Kearns v Delta Steeplejacks Ltd

This action arises out of the employment of Mr David Kearns by Delta Steeplejacks Limited (“Delta”) for a periods totalling about seven or eight years between 1981/82 and 1990/91. He worked as a steeplejack. During those times he worked on various chimneys, power station cooling towers, power station buildings, flare stacks and on an asbestos roof. The action was also brought against another of Mr Kearns’ employers but was discontinued before trial.

Mr Kearns gave evidence at trial of the circumstances of his exposure to asbestos in each situation. Whilst working on chimneys he was exposed to asbestos blankets used between courses of brickwork and asbestos rope used in the maintenance of chimney caps. Whilst working on cooling towers he cleaned and replaced asbestos eliminator slats and asbestos distribution pipes. Whilst working on power station windows he worked on the removal and replacement of windows which involved removing and replacing asbestos caulking. Whilst working on flare stacks he removed asbestos gaskets at the top of the stacks. He had cleaned an asbestos roof with a jet spray.

Mr Bird, managing director of Delta, conceded in evidence that Mr Kearns had been exposed to asbestos, having maintained in his witness statement that the level of exposure had been exaggerated.

Each party instructed engineering experts, respectively, Mr Glendenning and Mr Stear, who produced lengthy reports on exposure to asbestos, together with supporting documentation. They also prepared a joint statement, which focussed on the main issues in the case. It was agreed that it was not necessary for them to attend to give evidence as the issue of whether Mr Kearns was exposed to asbestos was a question of fact.

The primary duty under the Control of Asbestos at Work Regulations 1987 was to prevent exposure (Reg 8(1)(a)). If prevention was not reasonably practicable, the employer was required to reduce exposure to the lowest level reasonably practicable (Reg 8(1)(b)) and in any event below prevailing standards. Where it was not possible to reduce exposure below prevailing standards, the employer was required to provide respiratory protective equipment (Reg 8(2)).

The engineering experts agree that in relation to the work activities described by Mr Kearns, Delta should have prevented or minimised his exposure to asbestos. They also agreed that in accordance with the relevant HSE Guidance Note EH 10 Mr Kearns’s exposure should not have exceeded the relevant control limits for occupational exposure to asbestos unless he was wearing appropriate respiratory protection.

Ms Adams QC conceded, at the conclusion of Mr Bird’s evidence, that Delta was in breach of its duty to prevent Mr Kearns’s exposure to asbestos dust as far as reasonably practicable or to reduce such exposure to the lowest level reasonably practicable, as required under the Control of Asbestos Regulations 1969 and the Control of Asbestos at Work Regulations 1987. Ms Adams QC accepted that there was insufficient evidence of effective precautions being taken by Delta.

I have heard no evidence in relation to the other employer, albeit the trial bundle contains a witness statement from Mr Kearns’s other employer and his exposure to asbestos during that period is considered in the experts’ reports.

The experts agreed that in the event that Mr Kearns’ evidence was accepted then he was routinely and extensively exposed to asbestos dust, whilst he was employed by Delta. They also agreed that in those circumstances the exposure dose is likely to have been very high. Mr Glendenning considered that if Delta’s evidence was accepted, then on the basis of Mr Bird’s evidence, the exposure was lower than that suggested by Mr Kearns, but the extent to which it was lower cannot be quantified. Mr Stear considered that, particularly, if asbestos blankets were not disturbed the exposure would probably have been low and/or as low as reasonably practicable if precautions were taken. As I have said they agreed that if the other employer’s evidence was accepted the exposure with that employer would have been nil.

Having considered Mr Kearns’ and Mr Bird’s evidence, both written and oral, and the documents in the case, I am satisfied that Mr Kearns was doing his best to assist the court with his recollection of his exposure to asbestos whilst he was employed by Delta. Mr Bird’s evidence, as recognized by Ms Adams QC, does not dissuade me from that course. I was impressed by Mr Kearns’ description of working with the asbestos blankets whilst he was employed by Delta, which Mr Stear concedes is of relevance to the exposure dose. The engineering experts are agreed that, if Mr Kearns’ evidence is accepted, then his exposure to asbestos, whilst working for Delta, was very high. This would equate on Mr Glendenning’s analysis to 30 fibre ml/years, as opposed to Mr Stear’s analysis in his report of 5.2 fibre ml/year. Allowing for some limited inaccuracy of recollection over years, I would assess Mr Kearns’ exposure at 25 fibre ml/year or more.

Mr. Bowley, in opening the case for the Mr Kearns, accepted that the apportionment exercise would have to be carried out even though Mr Kearns had discontinued the claim against the other employer. He accepted in opening that, simply because Mr Kearns had made the decision to discontinue that part of the claim, it did not mean he could avoid the effects of apportionment when the Court came to consider it for the purposes of any judgment against Delta.

The experts prepared calculations in the reports on apportionment based upon a dose based assessment, and in Mr Glendenning’s case also a time based assessment by reference to the period of time Mr Kearns was employed by each employer, 7 years with Delta and 11 years with the other employer. Both experts recognise the imprecision of a dose based assessment, however, Mr Glendenning prefers a time based assessment whereas Mr Stear prefers a dose based assessment. The experts agreed an apportionment of respectively 14% or 17% for Delta, based upon their assessments of exposure, and of 39% for Delta based upon time exposure.

Mr Bowley submits that time exposure is a broad-brush approach often used in disease claims involving divisible injury (including divisible asbestos related injury such as pleural thickening) where exposure with different employers is likely to have been broadly similar and/or the evidence of exposure is such that precise calculations of dose and apportionment are impossible. Ms Adams QC takes a contrary view and, in written submissions, refers me to Holtby v Brigham & Cowan (Hull) Limited [200] 3 All ER 421, particularly at paragraphs 20, 21 and 37. She submits that whilst it may be sensible to utilise a time exposed basis when there is insufficient evidence to do otherwise, the dose relationship is the most appropriate way of addressing an exercise “shot through with imprecision” where it is available.

Although I have accepted Mr Kearns’ evidence on the scale of his exposure to asbestos whilst he was working for Delta, I am not in a position to make findings as to his exposure whilst he was working with his other employer. His evidence on this period was not challenged in cross-examination and I did not hear evidence from his other employers. It seems to me that in the absence of any findings on the factual evidence relating to the other employer, I should accept Mr Bowley’s submissions and adopt the alternative conclusion in the experts’ joint statement that the apportionment should be based on time exposure of 39%, upon which both experts are agreed. I also accept Mr Glendenning’s evidence concerning the imprecision of a dose based assessment.

The main issue that I have to decide is one of medical causation, whether (i) Mr Kearns suffered from bilateral diffuse pleural thickening, and, if he did so, whether it was caused by his exposure to asbestos or from other causes. There are two discrete aspects to the case on causation, first the damage to the right lung and second to the left lung. I have heard evidence from two chest physicians, Professor Jacob, who was originally Mr Kearns’ treating physician, and Dr Hind, on behalf of Delta. The radiography was available in court and they both gave evidence by reference to the images that were available.

Mr Kearns was born on 10^th November 1953. He started smoking at age 16 or 17. He smoked on and off until 2012. He started suffering shortness of breath in 2007, especially whilst climbing hills and on exertion. He was diagnosed as having cigarette induced COPD and uses inhalers. He is slow in the mornings getting going. His exercise tolerance is restricted to 20-30 metres up hills and 50-100 metres on the flat. He is unable to carry out any DIY, decorating, gardening or maintenance work. He was admitted to hospital in 2008 with an exacerbation of COPD. He has developed bilateral asbestos related pleural plaques. He has also developed diffuse pleural thickening in the right lung with blunting of the right costophrenic angle. There are no features to indicate any other asbestos related disorder or lung cancer. He has a respiratory disability of 60%, predominantly as a consequence of his COPD, 40%, and diffuse pleural thickening, 20%. His life expectancy is reduced by nine years by his COPD.

Mr Kearns had a fall in October 1999, damaging his cervical spine and lower lumbar spine L5/6 with fractured ribs whilst working. He underwent a right VAT evacuation with videoscopic thoracoscopy of a right sided haematoma. Two litres of blood were evacuated. He continued to receive treatment for right rib cage pain. He developed intermittent sharp chest pain on the right inter costal arch when he moved or bent forwards. He was admitted to hospital where diffuse pleural thickening was diagnosed. He was subsequently admitted for a ninth rib resection following which he developed a painful intermittent swelling beneath the right coastal margin.

Professor Jacob considers that Mr Kearns is suffering from bilateral pleural plaque disease and bilateral extensive diffuse pleural thickening. He believes that the diffuse pleural thickening in the right lung is caused by exposure to asbestos. Dr Hind believes that it developed as a result of the operation Mr Kearns underwent on 2^nd November 1999 for the evacuation of a haemothorax, following the fall in which he had fractured his ribs.

Professor Jacob disagrees with Dr Hind’s opinion and relies upon the sequence of x-rays after the operation which showed clearance. He maintains that if the clot had been retained it would have calcified, generating inflammatory reaction. When Mr Kearns saw Mr Barnard on 21^st December 1999 there was no indication of ongoing pathology in the pleura. The consultations and reports on the x-rays in 2001 make no reference to the pleural area. The report on the x-ray of 2^nd November 2001 recorded heart and lungs as normal. On 7^th January 2002 Mr Kearns underwent surgery to remove his ninth rib which was external to the chest wall. By 31^st January 2003 the chest x-ray had identified “right pleural effusion which would do for a haemothorax”. Professor Jacob accepted in cross-examination that it was not possible to tell from the x-ray whether the fluid was blood or not. He does not believe that the radiography report is correct. He believes that it was a new phenomenon where Mr Kearns was developing an infection or inflammation on the right lung.

The MRI scan of 5^th September 2003 did not comment on the pleura at all. The chest x-ray of 1^st September 2004 said “COPD but otherwise clear”. Professor Jacob considers that that an x-ray five years after the fall would have shown a retained clot, it would not have gone away but just got bigger and calcified. By 10^th May 2008 an x-ray recorded pleural based calcification on the right and diaphragmatic pleural plaques was noted. Dr Elliot’s x-ray on 10^th January 2013 showed blunting of the right costophrenic angle, which was unchanged in appearance from 2008. Professor Jacob also relies on the CT thorax scan from 10^th March 2013, which showed bilateral calcified pleural plaque disease in keeping with asbestos exposure, “sufficient to diagnose pleural thickening”. Professor Jacob considers that there was huge calcification on the diaphragm, which is away from the base where the haematoma occurred in the upper lobe. As to Mr Kearns’s right lung his view is that the change is only explained by exposure to asbestos.

Dr Hind agrees that Mr Kearns developed evidence of diffuse pleural thickening in the right lung, which he based on the various interpretations of his recent chest x-rays, with resultant blunting of the right costophrenic angle. He considers that this dates back to his traumatic chest wall injury in 1999, when he fractured several ribs on the right side. He draws attention to the fact that those fractures were complicated by haemothorax which required evacuation with a videoscopic thoracoscopy. Subsequently he underwent resection of his right ninth rib, following non-union. Thereafter he maintains that all of the chest x-rays have been reported as showing a continuing abnormality within the right lower chest, indicative of diffuse pleural thickening. Dr Hind’s opinion is that all changes in Mr Kearns’ right lung followed his fall in 1999, which he described as “a dreadful fall” where he bled two litres of blood into the pleural space.

Dr Hind explained that the parietal pleura is stuck to the inside of the rib cage and the visceral pleura is the inner tube. There is a space between the two pleuras where there is slight lubrication. In his view both the visceral and parietal pleura have become fibrosed as a result of the haemothorax, stopping the diaphragm moving. The parietal pleura goes down the side of the ribs over the dome of the diaphragm before joining the visceral pleura. The diaphragm is controlled by the frenetic nerve that instructs it to contract. The fibrosis is at the point where the blood has sunk which is very irritating. The blood was in the space between the parietal and visceral pleura. There was a chemical reaction followed by an inflammation, which caused the pleura to thicken and fuse together.

Professor Jacob considers that the CT scan of 6^th November 2013 showed a small patch of inflammatory change in the left lower lobe base, which was a progression of pleural disease. The report on the x-ray from Dr Barlow on 5^th April 2014 recorded bilateral calcified pleural plaques in keeping with asbestos related pleural disease. In the joint statement he said that the x-ray shows blunting of the left costophrenic angle, which he modified in his oral evidence. Professor Jacob also considers that there was pleural thickening at the base of the left lung where he describes atelectatic or parenchymal bands, and an area of rounded atelectasis higher up the lung. He describes it as a feature of visceral pleural thickening not pleural plaque. He agrees that the rounded atelectasis would have to be near the area of pleural thickening. He describes pleural thickening on the left side with atelectasis calcification and two layers of pleura compacted together, with strands of coming out which he described as crow’s feet.

Dr Hind’s evidence is that Mr Kearns’ costophrenic angle was not obscured on his left lung, however, on the right lung the diaphragm is slightly higher with blunting. His view is that there is evidence of focal visceral pleural thickening, affecting the parietal and visceral pleura. The fluid effusion is as a result of asbestos exposure that settles in the pleural space. The fluid is irritating causing inflammation of the parietal and visceral pleura. As the fluid is absorbed it leaves behind thickening and scarring. The fluid is a known consequence of asbestos. The asbestos fibres inhaled find their way into the visceral pleura, causing it to weep fluid on the outside. The fluid falls into the costophrenic angle acting like a gutter.

Dr Hind considers that there is insufficient evidence of diffuse asbestos related pleural thickening. He considers that the CT scan on 5^th March 2013 shows extensive clearly defined bilateral and heavily calcified pleural plaques, at most they are 8mm thick around the chest wall. On the left there are a few parenchymal bands related to the extensive diaphragmatic plaques extending from the anterolateral pleural plaques and from the left diaphragm. One is crossing from the left diaphragm to the costophrenic angle, the bands indicating involvement with the visceral pleura. The pleural plaque extends over 7 x 8 cm without involvement of the costophrenic angle. Dr Hind does not consider that the pleural plaques meet the size criteria for the definition of diffuse pleural thickening. He does not consider that they are interfering with the function of the left diaphragm. He disagrees that the April 2014 x-ray shows blunting of the left costophrenic angle such as occurs in diffuse asbestos related pleural thickening.

Both experts agree that part of the difficulty as regards the cause of Mr Kearns’s diffuse pleural thickening is that neither of them have seen the radiography dating back to the late 1990s.

The oral expert evidence has gone far beyond the content of the experts’ medical reports in establishing causation. I have found the demonstration of the radiology by both experts during their course of the evidence to be helpful in explaining, as well as exploring, difficult issues on causation. The conclusions which I have reached are as follows.

As to the right lung, both experts are agreed that there is evidence of diffuse pleural thickening, they disagree as to the causation. I am satisfied that the diffuse pleural thickening in the right lung was caused by asbestos exposure. The evidence from Mr Kearns, ultimately accepted if not wholly by Ms Adams QC, was that he had been exposed to high levels of asbestos during the period of time that he had worked for Delta. Whilst Dr Hind legitimately explored the hypothesis that the admitted diffuse pleural thickening was caused by the fall Mr Kearns sustained in October 1999, I am not satisfied that he has made his argument out. Although the earlier radiography is not available, I accept Professor Jacob’s evidence that the consultation records and radiology reports in the period of time after the fall (except for the x-ray report in 2003) are inconsistent with there being sequelae following the evacuation of the blood from Mr Kearns’ lungs. In reaching this conclusion I place emphasis on Professor Jacob’s evidence that the clot would not have gone away and would have calcified, causing inflammatory changes. Accordingly I am satisfied that diffuse pleural thickening present on the right side is due to exposure to asbestos and not to trauma in October 1999.

As to the left lung the position is somewhat different, in that there is a dispute between the two experts as to the presence of diffuse pleural thickening. It is agreed that there are pleural plaques in the left lung. I have had the opportunity of listening to Professor Jacob seek to explain, by reference to the radiography, where he considers that there was diffuse pleural thickening in the left lung, largely by reference to the presence of atelectatic bands. I am not satisfied that he has established that there was diffuse pleural thickening either by reference to the ateletic bands or the size of the area required. I am also satisfied that Professor Jacob modified his position on the costophrenic angle being obscured, accepting in oral evidence that the radiological evidence did not show it to be so. On this issue I prefer the evidence of Dr Hind that, whilst there is evidence of pleural plaques, there is insufficient evidence of diffuse pleural thickening. Accordingly I am not satisfied that the changes on the left side amount to diffuse pleural thickening nor do I consider that the changes on the left side amount to actionable injury, in other words that they amount to an injury which is more than de-minimis.

The experts are agreed that Mr Kearns has a respiratory disability of 60%, which is probably a consequence of cigarette-induced COPD of 40% with the remaining 20% as either asbestos related or due to post traumatic thickening of the right lung. Dr Hind considers that the chances of asbestos-related pleural plaques progressing in the future is 10-20% and will most probably never result in any respiratory disability, for example, breathlessness or chest pain. Dr Hind considers that his chances of developing diffuse asbestos-related pleural thickening are in the order of 1% and malignant mesothelioma 3%.

In these circumstances I am asked to assess general damages for pain, suffering and loss of amenity on a provisional basis, based upon Mr Kearns’ respiratory disability attributable to the diffuse pleural thickening of his right lung caused, as I have found, by his exposure to asbestos. The Judicial College Guidelines (13^th Ed.) recommends a bracket of £29,900 to £80,4500 in respect of:

“(c)

Asbestosis and pleural thickening—where the level of disability attributable to asbestos will be in excess of 10% causing progressive symptoms of breathlessness by reducing lung function. Awards at the lower end of the bracket will be applicable where the condition is relatively static. Higher awards will be applicable where the condition has progressed or is likely to progress to cause more severe breathlessness. Awards at the top end of the bracket will be applicable where mobility and quality of life has or is likely to become significantly impaired and/or life expectancy significantly reduced. This is a wide bracket and the extent of respiratory disability will be highly significant with disabilities of 10-30% being at the lower end, 30-50% in the middle and in excess of 50% at the higher end.”

Based upon a 20% respiratory disability due to asbestos, I accept Mr Bowley’s submission that general damages for pain, suffering and loss of amenity, on a provisional basis, should be assessed at £40,000. I also award special damages of £300. To this figure it is accepted by both parties that I must apply a reduction to reflect the apportionment between Mr Kearns’ two employers, referred to in paragraph 14 above. Accordingly I reduce the figure of £40,300 by 39%, making a total award of general damages for pain, suffering and loss of amenity of £15,717.

In view of my findings I consider that this a case in which an award of provisional damages shall apply.

It is agreed by the parties that the risk conditions shall be as follows: (a) mesothelioma, (b) progression of diffuse pleural thickening due to asbestos causing a significant increase in respiratory disability, (c) asbestosis, and (d) lung cancer caused by asbestos. It is also agreed that the period during which Mr Kearns, or his estate or dependants, shall be entitled to apply for further damages in the event that any (a) to (d) are alleged to have developed, is during the life of Mr Kearns and/or within 3 years after the date of his death. I direct that copies of the statement of case, pleadings, Mr Kearns’s witness statements, the medical reports and joint statement of Professor Jacob and Dr Hind, and a copy of this judgment shall be preserved and filed with the case file.