left side with another one on the diaphragm.  These are almost certainly related to his previous work as an industrial painter 40 years ago.

The lesion looks benign but we may have to consider a biopsy of the large one in the anterior chest…".

21. The Claimant could not recall any discussions with the consultant over and above those recorded by Dr Jones himself; but he denied telling the consultant that he had been exposed to asbestos as a painter, and had not been exposed as a boilerman – and there are no notes of his possible exposure to asbestos in the contemporaneous notes taken by Dr Jones. In any event, it now appears uncontroversial that the Claimant's only exposure to asbestos was as a boilerman as I have described.
22. Dr Jones' letter of 24 November must have reached Dr Cooke a couple of days after it is dated; because, on 28 November 2000, Dr Cooke saw the Claimant at the surgery to discuss it. The Claimant remembers being called in. It was quite an important consultation, because a lump had been found in the Claimant's lung and a biopsy was required to ascertain whether it was malignant or not. There was a chance that the lump was cancerous. The GP record of this consultation refers to "asbestosis", but the Claimant (rightly) understood this to be used as an umbrella-term to include all forms of asbestos-related disease. The note says that a biopsy and ECG was awaited. It also says:

"Considering claim now against employer from when he was a boilerman in Cardiff."

23. In paragraph 88 of his statement dated 31 March 2015, the Claimant said that, until he was told in 2012 that he had "pleural thickening", he had always assumed that his shortness of breath was due to his smoking and the associated COPD. However, he frankly accepted in cross-examination that, although he thought that his heavy smoking might have contributed to his condition, he was not diagnosed with COPD until 2007; and, from 2000 onwards, he believed that his breathlessness and chest pain resulted from exposure to asbestos while he was working for the Council as a boilerman.
24. Following his consultation with Dr Cooke, the Claimant telephoned Gee & Edwards, solicitors in Swansea who specialised in personal injury claims. On 5 December 2000, a Mr Owen of that firm attended the Claimant at his home. He told Mr Owen that he had been told by Dr Jones that he had "asbestosis". Mr Owen's note records that he explained the three year limitation period to the Claimant; but that did not appear to be an immediate problem as no one had before raised with him the possibility that he had a chest condition let alone an asbestos-related condition related to his work.
25. Although the Claimant appears to have been confused about dates of exposure, he made clear to Mr Owen that he considered he had been exposed to asbestos when, and only when, he was a boilerman at the schools meal service kitchen building in Tremorfa. In the event, the Claimant's employment history occupied the solicitors a good deal over the next few weeks. However, on 6 February 2001, Mr Owen sent the Council a letter before action (with some follow-up correspondence responding to particular queries), identifying "asbestosis" as the injury complained and the correct building in Tremorfa as the source. The dates suggested were, however, incorrect, the letter suggesting that he was employed there in the period 1971-4. Nothing now turns on that error.
26. The Claimant was made well aware that the changes to his pleura that required further investigation were attributable to exposure to asbestos; and he knew that his only exposure to asbestos was as a boilerman at the school meals service premises in Tremorfa. Attribution in that sense has always been clear. Of course, this was pre-Rothwell; and, in 2001, it was generally thought that a symptomless asbestos-related condition was actionable. Therefore, at an early stage of investigation, solicitors might reasonably not have been focusing on whether and what symptoms resulted from the condition. However, in his evidence, the Claimant was clear: at that stage and ever since, he considered that, whilst his heavy smoking may also have made a contribution, his breathlessness and pain in the chest resulted from an asbestos-related condition caused by exposure to asbestos when he was employed by the Council as a boilerman.
27. In the meantime, Dr Jones had sent a second letter to the Claimant's GP on 6 December 2000, but only in relation to matters arising from the first consultation, as follows:

"This patient's CT scan confirms that the lesion on the x-ray in the left upper lobe is actually pleural in origin.  It is sharply defined and has a few flecks of calcification so probably represents a large innocent pleural plaque.  There is also another calcified pleural plaque on the right hemi-diaphragm.  These changes are related to occupational exposure to asbestos.  Because the lesion on the left upper chest is so large we will attempt a biopsy to exclude malignancy but this seems unlikely.  CT scan also shows a large fat pad around the heart and a small pericardial effusion.  Arrangements have been made for him to have a CT guided biopsy in the next week or so and he has an exercise stress test booked for 13th December.  Further information will follow later."

Things were therefore still worrying, as malignancy could not be ruled out before the biopsy on the large "plaque" had been performed.

28. The biopsy was duly performed on 12 December 2000, again at Withybush Hospital. The histopathological report read as follows:

"Sections show a fragment of markedly fibrous pleura, with some attached and lightly inflamed fibro-fatty connective tissue. The appearances would be consistent with your clinical suggestion of a simple pleural plaque, and there is certainly no evidence of dysplasia or malignancy in this specimen".

The letter from the hospital back to Dr Cooke was in similar terms:

"This gentleman underwent CT guided biopsy of the anterior pleural mass, histology from which showed markedly fibrous pleura and inflamed fibro-fatty connective tissue with no evidence of dysplasia or of malignancy. I will write to you again when the results of the stress test are available."

The Claimant said that he remembered being given that news – especially the good news about the absence of any malignancy – by his GP.

29. Thereafter, the Claimant lost interest in matters somewhat. He failed to attend appointments with Dr Jones at Withybush in June and August 2001, resulting in the hospital saying that they would not book another appointment unless requested by the GP to do so. The possible claim against the Council through Gee & Edwards was also not pursued. Although the Claimant was critical of the solicitors for simply letting the matter drop, in cross-examination, again very frankly and openly, the Claimant said that he was not particularly taking an interest in pursuing a claim and, he said: "Quite possibly, I thought I would knock it on the head." He said that he took this view because, although he was still breathless and sometimes had chest pain – and, indeed, over time these were worsening – his condition "was not bothering [him]" and it did not really prevent him from doing the things that he wished to do. For example, he could still without difficulty get to the shops and climb the stairs.
30. Nevertheless, on 28 September 2001, Dr King at the Claimant's GP Surgery wrote to the hospital saying that the Claimant had a "history of asbestosis" and his symptoms were becoming progressively worse, with increasing chest pain and breathlessness, and some light-headedness (possibly due to a chest infection). He appears to have been seen at the hospital, and x-rayed, in March 2002. There he admitted to heavy smoking – more than 30 cigarettes per day and to breathlessness on moderate exertion which had been going on for some time but which had not worsened recently. He had no chest pain. He said that he was fine going round the shops at walking pace, and slowly climbing stairs – but he had to stop for breaks when climbing steep hills. The consultant wrote back to Dr King in a letter dated 16 April 2002. That records the diagnosis as:

"… large pleural plaque left lung – histology confirmed as benign December 2000… The pleural plaque on the left is unchanged from previous films. The one on the right is possibly slightly larger… No further investigation or follow up is required at this time.

The staff grade also wrote an undated letter, essentially repeating those findings and saying:

"As far as his chest problems are concerned…, he does not feel his level of breathlessness has changed particularly over the last year to 18 months and was reassured of the unchanged [x-ray]."

31. In 2003, the Claimant was admitted again with chest pains, and increasing breathlessness for a month which (it is recorded) improved after admission. He had new x-rays and a CT scan, which showed no new findings. A letter from the consultant to the Claimant's GP surgery said:

"His symptoms are of chronic breathlessness which would appear to be related to his heavy smoking."

His discharge summary gave his diagnosis as "pleural plaque". No review was planned.

32. The Claimant does not appear to have attended the chest clinic again for several years, until 2011. However, in about September 2007, in circumstances not entirely clear, he was diagnosed with COPD and given an inhaler and antibiotics from time to time; and, oddly (given the earlier diagnosis of COPD for which he continued medication), on 10 June 2008, a letter from his GP confirmed he was suffering from "asbestos plaques on the lungs, renal stones, hypertension" (with no mention of COPD), and "the lung disease does result in him being breathless when walking long distances".
33. In October 2011, the Claimant was again referred to the chest clinic at the Withybush Hospital, under Dr Tim Lewis, because his breathlessness was worse and thought not optimally managed by his medication. The Claimant told the hospital that he had had shortness of breath for 10-12 years, but it had increased in the last year. At the consultation on 14 October, that medication was changed. Further CT scans performed – the first confirming the "calcified pleural mass and pleura lesions", and a second in January 2012 identifying "pleural plaques with pleural thickening" – and a video-assisted thoracic scan (or "VAT scan") also performed. A further biopsy was arranged, which showed no malignancy.
34. At a multidisciplinary ("MDT") team meeting (recorded in a letter from Dr Lewis to the Claimant's GP dated 20 January 2012), it was agreed:

"Diagnosis: Benign neoplasm of bronchus and lung.

MDT meeting discussion: Pleural plaques only, no malignancy….

The patient may not yet be fully aware of this information but it will be discussed at their next clinic appointment."

35. The conclusion of Dr Lewis, set out in a letter to the Claimant's GP dated 16 February 2012, was that:

"He has diffuse pleural thickening so he may be eligible for both State and Civil compensation for asbestos related disease.

Mr Summers' dyspnoea [i.e. shortness of breath] is, I suspect, due to his smoking history despite the lack of any obvious obstructive element to his spirometry and there may also be an element of lack of physical conditioning."

Dr Lewis wrote to the Claimant directly the same day, as follows:

"Following your recent visit to the clinic we can confirm that the specimens taken at Swansea are all benign with no evidence of cancer.

No compensation is available from the State or previous employers or insurance companies for asbestos pleural plaques but you do appear to have what is known as diffuse pleural thickening and you may be able to make a claim for this. (I cannot guarantee this as I am not the person who makes the decision.)

We would advise you to make both State and Civil compensation claim as you have nothing to lose apart from a little time by doing this.

Some details of how to go about this are enclosed for your convenience."

The Claimant was discharged from the hospital, on the basis that nothing could be done for his respiratory condition, other than the revised medication for his COPD with which he was already being provided.

36. No doubt encouraged by Dr Lewis's letter, the Claimant made a claim for Industrial Injuries Disablement Benefit on 16 February 2012, in which he stated:

"About 13 years ago I was complaining about my breathing. I had an x-ray and then a lump was found and I had a biopsy but was told it was fine. My chest was getting worse and I had an x-ray last year and in January 2011 I went into Morriston and they tried to take a lump again. I've had scans and I've been told I have pleural thickening."

The implication there is that the Claimant's problems with his breathing and chest pains, since about 2000, were caused by his exposure to asbestos in the course of his work – an unsurprising suggestion by the Claimant, given that he has always believed that they were. That claim was rejected on 15 May 2012, on the basis that the Claimant does not suffer (and has never suffered) from Prescribed Disease D9 (pleural thickening, as defined for the purposes of the benefit), a decision confirmed on appeal to the First-tier Tribunal (Social Entitlement Chamber) on 28 November 2012.

37. In respect of the Claimant's current condition, Dr Sinclair and Dr Moore-Gillon were all but agreed. Their joint memorandum dated 20 February 2015 stated as follows:

"(1) Mr Summers has pleural plaques, the appearances of which are typical of those due to asbestos exposure.

(2) Responsibility for causation of his asbestos-related pleural plaques may be apportioned between those periods of employment in which there was asbestos exposure according to the proportion which each contributed to the totality of his asbestos exposure.

(3) Pleural plaques are usually regarded as not causing respiratory disability whilst asbestos-related diffuse pleural thickening is generally regarded as being capable of causing disability. There appears to be some debate in the case of Mr Summers as to whether he has diffuse pleural thickening and, indeed, we note that he has been turned down in his application for Industrial Injuries Disablement Benefit for that condition.

We state that it is well recognised that pleural plaques may rarely – if sufficiently extensive and confluent – give rise to disability.

In the particular case of Mr Summers we believe that whatever the label applied to his pleural condition we consider that it has both been caused by asbestos and is giving rise to disability. We consider that he should be eligible for Industrial Injuries Disablement Benefit.

(4) Mr Summers does not have asbestosis, i.e. he does not have diffuse interstitial pulmonary fibrosis caused by exposure to asbestos.

(5) Mr Summers has chronic obstructive pulmonary disease, including in particular emphysema and small airways disease. We attribute this to smoking and not to asbestos exposure.

(6) …

(7) We estimate Mr Summers' overall cardiorespiratory disability at around 50%. Contributing to this are his asbestos-related pleural condition, COPD, obesity and general physical deconditioning.

(8) Of this 50%, Dr Moore-Gillon considers that 20% (i.e. two fifths of the total) is due to the consequences of asbestos exposure, while Dr Sinclair estimates this proportion at 30%.

(9) …".

For the purposes of this trial, the minor disagreement between the experts in paragraph (8) is immaterial. I shall proceed on the basis that about half of the Claimant's respiratory symptoms is due to asbestos-related disease, and half due to other causes.

The Date of Knowledge: Discussion and Conclusion

38. On the basis of the evidence, Mr Phillips conceded – rightly – that he must accept that, from late 2000, the Claimant considered that exposure to asbestos whilst he worked at the Council's premises as a boilerman at least materially contributed to the breathlessness and chest pains from which he suffered at that time and since. However, I could not properly conclude that he had the requisite knowledge for the purposes of sections 11 and 14 of the Limitation Act 1980 until he was told in February 2012 that he suffered from "diffuse pleural thickening". Whatever the Claimant thought, he submitted there is no evidence that he suffered from anything more than symptomless pleural plaques in 2000 – or, indeed, at any time before 2011-2. The Claimant's belief that he was suffering from symptoms of breathlessness and chest pain as a result of an asbestos-related condition from 2000 was simply wrong. The symptoms from which he suffered in 2000 arose from other causes, notably his smoking.
39. That was a bold submission, ably put – but I am unpersuaded by it. In my judgment, the Claimant suffered from a symptomatic asbestos-related condition from 2000 – that is when his cause of action arose – and he first had knowledge that his injury was significant then. Consequently, the limitation period applicable under section 11(4) expired well before 2011.
40. In coming to that conclusion, I have particularly taken into account the following.

i) In respect of the facts about a prospective claim of which an individual must have knowledge under section 14(1), in 2000 the Claimant knew that he had been injured, in the sense that he had suffered pleural abnormalities; and that that injury was attributable to exposure to asbestos dust whilst in the employ of the Council and as a result of its act or omission. It is therefore not in dispute that the Claimant had knowledge of all relevant facts, except (the Claimant contends) knowledge that his injury was "significant".

ii) I respectfully agree with the joint memorandum of the experts which concluded that it would be an arid exercise to attempt to categorise the Claimant's condition as "pleural plaques" or "diffuse pleural thickening". Whatever label might be attached to the condition, as an injury it would be "significant" if it was (or as soon as it became) symptomatic (i.e. there were more than very minor symptoms) and would not be "significant" if it were asymptomatic.

iii) The use of medical terms in this area has changed, and become more specific, over time. In this case, the terms used by the medics contemporaneously are inconsistent and of limited value in determining whether they considered the asbestos-related condition to be symptomatic. After the 22 November 2000 consultation, Dr Jones used both of the terms "large area of pleural thickening" (letter to Dr Cooke of 24 November 2000) "sharply defined… large innocent pleural plaque" (letter to Dr Cooke of 6 December 2000). Even as late as the January 2012 MDT, the condition was talked of in terms of "pleural plaques only…"; although, by then, of course it was understood that the Claimant's symptoms arose from something more than simple, asymptomatic pleural plaques. The position is made more complicated by the following:

a) From a clinical point of view whether a patient is suffering from pleural plaques or diffuse pleural thickening is of limited value, because neither is treatable. What matters from a clinical point of view is whether the condition is malignant (cancerous) or benign (non-cancerous). Thus, in 2012, once the Claimant's condition was confirmed as being benign, the hospital simply discharged him – although giving him advice as to how he might pursue a claim for the symptoms that they considered resulted from the condition. "Simple" pleural plaques may therefore be used, not to differentiate the condition from diffuse pleural plaques, but rather from a malign condition.

b) Until Rothwell in 2006, asbestos-related conditions were thought to be actionable whether symptomatic or not.

c) Pleural plaques can, occasionally, be symptomatic.

iv) I accept that the medical records do not point consistently one way: for example, there is reference in the Dr Jones' 6 December 2000 letter to the lesions being "sharply defined", and the consultant in 2003 reported to the Claimant's GP that he thought the symptoms of chronic breathlessness appeared to be related to his heavy smoking. Nevertheless, the contemporaneous medical records from 2000 regularly refer to something more than "pleural plaques"; and they suggest that the clinicians considered that, whilst the pleural condition was benign, there was something more than straightforward pleural plaques present. This makes it more likely that the pleural condition was symptomatic.

v) Although parts of the expert evidence suggest the Claimant might be regarded as suffering from two conditions – asymptomatic pleural plaques and symptomatic diffuse pleural thickening – their joint memorandum appears to postulate a single condition of uncertain label. The contemporaneous medical records do not suggest more than one condition. Although the thickened area of the pleura may have altered over time – for example, by engaging more with the underlying morphological structures – the physiology appears to have changed little in nature. The Claimant was told of "Christmas tree-like" projections from the "lump" at a very early stage. Furthermore, although the frequency and severity of the breathlessness and chest pains has increased over time, the nature and type of symptoms was described by the Claimant in consistent terms over the whole period. The Claimant's condition is best considered as a single progressing condition, rather than one (symptomless) condition being overlain by a second (symptomatic) condition.

vi) In their joint memorandum, the experts do not deal with the question as to when the asbestos-related condition became symptomatic. However, in paragraph 9.10 of his report dated 17 February 2013, Dr Sinclair says;

"There is evidence of progression of Mr Summers' diffuse pleural thickening, as demonstrated by him having a forced vital capacity of 2.95l in 2007, which by 2012 had reduced to 2.46, a reduction of approximately 500ml whilst forced expiratory volume in 1 second has reduced from 1.97l to 1.76l. The greater reduction in forced vital capacity confirms progression of diffuse pleural thickening as opposed to COPD…".

That suggests that Dr Sinclair is of the view that the Claimant first suffered from diffuse pleural thickening by 2007 at the latest. Dr Moore-Gillon, on page 16 of his report dated 20 February 2015, did consider the onset of symptoms:

"Dating the onset of disability due to asbestos-related problems (and their associated parenchymal lung changes) is very difficult…. My general feeling is that the asbestos-related pleural change has probably progressed only extremely slowly if at all and that Mr Summers became aware of progressively worsening symptoms because of progression of his airways disease with continued smoking."

That is far from a firm or confident view. However, the experts are agreed that the Claimant has parallel conditions involving his chest, those involving the pleura being asbestos-related and others not being caused by exposure to asbestos but rather tobacco smoke. It is common ground between the experts that the latter has progressed (and continues to progress) more quickly than the former. Dr Moore-Gillon appears to suggest the early respiratory symptoms suffered by the Claimant were a result of his asbestos-related disease, and his COPD has been responsible for a higher proportion of the more recent symptoms.

vii) Although an increase in the Claimant's asbestos-related chest symptoms has been masked by an even greater increase in COPD-derived chest symptoms, the symptoms from which he was suffering in 2000 are characteristic of pleural thickening, they have not changed in their essential nature, and one characteristic of pleural thickening is that it is progressive.

viii) The Claimant's own evidence is also noteworthy. As I have described, although he thought that his heavy smoking may have contributed, he considered that, from 2000, his breathlessness and chest pains were due to the asbestos-related changes to his pleura. I accept that there is no direct evidence from the Claimant, or anyone else, to the effect that he was told by the medics in 2000 that his asbestos-related condition was symptomatic – and I have explained why that may not have been at the forefront of their minds – but it is clear that, after his various consultations, the Claimant was left with the impression that his breathlessness and chest pains did derive from his pleural condition. Of course, in 2000-1 it would have been thought open to him to pursue a claim for his pleural condition even if it were symptomless. However, he said that he did not pursue a claim (and did not attend chest clinic appointments) after the negative biopsy in 2001, not because he thought that he had no asbestos-related symptoms, but because those symptoms he believed were asbestos-related did not bother him and he did not consider those symptoms (although worsening) were sufficiently debilitating to make pursuit of a claim worthwhile.

ix) In my judgment, on all the evidence, it is therefore far more likely that some of the Claimant's breathlessness and chest pains in 2000 were caused by his pleural condition; and the Claimant's understanding then that they were so caused was true.

Conclusion

41. I therefore conclude that the Claimant's date of knowledge for the purposes of sections 11 and 14 of the Limitation Act 1980 was well before 18 August 2011.
42. This claim thus fails; and I shall direct judgment be entered for the Defendant.