Professor Carl Heneghan (Son and Administrator of the Estate of James Leo Heneghan, Deceased) v Manchester Dry Docks Ltd and Others
| Jurisdiction | England & Wales |
| Judge | Mr Justice Jay |
| Judgment Date | 11 December 2014 |
| Neutral Citation | [2014] EWHC 4190 (QB) |
| Docket Number | Case No: HQ12X03121 |
| Court | Queen's Bench Division |
| Date | 11 December 2014 |
[2014] EWHC 4190 (QB)
IN THE HIGH COURT OF JUSTICE
QUEEN'S BENCH DIVISION
Royal Courts of Justice
Strand, London, WC2A 2LL
Mr Justice Jay
Case No: HQ12X03121
David Allan QC and Simon Kilvington (instructed by Pannone Part of Slater & Gordon) for the Claimant
David Platt QC (instructed by Berrymans Lace Mawer LLP) for the Defendants
Hearing dates: 25 th and 26 th November 2014
Approved Judgment
I direct that pursuant to CPR PD 39A para 6.1 no official shorthand note shall be taken of this Judgment and that copies of this version as handed down may be treated as authentic.
Introduction
Mr James Heneghan was born on 8 th March 1938. During the course of his working life, he was exposed to respirable asbestos fibres and dust. In November 2011 Mr Heneghan began to develop symptoms of adenocarcinoma of the lung, and a diagnosis to that effect was made in early 2012. He died from the disease on 3 rd January 2013.
The deceased was employed by the six Defendants on a sequential basis between 1961 and 1974. There were earlier employers who have not been sued. Owing to the lack of available records, the precise dates of his various employments are unclear, but the parties are agreed that the deceased's exposure to asbestos over the course of his working life can be quantified, and that the total exposed "share" of those Defendants who have been sued is 35.2%. As between the six Defendants, the distribution of their respective exposures has also been agreed, and ranges from 2.5% to 10.1%.
Consequent upon the deceased's death, claims have been brought in the usual way under the Law Reform (Miscellaneous Provisions) Act 1934 and the Fatal Accidents Act 1976. The Claimant, Carl Heneghan, is the son of the deceased and, I note, Professor of Evidence-Based Medicine at the Department of Primary Care Health Sciences at the University of Oxford. Unfortunately, the deceased's widow, Mrs Doreen Heneghan, is not in good health.
Liability has been admitted by all six Defendants, and Judgment was therefore entered against them on 21 st December 2012 (Order not sealed until 14 th January 2013). On that occasion, Master McCloud ordered the trial of three issues. Given that the issues of contributory negligence through smoking, and quantum, have now fallen away, the sole live issue for this Court to determine is "whether each Defendant is liable for damages in full or for only a portion of the damages". If the Claimant's case is right, it is common ground that he should receive the sum of £175,000, being the damages in full figure contemplated in the Master's Order; but if the Defendants' arguments prevail, it is equally not in dispute between the parties that the Claimant should receive £61,600, based on the total "exposed" share of 35.2% of the gross sum.
One might be forgiven for thinking that the answer to this issue ought to be found in previous authority, because it must have arisen in the past. As it happens, this issue has not been previously determined. In these circumstances, the present case gives rise to problems of some difficulty and importance.
The nature of the agreement of the parties means that lay witness evidence is not required. The expert engineering evidence is agreed, but needs to be summarised in order that the issue in contest may be properly understood. The medical evidence is largely agreed, save for two points which I will need to examine.
The Engineering Evidence
In his detailed and helpful report dated 16 th May 2012, Mr John Raper has considered the deceased's levels of exposure to asbestos fibres referable to his employment with ten employers over many years. Mr Raper has examined the deceased's work history and the various tasks undertaken over time, from which data he has been able to draw reasonably solid inferences of the likely levels of asbestos exposure. The deceased's aggregate asbestos dose was of the order of 133 fibres/ml years. The six Defendants' cumulative exposure was 46.9 f/ml years, and the exposure attributable to the employers who have not been sued was 86.2 f/ml years, yielding an apportionment division of 35.2%.
Mr Raper has also been able to analyse the deceased's exposure on a Defendant-specific basis. This analysis has produced doses or exposures ranging between 13.4 f/ml years (for the Third Defendant), in other words 10.1% of the total exposure, and 3.3 f/ml years (for the Fourth Defendant), in other words 2.5% of the total exposure.
The significance of these figures may be properly discerned when consideration is given to the Helsinki criteria, formulated by an international panel of experts in 1997. According to a strict application of these criteria, cumulative exposure of 25 f/ml years is sufficient to enable an inference properly to be drawn that lung cancer in any individual case is attributable to asbestos, provided that there is a minimum ten year interval from first exposure to onset of the cancer.
These criteria have been refined over the years. The 25 f/ml year criterion remains appropriate for exposure to mixed fibre types with a preponderance of amphiboles. If exposure involved equal quantities of amphiboles and chrysotile, then cumulative exposure of 40 f/ml is probably necessary to double the risk of lung cancer. And the exposure threshold is much higher in a case of exposure to commercial chrysotile only.
Given that the deceased's exposure of 133.1 f/ml years included 114 f/ml years of amphibole, the relevant threshold applicable to his case is likely to be below the figure of 40 f/ml years mentioned above. The parties have been content to proceed on the agreed basis of a more than fivefold increase of the risk of lung cancer in the instant case – taking the cumulative exposure to asbestos fibres over the whole of the deceased's employments.
The Medical Evidence
Dr Robin Rudd (for the Claimant) and Dr John Moore-Gillon (for the Defendants) gave oral evidence in line with their reports. Each is pre-eminent in his field, and intellectually formidable. Both amplified slightly on their reports, and following their respective cross examinations it became quite clear where the slight differences between them lay.
I begin with the common ground.
The deceased's lifetime risk of developing lung cancer had he (a) not smoked and (b) not been exposed to asbestos fibres, would have been in the order of 0.5%. His smoking increased the risk to 2% or thereabouts: in other words, it increased the baseline risk by a multiple of four. Dr Rudd explained in his first report that the effects of smoking and asbestos exposure were not merely synergistic but multiplicative. In short, given the fourfold and fivefold increases in risk which I have mentioned, the risk of this deceased developing lung cancer was more than twenty times the baseline risk. Put another way, given that the deceased was a smoker, the risk of his developing lung cancer at these levels of asbestos exposure were more than five times greater than they would have been had he just been a smoker. Dr Moore-Gillon did not disagree with the multiplicative approach or these figures.
On 12 th November 2013 the medical experts produced a Joint Statement to the Court, points 2, 3 and 5 of which are relevant for present purposes:
"2. His risk of lung cancer was increased by smoking and by asbestos exposure.
3. On the balance of probabilities he would not have developed the lung cancer if he had not been exposed to asbestos.
…
5. The risk that lung cancer will develop increases with the amount smoked and with the dose of asbestos received. If a lung cancer does develop, then the duration and severity of symptoms and the eventual outcome are not affected by the amounts of smoking or asbestos exposure which led to that increase in risk."
The medical experts are also agreed about the multiple mechanisms involved in the carcinogenesis of asbestos-related lung cancer. This involves a consideration of the microbiological processes occurring in cells, in particular cellular DNA, of the inhibitive effect asbestos has on programmed cell death, and of the reduction in the effectiveness of the body's natural defences against cancer caused by the presence of asbestos fibres in lung tissue. The precise detail does not matter for present purposes; it is sufficient to record that the experts are in general agreement that anything between four and seven stages in cellular mutation is required before the emergence of a cancer cell which may potentially progress to become a clinically apparent carcinoma of the lung.
The differences between the experts, such as they are, emerge from comparing the Appendix to Dr Moore-Gillon's report dated 22 nd January 2013 with Dr Rudd's report dated 22 nd May 2014. Mr David Platt QC made the forensic point that Dr Rudd should have drawn attention to these differences in the Joint Statement because the obligation under the CPR is to identify both the areas of agreement and disagreement. Although I agree with Mr Platt that it would have been more helpful had Dr Rudd raised the issue at that juncture, I have to say that in the end nothing really turns on this.
These conclusions in Dr Moore-Gillon's Appendix are not shared by Dr Rudd, and so I set them out in full:
"My view though is that whilst it is not possible to infer a causal connection between all inhaled (and retained) asbestos and the development of lung cancer, it is perfectly reasonable to consider its role in...
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