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	England and Wales High Court (Queen's Bench Division) Decisions
You are here: BAILII >> Databases >> England and Wales High Court (Queen's Bench Division) Decisions >> Griffiths & Ors v British Coal Corp & Anor (Summary) [1998] EWHC 2008 (QB) (23 January 1998) URL: http://www.bailii.org/ew/cases/EWHC/QB/1998/2008.html Cite as: [1998] EWHC 2008 (QB)

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		BAILII Citation Number: [1998] EWHC 2008 (QB)

IN THE HIGH COURT OF JUSTICE
QUEEN'S BENCH DIVISION


		Cardiff High Court
		23rd January 1998

B e f o r e :

THE HONOURABLE MR JUSTICE TURNER
____________________

Between:


	Griffiths and others
	- and -
	British Coal Corporation and another

____________________

Issue 2
____________________

HTML VERSION OF JUDGMENT
____________________

Crown Copyright ©


 


MR JUSTICE TURNER:

This summary is to be read as being consistent with the main judgment: to which reference should be made in any instance where the evidential basis or forensic interpretation is/are in doubt.

Introduction

The eight cases which are now before the court represent the tip of an iceberg. When appointed as the judge to try a number of actions which were proceeding in High Court District Registries and County Courts in many different parts of England and Wales there were already over one hundred such actions in being, while a further six thousand or so other actions had been threatened or notified to the defendants. The decision was taken to try a limited number of the actions through to judgment with the objective of raising, within those actions the greatest number of issues in regard to liability and medical complaints that could be conveniently accommodated within a reasonable trial schedule. In the event these eight 'lead actions' were selected by the parties themselves.

The injuries in respect of which the plaintiffs all seek compensation are to the respiratory system. They are said to have resulted from exposure to mine dust in the course of employment by the former National Coal Board (NCB) which, since the 5^th March 1987 and pursuant to the provisions of the Coal Industry Act 1987, has been known as the British Coal Corporation. For ease and consistency of reference the defendants will be referred to throughout this judgment as 'British Coal'. The periods over which the claims arise go back many years. The liability of British Coal only commenced with vesting of all the assets of the existing private colliery companies under the provisions of the Coal Industry Nationalisation Act 1946 on the 1^st January 1947. It has been necessary in some of the cases, however, to investigate working conditions as they existed so long ago as the early 1930's.

The court has been concerned to investigate whether or not any of the lead plaintiffs has been able to demonstrate that the respiratory illnesses of emphysema, chronic bronchitis, asthma or small airways disease were caused by exposure to coal mine dust and, if so, whether such exposure was caused by actionable fault on the part of British Coal. The generic medical issues identified above have been the concern of the medical profession for many years. There has been a general perception that the respiratory health of miners has been impaired as the result of the working conditions to which they were exposed in the course of their work underground. It should be noted that it is probably within the general knowledge of most that a particular disease, pneumoconiosis, is one from which it has been known for very many years that many coal miners have suffered. That disease is now known to be caused by the coarser fractions of coal dust which do not reach the innermost parts of the lungs. These actions have been concerned only with the finer (respirable) fractions of dust which are capable of reaching the deepest parts of the lungs.

The framework of the main judgment is first to look at underground coal mining generally and to examine the methods which have been used to win coal in the period with which the cases are concerned. This is with a view to an understanding of the terminology of mining and the circumstances to which the detailed engineering evidence in the case was directed. This will be followed by a review of the generic engineering evidence and then, in its turn, by the generic medical evidence. Finally, the cases of the individual lead plaintiffs will be considered. This summary follows the same course.

The Generic Liability Issues

The Legal Framework

Under s 1(4)(a) of the Act of 1946, British Coal came under a general duty to secure the safety, health and welfare of their employees, but these are general duties which are not actionable by an individual miner. Under the same Act, primary obligation of British Coal was to work, get and the make of supplies of coal available. The safety and health obligations were expressed to be subordinate to the primary task of British Coal - which was to produce coal. This is not to say that there was any direct evidence given in this case that the Board, in possible contradistinction to managers and officials deliberately to put production of coal ahead of the welfare of its work force. There was abundant evidence which emanated from a variety of sources that officials interpreted their duties as requiring the production of coal first and the taking of precautions in respect of health second. This may be understandable in the context that on the one hand respiratory disability, with which alone this case is concerned, is the result of long term rather than short term exposure, if at all and is not, therefore, immediately affected, by day to day conditions underground. While on the other hand the use of methods of suppression tended to impede efficient production and frequently was the occasion for dissent or resistance by or on behalf of the miners themselves since such methods impacted on production with an effect on wage levels.

For many years prior to 1947 there had been industry-wide concerns about chronic pulmonary disease, especially in the mines of South Wales. In 1936 the Medical Research Council (MRC) was appointed to investigate. It reported [Bedford & Warner] in 1943 and found that there w as evidence of an association between the incidence of pneumoconiosis, by which was meant all respiratory disease, and the calculated mass concentration of particles, particularly those below 5 microns in size both of coal and of mineral matter other than coal.

Setting up of Pneumoconiosis Field Research (PFR) - 1954

The objective was to undertake a field research in order to determine how much and what kinds of dust cause pneumoconiosis (in the narrow sense) and to establish what environmental conditions should be maintained if mine workers are not to be disabled by the dust that they breathe during the course of their work. The papers which were produced by the PFR, which subsequently became the Institute of Occupational Medicine (IOM) as the results of the research became available are numerous and, generally accepted to be, of high quality.

Standards and Sampling

After the Second World War, miners who were found to be suffering from pneumoconiosis were effectively excluded from working for British Coal and faced unemployment of uncertain duration, owing to their lack of skills other than those which they had acquired as miners. There was however an acute shortage of labour in the mines. It was in these circumstances that British Coal, with the full support of the Trades Unions, proposed a scheme for the employment of pneumoconiotics. It allowed (a) the employment of those men whose condition was "seriously incapacitating" "in approved dust conditions" on the surface, expressly said to be reasonably dust free (b) where the disease was in an early stage, a man was allowed to continue to work "without danger to his health provided that the work is "in approved dust conditions"

This introduced the concept of 'approved conditions' which led to what was to become the predominant theme of the approach of British Coal to respirable dust, the aim to have as few faces as possible 'unapproved'. The standards of dustiness introduced by the scheme changed over time, normally as a result of the introduction of new and improved sampling equipment. During the hearing much time was spent debating whether each new standard was a relaxation or tightening of the previous one.

The original scheme, which provided for the establishment of upper limits of dust concentrations in different working environments, was introduced in 1949. In 1956 a new protocol was introduced which was intended to remedy some of the weaknesses of the original scheme. The main one of which had been that the sampling instrument [mainly Short Term Thermal Precipitator, but also PRU handpump] could only take samples over a short period, which left the problem of how to obtain samples which would be representative of conditions throughout a shift. The new protocol was intended to produce uniformity by demanding that 'mean shift averages' as opposed to 'periods of maximum dustiness' should be used which is what the 1949 scheme had provided. Without doubt this change did not involve a tightening of the standard, it was argued by the plaintiffs that it had introduced a relaxation of the standard, but I did not find it necessary to make a decision on this point.

The next revision of the protocol took place in 1965, as the necessary consequence of the introduction a full shift sampling instrument [the Long Running Thermal Precipitator]. The intention was that this new standard should be equivalent to the previous (1956) standard. Whether it was or not, was a matter which was again much debated, but which I, in my turn, do not find it necessary to decide. What is, or may be, of greater importance is that as late as 1965 British Coal was not taking the opportunity to tighten the standard. The reason asserted was that since the gravimetric standard would be introduced in a few years, it would create unnecessary duplication of effort if it was done and that there was not yet a rational or scientific basis upon which to set a new standard. It remained what it had always been known to be "arbitrary". The standard was in any event a stop gap because on the horizon was the PFR's first major report on the ISS cohort and the widespread availability of a pit-worthy gravimetric sampler.

The gravimetric sampling and the setting of standards appropriate to it were introduced in 1970. The setting of this standard awaited the first major results from the PFR, the Interim Standards Study (ISS). The standard so derived was not intended to be so severe that it could not be met with contemporary techniques of dust suppression. Due to the nature of the change from particle to gravimetric standards, some faces that were previously approved failed to meet the new criteria. However, it is apparent that once collieries knew that they were not meeting the standards they set out devising and implementing schemes for reducing dust which depended, not so much on new technology but, on making better use of existing technology. In large measure they succeed. The distinction is critical. The fact that without new machinery or technology, those new standards could be met shows that more could and should have been done before that time to concentrate effort on the task of minimising exposure of miners to respirable dust. This was, of course the statutory obligation on British Coal which had been introduced by the Mines and Quarries Act 1954 and which, statute or no, had been the common law obligation to which they had been subject since vesting day. Measurement, as has been said before, was merely a means of providing a quantitative check on the success of the steps taken to reduce exposure to dust. It did not affect the basic obligations as employer to which British Coal was subject.

Approved Conditions scheme: From the start British Coal had known of its limited purpose (as described above) But British Coal appear to have been mesmerised, or corrupted, by the notion that it was only if a face was 'not approved' anything needed to be done to reduce the concentration of dust at such a face. It was not for lack of expertise that such a position was allowed to develop and become institutionalised. British Coal employed a number of talented research and development engineers in the field of dust suppression and measurement. The problem was that they were not given either their heads or the resources to do what was necessary, until statutory regulation, long opposed by British Coal, had become an inevitability.

The 1975 Respirable dust regulations did not in themselves change the 1970 standard which the defendants had set for themselves, but did give the mines inspector the power to enforce them.

One of the criticisms that has been raised by the plaintiffs against British Coal is that until 1970, British Coal used a particle counting method to measure the level of dustiness on particular faces. In 1943 Bedford and Warner had suggested that pneumoconiosis (in the wide sense) was related to weight of coal and not the number of particles inhaled and the plaintiffs therefore complained British Coal should have produced a suitable gravimetric sampler far sooner than they did. The evidence satisfies me that, had the will been there, in upper management of British Coal, a pitworthy gravimetric sampler both could and should have been introduced some five to ten years earlier than in fact it was. Although, this finding is made, it must still be remembered that the mere delay in producing an effective sampler does not represent a finding of causative fault for reasons which have already been given. The evidence satisfied me that had an efficient gravimetric sampler been introduced into the mines by, say 1957 (ten years after vesting date) as I have found it ought to have been, the defendants would have had no choice but to implement a programme of dust suppression and control that would have had a general effect in reducing exposure of men to respirable dust. But there would still have remained the institutionalised weakness of the system of "approval and 'non approval' of faces.

A prophetic epitome of all this was made in October, 1952, by Sir Charles Ellis, then Chairman of the Scientific Committee of the NCB. He had written a detailed memorandum which debated the issues both for, but mainly against, the making of the Order (now the 1975 Regulations) which the Union had been seeking at that time. Sir Charles took the view that:

(a) since the standards of dustiness being sought were then arbitrary and empirical there was no case for their statutory imposition

(b) sampling techniques and methods of measurement were liable to change

(c) the instruments of measurement were far from being satisfactory

(d) continuous sampling was desirable but production of a suitable continuous sampler was a long way off

Sir Charles was also alive to the essentials of the problems in that he acknowledged it had to be realised that sampling as such was no substitute for the efficient maintenance and operation of proved dust suppression measures which would achieve standards of air cleanliness that had been agreed with the NUM and Ministry of Fuel and Power as being "desirable".

Since 1970 and the coming into force of the 1975 Regulations:

(a) standards of dustiness were no longer arbitrary because the work carried out by the ISS enabled standards to be set which, if observed, would enable a probability estimate to be made of the risk of respiratory disease occurring in miners;

(b) sampling techniques were perfected,

(c) an instrument of a kind capable of measuring the mass of dust, which had existed, and had been recognised as necessary in 1943, was now available;

(d) that instrument also included a capacity for continuous sampling.

And perhaps most important of all, it was fully recognised by all levels of management that the proper objective was no longer 'approval' alone but the attainment of conditions which met the statutory obligation which had been created by s. 74 of the Act for 1954 and which had come into force on the 1^st June 1957. Once Regulations were in place there was a substantial improvement in dust levels as a whole and not just those at the upper level of what was permissible under the Regulations.

The conclusion is inescapable: if British Coal had devoted themselves as zealously in the years between 1947 and 1970 as they did, and had to do, after 1970 and especially 1975 to the suppression and control of respirable dust, there is every reason to suppose that the exposure of large numbers of men to avoidable concentrations of such dust would not have taken place. I am not unmindful that British Coal had many other matters which were pressing upon them, especially was this so in the early days of their existence. But long term health of the workforce had been recognised as an important objective to be obtained. To the extent that they failed in the respects which have been here discussed it can fairly be said that they were seriously at fault.

The risk posed to miner's health by respirable mine dust was known at the time of nationalisation. Accordingly, British Coal employed scientists and engineers whose functions included not just research into the causes and nature of respiratory ill health but into methods of reducing the creation and dispersion of dust as well. Broadly, there are three main areas of activity underground with which this part of this litigation was concerned. These were:

1. Conditions at the face;

2. Contamination of the intake;

3. Conditions in headings of stone or coal or a combination of both.

The progress of this research, including its eventual introduction into the pits, can be conveniently charted through the reports of HM Chief Inspector of Mines which were issued on a near annual basis. What clearly emerges from these reports and is evident from the many internal documents of the Board referred to at length during the hearing, was not just the general criticism which can be accurately stated as the defendants "could have done better if they had tried" but, and depressingly, the recurrent theme of many of those criticisms. They also show that in many instances there was a long lead time between 'research' and 'first use' which is compatible with what I have found to be the leisurely approach to the introduction of the gravimetric sampler as described above.

The internally promoted Destroy Dust Campaign which commenced in 1971 produced a distinct and significant improvement in the suppression and control of respirable dust. However, there is nothing in the evidence to suggest why such a campaign could not have been set up and been equally successful twenty years earlier. For example, in 1959 the South Wales NUM published a booklet entitled The Control of Dust in Mines which made clear the importance of having an educated workforce. The problem was in reality one of culture and while such a campaign has a part to play, ultimately it appears only statutory sanctions, or the threat of them, would provide colliery managers with the powers they needed to produce such a change of culture.

Respirators

Perhaps the most obvious way to have lessened the impact of dust exposure on the individual was for him to have been provided with respiratory protection. Before mechanisation was widely introduced, coal mining was not only an arduous occupation, but also it was one performed in conditions which were frequently physically confined in narrow seams as well as conditions which were hot and humid. None of these considerations were conducive to the wearing of any article which would have had the immediate effect of worsening the subjective impact of those working conditions let alone one which tended to impede the ability to breathe freely. Although respirators existed before vesting day, they were relatively crude and were uncomfortable to wear. After nationalisation and with the introduction of 'approved conditions' of working for pneumoconiotics the perception of British Coal, and in fairness to the Trades' Unions also involved, was that the widespread introduction of the use of respirators would distract the attention of British Coal and that of their officials and workmen from the task which was fundamental to reduction of levels of exposure to respirable dust, namely the suppression of it at source and control thereafter.

It is now possible to fast forward to 1971, when the advent of statutory regulation was not far away and British Coal produced a U-turn in its policy in regard to respirators. Their new position being that the dust respirator should be regarded as the last line of defence in the whole system of anti-dust measures. Given what had been the open opposition of British Coal to the wearing of masks, it is little surprise that, in general, there was an undisturbed culture among miners which looked with disfavour on the wearing of masks, even if conditions would have made such a course sensible by reducing the discomfort and health risk from exposure to high concentrations of dust. Apart from considerations of culture, which would have required substantial education or persuasion to overcome, there remained the added disincentive to the wearing of respirators namely the physical discomfort in a number of discrete and identifiable respects which accompanied their use. A memorandum prepared by the IOM for the National Dust Prevention Committee (NDPC) dated 17^th March 1972 fully addresses the issues raised and stated that "a greater use of dust respirators could probably do more to eliminate dust disease among coal miners than any other course that is technically feasible at the present time - and at a fraction of the cost. "

I accept the evidence presented which would suggest that 50 per cent protection from total dust would have been achieved if a respirator was worn for as little 25 per cent of the shift and that suitable respirators, such that it would have been reasonable to expect a conscientious miner to have worn for a part of his shift would have been available by the mid 1960's.

Furthermore, there was ample evidence which demonstrated that miners' traditional reluctance to use respirators could be, and in certain pits had been, successfully overcome. The regional differences in respirator take-up make good this point. This finding is sufficient to dispose of the possible argument that the defendants should not be found to have been in breach of duty because it had not been shown that miners would have worn respirators.

In deciding how to apply these considerations in a practical way requires that allowance will have to be made for the fact that overmen in particular, and deputies to a lesser extent, will have had to remove their respirators for appreciable periods when giving instructions to miners for whom they were responsible as well as the fact that working conditions for all may well not have been conducive to the wearing of respirators for much, if not most of their working time underground. For the face worker, other than machine driver, who had performed physically arduous work, there is difficulty in proving that he would have used a respirator even if such had been supplied and he had been suitably instructed.

The extent of the exposure of the individual to dust

In the endeavour to find, in the individual case, the extent to which any particular miner was exposed to excessive or tortious dust, implicitly there are two baselines for which search has to be made. Specifically, this means that a measure has to be found first for total exposure and, secondly, the theoretical minimum exposure to which only such miner was or should have been exposed. The million (plus) documents disclosed by the defendants provide at best a fragmentary and at worst a non-existent picture of what each individual plaintiff s working conditions were like during a working life of 30-40 years. There is also the added problem that for a number of reasons the dust records are known to be inaccurate, in particular there is abundant evidence that there was frequent falsification of the measurement process by such means as taking abnormal steps to ensure that all available suppressive measures were in use both on the face and in the intake before periods of measurement began, occasional improper use of bondina sheets to filter the air before it reached the measuring instrument also took place. The samplers were usually not men of the highest calibre for whose work deputies and colliers had little immediate interest since it tended to get in the way of production.

The documents also do not provide a sufficiently detailed picture of working conditions across the whole of the face from intake to return, of conditions in stable holes at either end of the face, let alone of conditions in headings and drivages where some of the plaintiffs spent extended working periods and which were subject to special problems of ventilation. Another problem was the need to convert measurements for dustiness in a given volume of air in terms of number of particles (for example made by a thermal precipitator) into weight of dust (gravimetric) so that they could be compared and correlated so as to obtain a cumulative lifetime dust exposure figure. The hope had been that it would be possible to ascribe a numerical value in any given case to an individual's dust exposure but this proved to be hopelessly optimistic and was tried in vain. It is unlikely that anything approaching a true reflection of actual exposure could ever have been realised. Despite this formidable list of actual and potential sources of difficulty and error, both by omission and commission, the parties and their experts assiduously embarked on the task of seeking to "put some numbers down" for individual plaintiffs and, to heavily qualified effect, succeeded in their objective. What conclusion can most probably be drawn from the exercise is that although there may be considerable doubt about the absolute value of these 'numbers' the experts' figures, when computing for those individual plaintiffs which they were able to attempt, did provide a spread of results from which a reasonable comparison between miner and miner could be attempted.

Records are, of course, only a part of the source material available to be treated as evidence upon which the court can proceed to evaluation the exposure of an individual to dust. This is an oblique reference to the existence of the eye witness evidence of what working conditions had been like in practice. It would be unwise, however, to place too great reliance on such evidence. At best it depended on distant recollection, extending in one or two instances for over sixty years.

The generic conclusion is that British Coal failed:

1. To take all reasonable steps to minimise the creation and dispersion of respirable dust by the introduction and use of known and available dust suppression techniques from about 1949 to 1970 and to a lesser extent thereafter.

2. Such techniques included, but were not limited to:

a. Face infusion;

b. The use of pneumatic picks equipped with water sprays;

c. Water designed into coal cutting and getting machines at the pick face;

d. Spraying fallen coal and 'muck' with water;

e. Reduction of firing, especially on production shifts;

f. Attention to chutes, enclosed transfer points and joints on conveyor systems;

g. Ventilation in headings and drivages.

3. To ensure that suitable instruments for measuring dust were developed and introduced at as early a stage as was practicable.

4. By adhering to the misleading concept of face 'approval' and 'non approval' to institute an efficient system for ensuring that the obligation as in 1. above was met.

The Generic Medical Issues

Out of a trial which lasted 102 court sitting days taking evidence, almost exactly one half were devoted to consideration of the generic and individual plaintiffs', medical evidence. This helps to provide some indication of the scope and complexity of the medical issues litigated in the course of the hearing. All parties to the present litigation relied upon the evidence of consultant physicians and epidemiologists. The plaintiffs also led evidence from a medical statistician. There was frequent reference to the papers generated by the Pneumoconiosis Field Research (PFR). The former deputy director of the Institute of Occupational Medicine (IOM), Dr Jacobsen, reluctant at first to give evidence because he felt his impartiality could be impugned by so doing, was nevertheless prevailed upon to assist the court and gave evidence when called on behalf of the plaintiffs.

Diseases of interest in this litigation

The historical position is that for many years there has been a recognition that coal mine dust has a generally adverse effect on the lungs of those who inhale it. The most obvious example of this is the disease now called coal workers pneumoconiosis (CWP). It is a condition detected radiologically, during life. But detection is well short of being assured in every case. The disease takes one of two forms, namely simple or complicated, the latter being otherwise known as pulmonary massive fibrosis (PMF). It is generally accepted that simple pneumoconiosis does not cause respiratory disability and is not usually progressive, in the sense that once exposure to mine dust ceases, the condition does not significantly progress. PMF, by contrast, is usually progressive and, certainly in its more advanced forms does cause respiratory disability which may ultimately lead to death. PMF may develop from any one of the simple forms of pneumoconiosis, although it is more common to find that it does so in those individuals who suffer from grade 2 or higher.

Chronic bronchitis as defined by the Medical Research Council (MRC) is a functional, rather than disease based, definition and consists of 'sputum production on most days for at least three months in the year for at least two consecutive years'. When reading all medical papers that are in evidence, it is important to remember that the term chronic bronchitis was frequently used loosely and, with the exception of tuberculosis in the early papers especially, covered all diseases and abnormal conditions of the respiratory tract.

Emphysema is a pathological definition of a condition in the lung characterised by abnormal permanent enlargement of the airspaces distal to the terminal bronchioles with concomitant destruction of the walls of the airspaces, but without fibrosis. The functional result of this disease is the destruction of the alveolar walls which are the gas/blood exchange area of the lungs resulting in the mismatch of exchange of oxygen to, and carbon dioxide from, the blood. Because the lungs have to work harder to try to match the demands of the blood supply for more oxygen, the result will be breathlessness.

Emphysema may be of two different types, namely panacinar or centriacinar. Centriacinar emphysema predominantly affects the central parts of the acinus, that is the part of the lung tissue proximal to the respiratory bronchiole. This is also commonly referred to as centrilobular emphysema. Panacinar emphysema affects the whole of the acinus, but characteristically is most pronounced in the lower lobes of the lung. There has been considerable debate during the hearing of these cases as to the existence of a third category of emphysema, focal dust emphysema. The plaintiffs' contention espoused by Dr Rudd is that focal dust emphysema differs from centriacinar emphysema only by virtue of the presence of retained dust in a focus, and that it is not a separate disease entity in itself. The contention advanced by British Coal is that focal dust emphysema results from the deposit of respirable dust around the respiratory bronchioles and it is this which causes atrophy or loss of tone in the smooth muscle of the bronchiolar wall. It remains closely confined to its point of origin around the bronchiole and does not extend into the alveolus. It is British Coal's further contention that emphysema may result from the mechanical effects of scarring due to presence of a heavy dust load.

Small airways disease is a functional description of a condition which results from airway narrowing in the distal bronchioles. It may exist independently of emphysema. The condition cannot be diagnosed on the basis of a clinical assessment alone. But, if there is evidence of reduced flow in the small airways without evidence of emphysema then a differential diagnosis of small airways disease can be made.

Asthma is a condition characterised by variability of symptoms such that at times there will be a normal, or near normal function, while at others there may be severe limitation of air flow. It is diagnostic and characteristic of the condition that following inhalation of a bronchodilator drug, there may be a significant improvement in airflow.

Complicating a sure attribution of the cause of the development of any one or more of these conditions is the effect of smoking. It is common ground that smoking can, and frequently does, cause or exacerbate any one or more or all of these conditions. The precise mechanism by which smoking does so is not definitely established. Neither can the plaintiffs define the mechanism of causation of the suggested link between exposure to mine dust and these conditions, which is fundamental to this part of their case.

Types of studies examined

Epidemiology is the study of how often diseases occur in different groups of people and why. Broadly there arc two types of in-life epidemiological study which may be undertaken. These are first longitudinal studies in which subjects are followed over time with continuous or repeated monitoring of risk factors or health outcomes, or both. Secondly there are cross- sectional studies in which a group of patients who have developed a disease are selected and their past exposure to suspected aetiological factors is compared at a particular time to those who do not have that disease or that degree of disease. In addition to the in-life categories there are two others based on studies made after death. These are mortality and post-mortem. The object of conducting mortality studies in relation to miners was simply to see if a miner was more likely to die from chronic bronchitis or emphysema than men engaged in other occupations. The post-mortem studies examined the lungs of miners to identify the amounts and types of emphysema and relate those findings with the amount of coal dust contained in simple foci in the lungs.

An important qualification to all epidemiological studies is that the results should be viewed in the context to which they relate. If a statistically significant association is found which is at variance with other evidence (which in this case would be medical or biological), then the conclusion suggested by the study may properly be ascribed to chance and hence of no or little value. However, the individual plaintiffs require more than convincing studies if they are to succeed. Dr Jacobsen put the subject in context when he said:

I agree that there is no way in which the epidemiological data or smoking or a dust exposure can identify whether an individual who may be suffering a loss of lung function and who may have been exposed to both insults has his loss of lung function attributable to one or the other. The epidemiological data... does not help you to solve that problem on its own.

Clinical judgments are required and criteria, measuring of both insults are required....

If you have a coal miner who suffered a loss of function then you would have to consider all the factors, his smoking habits and his dust exposure.... but the epidemiological data do not make that decision for you.

The plaintiffs expressly relied in their opening submissions on a number of epidemiological studies based on the results obtained from the PFR. British Coal in their opening submissions sought fundamentally to undermine the plaintiffs' case on this by attacking the validity of the methods and conclusions of the PFR itself.

The PFR studies were conducted at the pit head with the equipment for measuring the Forced Expiratory Volume of Air in one second (FEV₁) installed in vans specially equipped for the purpose. This measuring equipment was antiquated compared with today's hospital based equipment, a factor which clearly impacted on the accuracy of the individual measurements. During the evidence a number of problems were identified with the use of such equipment but were dismissed since they did not produce false statistical associations. In any event, whatever criticisms were made of the PFR's lung function measuring techniques, the general pattern of results at collieries from survey to survey was 'reassuring' and showed plausible reductions in FEV₁ The results also showed the well-recognised association of FEV₁ with age, build and smoking habit. In these circumstances the results had a validity sufficient for the purpose in hand.

In the healthy individual lung function increases with age until it reaches its peak at about twenty five years. Thereafter it decreases at the rate of about 30 ml per year, on average. The rate of decline varies between individuals by factors as much as two or three times, confirming what has been said in other contexts that there will be a natural spread of results in any biological process. In the same way there will be individual variations in the rate at which lung function declines with age. As between individuals, absolute levels of lung function will be found to vary even after correction for such known variables as height and age. In a population the normal distribution of lung function will be found to lie within ±1.96 standard deviations and five per cent will lie outside this range. Thus 2.5 percent of the population will have a lung function which will be one litre greater and 2.5 per cent one litre less than the mean. About 15 per cent of the population will have a 'deficit' when compared to the mean of more than half a litre. Given these known variables, there are obvious theoretical and practical difficulties in determining what was an individual's lung function before it became subject to insult of any kind.

The essentials of British Coal's opening position was that chronic bronchitis does not cause any significant loss of lung function, but causes imperceptible and barely measurable loss of function in a large number of miners, but that absent, any destructive effect on the cilia, chronic bronchitis does not constitute injury which is compensatable in English Law. They further contended that if, or to the extent that mine dust can cause emphysema, it does so to an insignificant mean extent and certainly has no material effect on lung function. Lastly, British Coal disputed that either small airways disease or asthma can be caused by exposure to mine dust.

However, after the evidence British Coal's position became that they accepted that some types of coal mine dust can cause a degree of loss of lung function which is not attributable to chronic bronchitis (properly defined) and that the amount of and the physiological reason for such loss remain in issue. They further accepted that such "degree of loss of... function" cannot be explained by reference to chronic bronchitis and that such loss may be up to 70 ml per 100 ghm^-3, as an average figure. It was further submitted that the pathological explanation for such loss is unknown, but that "emphysema may play a part". If emphysema is implicated it is because it causes a localised effect, unlike the severe effect seen in smokers with ceniriacinar emphysema. British Coal put forward that small airways disease and some form of restrictive condition may also play a part. However the submission that received the most emphasis was that there was no proper basis, for rejecting the possibility that, in any miner who has smoked, his loss of lung function was solely attributable to his smoking habit.

Dust may have made a contribution to the loss, but that cannot be proved.

Thus it would seem that, having been forced from their original position by the sheer weight and quality of the evidence marshalled by the plaintiffs, British Coal remain as doubters. British Coal may of course be correct in this new position although it has to be remembered that there is an obvious element of defensive opportunism being displayed. It has required careful analysis and evaluation.

By contrast, the plaintiffs' position has been consistent throughout. But, of course, consistency does not have to be the criterion of success although it has an obvious headstart over, defensive, inconsistency. The plaintiffs' position has not only been consistent, but has also been relatively straightforward. In relation to chronic bronchitis their position was that the condition may give rise to a right to compensation even though the condition is not permanent. The plaintiffs further relied on the fact that it was generally accepted wisdom in the medical profession that coal mine dust causes and contributes to centriacinar emphysema and is thereby causative of breathlessness and disability.

The point has already been noted that the plaintiffs are not able to prove what is the probable mechanism by which destruction of the alveoli takes place this being the principal physiological characteristic of emphysema. Collectively, the plaintiffs attempted to overcome this possible weakness (the inability to point to a definite mechanism whereby mine dust causes damage to the lungs) by referring to numerous and extensive epidemiological studies which have been conducted over a number of years and which they say, by way of evidence and submission, can amount to the proof which they seek. In response it was submitted on behalf of British Coal that the reliance by the plaintiffs on the results of the epidemiological research as supporting a case that exposure to mine dust is a cause of emphysema was an attempt to convert a blurred picture of a general scene into a highly resolved image of very specific application by flawed and inadequate evidence.

In his report on generic issues, Dr Rudd reviewed a large number of studies which have examined the relationship between exposure to mine dust and chronic bronchitis, emphysema and loss of lung function. From the many papers that were available for consideration, both sides to this litigation concentrated on a selected few. The majority of these core papers depend on the published results of the PFR (see earlier for its objectives) and therefore its objectives and methods require further to be explored. From 1951 until the conclusion of its work, the PFR was concerned, in addition to pneumoconiosis, with the very matters that are in issue in these proceedings. British Coal's initial position was that the conclusions from the principal paper Marine (1988) and other researchers using PFR/FEV₁ data lacked validity and, therefore, are unsafe.

It is necessary to briefly look at Marine (1988) as it was this paper which was responsible for the expenditure of the greatest time and effort, by both sides to this litigation. The authors of the paper, which included Dr Jacobsen, found that the effects of both smoking and exposure to mine dust could cause clinically important respiratory dysfunction and that the effects of each were additive. Understandably, therefore, this study lies at the very heart of the plaintiffs' case, albeit that its design meant that it did not help with the question of susceptibility (variability of response), as to which see later. It is legitimate to impute a recognition by British Coal of the potential importance of the study and so to understand the lengths to which they went in order to destabilise if not to discredit its main findings. To this end the court spent many days examining some of the raw data interpreted by Marine in minute detail. This examination, following the lead of British Coal's expert medical reports, investigated estimates of dust exposure, methods of measuring dust and the proper correlation between different dust sampling instruments, responses to questionnaires in relation to smoking habits, implausibility of some sequential measurements of FEV, of individual miners in longitudinal studies including the methods of recording FEV, and the like. This exercise revealed that there were a number of errors of recording of lung function that were incorporated in the data set used in the Marine study (although it was plain that it made no difference of any moment to the conclusions which could properly be drawn from it). However, many of the significant portions of the comments in the expert reports prepared for British Coal were exposed by Dr Jacobsen to be ill-informed, inaccurate and either unjustifiable or plainly mistaken. It is enough said as to the strength of Dr Jacobsen's evidence that by the time British Coal came to make their closing submission their position was that in general terms they did not seek to challenge the validity of the data upon which the studies were based although clearly the interpretation of the data remained a matter of controversy.

This did represent something of a sea change from British Coal's opening stance and was a proper reflection of the extent to which the full frontal attack on the PFR data and its methodology had been repulsed. This forced British Coal to redefine their case when Professor Berry came to give evidence. The areas of difference, as summarised by him had become:

1. If it is accepted that exposure to coal mine dust causes a reduction in lung function some remaining questions are: -

the size of the reduction both in absolute terms and in relation to the reduction caused by smoking;

the extent to which the reduction causes disability or contributes to disability;

whether there is evidence of susceptibility and, if so, the size of the susceptibility both in absolute terms and in relation to susceptibility to tobacco smoke.

2. The data of the PFR studies seem most useful for the above purposes since they relate to the situation in the British coal industry. Other studies act as confirmation of the PFR studies in a qualitative sense but are less useful quantitatively.

3. Various concerns have been raised in connection with the data of the PFR studies. It has been possible to address a number of these concerns by re-analysis of some of the data. Many of the conclusions have been shown to be robust to alternative definitions and, whilst some conclusions have been weakened, the overall pattern of results stands up.

The nature of this evidence and the challenge it mounted was on a relatively narrow basis that can best be described as "interpretation of the data". This was an elegant retreat from the position which had been occupied by British Coal, with the benefit of his assistance for the previous 88 court sitting days, but was still some way short of abject surrender.

The most significant longitudinal study was by Love & Miller of the IOM. The authors had examined the individual losses of FEV₁ from three PFR surveys and compared these to individual measured dust exposures during the same period and those partially estimated before the commencement of the period under study. They found that the loss of FEV₁ over the study period of 11 years increased with previous cumulative dust exposure after allowing for the effects of age, height, smoking and overall colliery differences. These results confirm by direct measurement inferences drawn indirectly from previous cross sectional studies of the relationship between FEV₁ and dust exposure. The paper supported the proposition that heavy exposure to dust can have an important impact on disability comparable in magnitude to that from smoking. While this paper did not provide any greater insight than the previous offering from the PFR or other research groups, its utility for the plaintiffs was that it was one of a number of papers which all tell the same story and therefore create a weight of evidence, which ultimately was unanswerable. Different insights into the same issue was provided by the evidence relating to death.

The importance of a mortality study may be to demonstrate, not that miners have a raised mortality when compared to non-miners as in a control study but, that as between miners with differing exposure to mine dust and emphysema mortality is raised when compared to those who do not suffer from emphysema. The key finding of the main mortality studies for present purposes is that miners exposed to excessive amounts of respirable coal mine dust are at increased risk of premature death, either from (PMF) or from chronic bronchitis or emphysema or to put it another way the papers show a clear trend toward a decrease in survival with increasing exposure to dust and age. British Coal attempt to discredit these studies. The main avenue of attack was that it had undoubtedly been a feature of the certification of death in coal mining areas that the cause of death may be wrongly ascribed to one condition (pneumoconiosis) when it should have properly been ascribed to another (emphysema or chronic bronchitis). However Dr Coggon's cross-examination on days 48 and 49 showed that the opportunity for bias due to mis-certification of cause of death had not operated. I have also found that the argument by British Coal that smoking had confounded the results to be unsustainable, for, as Dr Coggon said, among other reasons, the studies show that there was a clear increase in mortality from bronchitis and emphysema during follow-up in relation to higher cumulative exposure to respirable dust. No corresponding trait was observed for mortality from lung cancer.

Likewise the post-mortem studies provide another piece of the jigsaw. The study by Leigh (1994) which was among the best conducted provides strong support for the hypothesis that severity of emphysema in coalworkers is causally related to coal content in the lung and thus to exposure to coal in life. This study also confirmed the importance of age and smoking in severity of emphysema. In most post-mortem studies there is the inherent danger that bias can occur because only a small fraction of miners will have had an autopsy performed. The authors also claimed, rightly, as I find, that although selection bias is inherent in a study of this type there was no reason to believe that selection would have been influenced by severity of emphysema and lung dust content in such a way as artificially to produce the results found. Also Dr Rudd could not see why the selection bias would lead to false conclusions about the relationship between dust and emphysema and it might be added, since decrement of FEV₁ had been measured before death, loss of ventilatory capacity. Professor Berry in his evidence considered that the authors had achieved the objective which they had set themselves, subject to the possible bias from the sampling techniques, and accepted that the analytical technique was "in order".

One of the recurrent themes in the discussion of the epidemiology was the diminishing effect of dust. This was in issue throughout the evidence. The issue was whether the decreasing effect of dust per unit of exposure as age increases seen in the Rogan/Marine studies was a true effect or was artefactual. The conception is also referred to as the age x dust interaction. Although this issue recurred from time to time during the evidence, in the end the Defendants were driven to concede that "the evidence there is, (of such an effect) is inconclusive." In my judgment the most probable explanation for the apparent age x dust interaction found in Rogan/Marine was that it was artefactual, although (per Dr Rudd) it was plausible how, in a lung already heavily dust laden, each additional unit of dust would be unlikely to produce the same effect as in a less dust affected lung. The evidence in relation to the biological implausibility of the dust-age interaction being a true, rather than an apparent, effect was in my judgment and for practical purposes in favour of the former.

Drs Morgan and Pearson

These were the principal authors of the generic medical report submitted to the court and relied upon by British Coal. As has been seen above, their 'root and branch' attack on the PFR was successfully seen off by Dr Jacobsen with able contribution from Dr Rudd. At the conclusion of the evidence both written and oral from Dr Jacobsen, it should have been clear to all, except the blinkered, that the strategy of full frontal attack on the PFR was bound to fail and. that if any progress was to be made, a fresh and more focused approach would be required. Drs Morgan and Pearson however attempted to hold to the basis of their written reports. This was seriously in error and in my judgment resulted in both eminent physicians losing intellectual and professional credibility.

It is possible, at this stage in the analysis to discuss their failings jointly, although the major responsibility for them plainly lies with Dr Morgan. He has been a prolific writer of learned papers on the lung function of miners, in particular, for whom, in general terms as he would have it, the cause of the majority of their lung deficiencies was not the adverse effects of mine dust but tobacco smoking, with only a minor contribution being made to ventilatory deficiency by reason of chronic bronchitis (cough, sputum with some narrowing of, and turbulence in, the main airways). Historically, as can be seen elsewhere, there has been a significant learning process about the effects of coal mine dust on miners' lungs over the course of the last 40 years and more. This has largely derived from the results of the PFR. Dr Morgan is of an older generation who, in his early days, was both regarded as knowledgeable and highly respected as a chest physician. For almost 40 years now Dr Morgan has been based in the United States and Canada. In the United States, Dr Morgan was resident for a long time at Morganstown, West Virginia where for a number of years, he was director, and later Professor, of the Medical Research Station of the Appalachian Laboratory for Occupational Respiratory Disease. He was thus based in the geographical centre of one of the main coalmining areas in the United States. As was to be expected Dr Morgan was the author and co-author of many papers on the topic of the respiratory diseases of coal miners; see his curriculum vitae. During the course of the evidence in this case his thinking was shown not always to have been consistent.

It has also to be remembered that Dr Morgan had given evidence on behalf of the defendants in the case of Tanner v. British Coal Corporation in which judgment was given on 20^th December 1989. Parts of the Generic Medical report was lifted, almost bodily, from reports submitted in the earlier case. It will not have been overlooked that the Marine (1988) paper had been published only shortly before the hearing in Tanner. The judgment is strangely silent about this important paper. It might have been expected that, having regard to its importance, one side or the other would have introduced it into the evidence. By the time of the hearing of Tanner, Dr Morgan was much opposed in his thinking to the validity of the Marine conclusions and was in print in pursuit of that objective.

One of the many troublesome features of the approach of Dr Morgan to the issues in this case has been his inconsistency in regard to them. Such were the many errors and lack of balance in the written material and comment in the Generic Reports that, and as it became increasingly obvious, the ground was already prepared for an uncomfortable time in the witness box. While the full judgment contains a number of the many examples of Dr Morgan's difficulties, one example is not out of place in the summary:

Dr Morgan was being effectively cross-examined about his written comments in relation to the Cockcroft (1982) post-mortem study where he had said:

All autopsy studies have an inherent bias.... This makes it very difficult to reach conclusions that are applicable to the wider population of miners in general.

Since the control group are different from the subject group in respect of such an important variable as age which is known to be related to the prevalence of emphysema it is highly questionable whether any valid statistical comparison is possible.

Ultimately, Dr Morgan agreed that:

certainly some of (his comments were) inaccurate

and that he

(did not entirely) regard them as a valid and fair commentary on the paper.

In summary, much of his evidence was ill-considered, inaccurately and inappropriately referenced to published papers, partial and inconsistent with some of his own earlier published pronouncements.

The hope must have been that with Dr Pearson who had been a significant contributor to the Generic Reports, as well as having written on each plaintiff individually, a better picture in terms of accuracy, objectivity and fairness would have emerged. It is not just a sadness that that was not to be so. Indeed, it is not an understatement to say that a bad situation became worse. Pressure of work, a lack of familiarity with the subject matter could have explained why Dr Pearson performed so badly. In summary, his evidence was inaccurate in many places, inappropriate and unchecked references were given, partiality and lack of objectivity ran through the whole corpus of his evidence. In the Generic Medical report there was reference to an unpublished paper by Stenton (1996) which contained the statement:

Smoking is the most important cause of respiratory morbidity and mortality in the UK and is known to be capable of producing all the abnormalities within the mining population. Biologically the smoking story is both possible and plausible The study of benefit claimants (Stenton) is a large study which supports such a hypothesis but so too does much of the other data if one does not begin with a preconception that dust is harmful. (emphasis supplied)

Not only had Dr Pearson enthusiastically embraced this study, but he had gone further, even, than the study itself when he said:

I think the only conclusion in this study you can draw is that it is unlikely there is any association with dust. (Emphasis added)

whereas the study itself had said that its results offered "no support" for the suggestion that dust had an effect on ventilatory capacity. The paper was in fact unpublished and, I would judge would find it hard to be accepted by any responsible medical publishing house. In fairness to Dr Pearson he was not alone in placing weight on the paper. But it is to be observed that not only was Dr Pearson present for almost the whole of the trial (medical aspects) but also had access to the daily transcripts of evidence.

But Dr Pearson's failings were not just restricted to the Generic Reports, they spilled over into some, at least of the reports on the individual plaintiffs to which it will be necessary to turn at the appropriate stage in this judgment.

From the examples given, which are merely samples, it must by now be perfectly apparent why it would not be possible to sit comfortably with any decision which depended on the professional and intellectual approach of either of these two witnesses whose evidence has been reviewed in this section of the judgment. The decision by British Coal to proceed on their evidence could have been anticipated as high risk. The controversial nature of many of Dr Morgan's publicly stated views was well known, long before this litigation began, they had been given frequent airings in the medical press and had been as often effectively refuted as made.

Knowing of this high risk did not deter British Coal from seeking to find any weakness they could in the generic medical evidence relied on by the plaintiffs. But as so often happens in litigation, a good case becomes the stronger, the more it is tested. So it was here.

In conclusion, on Drs Morgan and Pearson I judge, adopting the approach taken in The Ikaricm Reefer [1993] 2 Lloyds Reports 68, that they wholly failed to appreciate the role which an expert witness is not just expected, but required, to fulfil when preparing reports for and giving evidence in litigation of this character.

I am quite satisfied that the position taken by Dr Morgan was that since his experience in the field was more extensive than any of the other witnesses he was entitled to hold to his dogmatic views despite the great extension of knowledge of the subject which had taken place, not only since the PFR first reported, but also since the decision in Tanner's case in which his views had been upheld. It was to Dr Pearson's disadvantage that he became caught up with Dr Morgan and it may show the disadvantages of not selecting experts who are truly independent one of the other. Dr Pearson had been a research fellow working with Dr Morgan at the University of Western Ontario in Canada where he had been for a period before returning to practice in the United Kingdom.

Does emphysema cause the observed loss of FEV₁ in coal miners?

The nature of the mechanism (pathogenesis) which causes loss of lung function in those who smoke and those exposed to mine dust occupied an significant part of British Coal's opening and closing submissions as well as the evidence adduced in the course of the trial. Their position was that the loss of FEV₁ was not caused by emphysema as properly defined. In their Generic Report British Coal's experts propounded the questions and answers which follow:

In considering whether dust induced emphysema plays a role in the development of airways obstruction in coal miners, the following questions need to be answered:

a) Is emphysema more common in coal miners than it is in the general population?

b) When emphysema is present in the lungs of a coal miner, has the inhalation of coal dust made a contribution to its development?

c) Assuming the answer to b) is in the affirmative, when coal dust induced emphysema is present does it cause either significant airways obstruction or other disabling impairment such as the reduction of the diffusing capacity?

There seems little doubt that the first two questions should be answered in the affirmative. The answer to the third and most crucial question is harder to find.

The importance of this topic for British Coal was that if it could be demonstrated that in the absence of fibrosis there could be no emphysema, those who had emphysema and only type M (macule - which had no solid centre greater than 1 millimetre in diameter) abnormalities, emphysema could not be related to the presence of dust. The results of the Ruckley studies did not enable British Coal to go that far and the results of the Leigh (1994) study showed, to the contrary, that there was strong evidence that emphysema in miners was causally related to lung coal content.

Dr Rudd was troubled by certain aspects of these studies, although he was not convinced that they went far enough, Dr Coggon was also not satisfied with the validity of British Coal's point "no fibrosis, no emphysema". It was the defendants' final submission that:

Unlike the loss of lung function found in miners, the emphysema found in miners is associated both as to its presence and its extent with the coal rank of the inhaled dust and with increasing category of simple pneumoconiosis. The emphysema that is caused by mine dust may properly be described as focal. It is generally found in the immediate vicinity of the fibrotic nodule. It has not been shown that mine dust causes emphysema to any material extent in the absence of fibrosis or that focal emphysema caused by dust is capable of causing any material loss of lung function.

which

is an indication that the loss of lung function is a response to the inhalation of dust which does not differ as between types of dust, whereas the emphysema is specifically related to, and probably a mechanical consequence of, the formation of fibrotic nodules in simple (CWP).

But this submission was at variance with Ruckley (1989) which had showed that fibrosis could exist without emphysema, men with PMF did not necessarily suffer from emphysema and that the failure of the study to show any association between pathological group M and emphysema was due to the lack of statistical power, because of small numbers, rather than demonstrating that emphysema could not occur without fibrosis.

Migration of emphysema from macule into the respiratory bronchiole

It was the general position advanced by British Coal that although no specific biochemical mechanism has been identified in relation to dust related emphysema it is possible that some form of biochemical response generates localised emphysema in the vicinity of the deposited particles. It was unlikely that that response would extend further into the lung. British Coal also pointed out that it is not necessarily the case that focal emphysema has a biochemical cause, since there exists a simple mechanical process directly associated with fibrosis.

Dr Rudd accepted that the initial development of emphysema was around the coal macules and nodules but insisted that in some way which he could not explain emphysema could radiate out from the macules and nodules to other areas of the lung.

Relying on Dr Stockley's evidence, the defendants submitted that this hypothesis was unproven and intrinsically unlikely. However, in oral closing submissions Mr Allan invited the court to consider that this evidence was at the limits of Dr Stockley's expertise. While Dr Stockley knew a great deal as to the mechanisms by which cigarette smoke causes emphysema he did not have the same working experience as regards mine dust.

The relevance of dust composition to emphysema

On this topic British Coal argued that the proportional coal content of dust exposure was related to the prevalence and extent of pneumoconiosis and of dust-related emphysema, but not to loss of lung function. This questioned the hypothesis that the loss of lung function caused by dust is the consequence of dust-related emphysema. If it were otherwise then proportional coal content of dust exposure would be expected to be related to loss of lung function.

It was also submitted that the relationship with coal rank which is common to pneumoconiosis and emphysema is more consistent with the view that dust-related emphysema is a focal condition, characteristically found in close proximity to the fibrotic nodule and aetiologically connected with it, than with the view that dust-related emphysema results from a generalised inflammatory response in the lungs such as could occur in consequence not just of the inhalation of coal dust but of any other particulate matter including the other components of mixed mine dust.

While I accept that the point, that the proportion of coal dust in the mine's atmosphere was relevant to causation of pneumoconiosis and emphysema, I reject it not only because of the tenuous nature of the inference which British Coal sought to draw from the evidence but also because it was inconsistent with the evidence of Dr Rudd and Professor Berry. The last named explicitly stated that he thought that the further evidence relating to pit effects which had come from the IOM excluded the possibility that the dust in one mine was more potent than that in the other for reasons which were not reflected in the measurement of exposure. He concluded that the difference in the pit effects were not related to the make up of the dust.

Small airways disease

This topic was relatively, starved, of interest and evidence and did not received detailed submission at the conclusion of the evidence. I have not found it necessary to arrive at a conclusion one way or the other, whether small airways disease is a condition induced by exposure to mine dust.

Susceptibility and The Common Pathway

As has been seen already, British Coal came to accept that there was almost certainly a degree of variability of response to mine dust. This was something about which all experts, whose evidence I can accept, had agreed. Dr Jacobsen expressed the proposition in robust terms such that if the proposition was not true it would have provided the only example of a biological system acting in a uniform way.

British Coal, however, contended that what was important was the extent and pattern of this variability. Professor Berry, while not denying that variability did exist, was prepared to assume that it did exist although a quantitative measure was he said 'elusive'. I have heard and considered the evidence of a number of experts on this issue who sought assistance from learned medical articles to support their views. However, it falls to the judge and not the epidemiologists or clinician to decide such a contested issue. While fully recognising that from the scientific perspective the experts have articulated their reasons for withholding an expression of firm opinion either way, from the forensic perspective, I am left in no real doubt. While I caution myself about making a priori assumptions there is, in my judgment, too much evidence which I have extensively reviewed which is either 'compatible' or 'consistent' with the existence of susceptibility as well as there being a spectrum of susceptibility to be able to ignore it. In particular I have been persuaded, on balance of probability that both the existence of susceptibility and its spread (variability) are biologically plausible and probable. More importantly, however, there is sufficient evidence in the papers by Love & Miller, Ruckley and Marine to prove that my conclusion does not depend for its validity on the possibly shaky foundation of a priori assumption.

British Coal relied on the difficulty which the features of susceptibility identified above create in the case of the individual miner exposed to mine dust:

1. Is he susceptible at all to dust?

2. If he is susceptible, where in the range of susceptibility (variability) does he lie?

3. Is the susceptibility to smoking or to mine dust or to both?

4. If chronic bronchitis develops as an early response to insult can the plaintiffs prove that exposure to mine dust in excess of the minimum will have made any or any significant difference to their condition?

The Common Causal Pathway

Running through the whole of the discussion is the possibility that if the actual mechanism which led to dysfunction in the smoker and miner was the same, the problem in relation to the proof of susceptibility would solve itself Having considered the extent of the variability in the effect of mine dust and found that it exists, it is necessary to consider how susceptibility to mine dust and cigarette smoke may in fact interrelate. This question is crucial in that the end point is to apportion in the individual smoking miner how much of the loss of lung function was due to the effects of smoking on the one hand and to exposure to mine dust on the other.

If the two susceptibilities do not overlap, in that a person who is susceptible to mine dust may not be susceptible to cigarette smoke (which is the antithesis of "the common causal pathway"), the problem becomes how an individual smoking miner can prove that his loss of function is due to his susceptibility to mine dust rather than, or even as well as, cigarette smoke. All such an individual would be entitled to recover, because that would be all he had proved, would be that he had suffered the average loss due to his exposure to dust - a relatively small amount compared to what would be available under Dr Rudd's matrix or any similar approach. The key, therefore, is whether the Plaintiffs have shown that there is a common causal pathway.

Does the proposed pathogenesis of emphysema help? It is an area which is of importance to both parties. If the Plaintiffs can demonstrate a plausible mechanism for the development of emphysema which is consistent with either smoking or dust as the cause of the emphysema, this would be evidence upon which the court could find that a common pathway existed. British Coal on the other hand submitted that the evidence did not point in that direction. It appeared to be common ground that the mechanism whereby smoking causes emphysema is incompletely, albeit increasingly, understood. It was also common ground that less work has been done in relation to the physiology of the causation of emphysema by dust. The plaintiffs could submit that Dr Stockley was prepared to accept that both plausible mechanical and biochemical mechanisms for mine dust causing emphysema existed.

On behalf of British Coal it was submitted that when considering the comparative patterns of susceptibility, the epidemiological studies were of no help. The submission proceeded to argue that to attempt to equate the patterns of susceptibility between smoking and mine dust was to make an unwarranted assumption, at least in the absence of sufficient evidence that the aetiology of the impairment of lung function caused by both insults was similar. British Coal point to the evidence on mechanisms of the pathogenesis of emphysema above, and submitted that it did not come near to establishing that there was a common pathway.

British Coal further submitted that there was evidence from Dr Coggon which effectively accepted that the analogy with smoking was made not on the basis of any positive evidence but rather as an assumption in default of any positive evidence. He was asked whether there was evidence that on balance of probabilities the effect of dust was analogous to smoking and replied:

It is a very different situation from some of the other things we have been discussing.

I can conceive a situation that in theory a new study might come out next year that would completely change where my judgment lay on that question, whereas I think it much less likely that a new study would come out that would alter my judgment on whether or not dust causes a reduction in FEV₁, because there is much more consistent evidence underlying that judgment.

This was a thoughtful answer which implied, as I interpret it. that he thought that 'on balance' the two insults produced analogous effects.

In his written evidence Dr Britton had said:

It is not necessarily valid to assume that susceptibility to one insult (smoking) is necessarily a marker of susceptibility to another (coal dust), but in the absence of evidence that an alternative procedure is more appropriate, it is reasonable to apportion coal dust and smoking effects [using average effects].

On behalf of British Coal their case was summarised in the following terms:

The logic of the argument for drawing an analogy between dust and smoking is flawed. To assume a common pattern of susceptibility to dust and tobacco smoke, in the absence of direct evidence, could only be reasonable if some ground could first be demonstrated for believing that the patterns were more likely to be the same than to be different. The "common pathway" is the only ground that has been suggested but is itself a matter of speculation which has not been proved.

The argument by analogy is potentially seductive. If what is being examined is emphysema as a distinct pathological condition, rather than a functional description which fits a number of differing, yet similar, pathologies, then if it is proved, as Fletcher has shown, that there is variability of decrement of FEV₁ to tobacco smoke, if the underlying pathology is the same when mine dust also causes loss of lung function, then it is logical to argue (by analogy) that the range of variability should be the same. Therefore the plaintiffs' cases would be assisted by showing a common pathway available both to tobacco smoke and mine dust as having a comparable effect in the susceptible population. Dr Coggon's evidence was to the effect that if different members of a group were susceptible to either dust or smoke but not both it would create problems for the theory of the common pathway.

The preponderance of the evidence has been directed towards establishing the probability that exposure to mine dust is a cause of loss of lung function in a minority of miners and that its effect is not limited to an even (mean) effect across the whole population of those who have been engaged in underground mining over their working life, as British Coal had contended. Equally the preponderant effect of the evidence has been to satisfy me that among the minority of miners so affected, there is both susceptibility and a significant range of variability of response or effect of exposure to dust. This finding is the crucial finding on this part of the litigation. It should perhaps be clarified by saying that it involves of necessity rejection of the contention advanced on behalf of British Coal that there is a separate pathological entity that goes under the name or description of focal dust emphysema.

Summary of findings on the Generic Medical Issue

My findings are as follows:

1. Coal mine dust (coal and stone) is a cause of centriacinar emphysema;

2. Such emphysema may, and usually does, lead to loss of ventilatory capacity most easily demonstrated by loss of FEV₁;

3. Confirmation that the causes and effects of tobacco smoke are as in findings 1 and 2 above;

4. It is probable, but not certain, that there is a common causal pathway to both cigarette and mine dust induced emphysema which usually gives rise to breathlessness;

5. Whether 4 is established or not, the effects are generally the same in that there is a spectrum of effect which in the majority is not clinically detectable but in the minority does produce a range of effects from simple impairment, frank disability and occasionally death.

6. In the individual smoker it is not possible to attribute the cause of breathlessness either to the one insult or the other, this is so whether or not there is a common pathway.

The legal consequences of these findings will be discussed under 'Apportionment'. The clinical consequences will be next discussed.

The Effects of Smoke and Dust on Ventilatory Capacity

Having explored the matter in evidence, particularly with Dr Britton, the parties have agreed that, on average, a person who smokes 20 cigarettes a day for 1 year [defined as "1 pack year"] will lose 15 ml of FEV₁ per year. Predictably, however, the parties do not agree on the size of the average dust effect. The studies to which reference has already been made which look at the relationship between FEV, and exposure to dust have all calculated what is the average effect of dust. As is to be expected, all of these studies throw up different figures. This question was also explored in the evidence from a different angle, by a search for evidence which could support the qualitative proposition that "average smoking equals heavy dust". In his main report Dr Rudd devised a matrix which sought to allow for the allocation of the losses of lung function as between smoking and dust. This matrix was based on the proposition that loss of lung function can be apportioned equally between smoking and dust if a person is an average smoker and has been heavily exposed to dust. British Coal chose not to cross examine Dr Rudd on his matrix. Instead they later referred to and relied upon the matrices prepared by Professor Berry which were based on different philosophies and which, it has to be observed, were not even in being at the time when Dr Rudd was giving evidence. Having considered all evidence, the best judgment on this issue that I can make is that the average loss in the dust susceptible will be a figure within the range 100 to 150 ml per 100 ghm^-3 say 125ml per 100 ghm^-3.

There, the parties effectively left the problem in the hands of the court with the implication in the invitation to 'do the best it could'. For the reasons developed in the section on Apportionment, although there has to be an element of 'broad judgment' in fixing the apportionment in the individual, it is possible to incorporate some methodological input into the process. That input is a reflection or distillation of the processes which led to the production of the matrices described in the reports of Dr Rudd and Professor Berry. Having examined the merits of each approach, Dr Rudd's is to be preferred. His matrix, to the extent that an estimate of the relative effects in any individual miner is required, was worked into, but not be decisive of, the apportionment since there are the other elements such as limitation and non-tortious exposure that have to be taken into account.

IIAC

In 1985 the Industrial Injuries Advisory Council ("IIAC") decided to investigate whether to recommend that the Secretary of State should prescribe the disease of bronchitis and emphysema in coal miners for the purposes of what has now become the Social Security Contribution and Benefits Act 1992. Its first report in 1988 IIAC concluded that although it was satisfied that exposure to coal dust can cause airflow limitation which is proportionately related to the level of dust exposure, the evidence suggests that in most cases, if not all, airflow limitation due to coal dust has only a small effect on FEV₁ and breathing capacity which is difficult to detect and measure reliably. It went on to say that on the current evidence, it could not say that occupational causation can be presumed with reasonable certainty in individual cases. This is because it is impossible to distinguish between airflow limitation due to smoking, which is the commonest cause of bronchitis and emphysema, and the probably smaller effects of occupational dust exposure. Among smoking miners, it is far more likely that any airflow limitation is due to smoking than to dust exposure. There is insufficient evidence on non-smoking populations for accurate assessments to be made of the effects of dust exposure alone. The Council's report ended with the plea for more research into this subject.

Such new evidence was in existence so that in 1992 it issued another report. This new evidence, in particular Marine (1988) led it to conclude that the new studies have provided answers to the questions addressed in its previous report. They have demonstrated that cumulative coal dust exposure is associated with a clinically important reduction in FEV₁ in both smokers and non-smokers, that coal dust has an important effect independent of tobacco smoking and that the risk of disabling loss of lung function is increased by more than two-fold in both smokers and non-smokers.

It was, therefore, recommended: "that chronic bronchitis and emphysema be prescribed in relation to current and past coal miners who have worked underground."

As the positioning of this section in the judgment suggests, IIAC's considerations is included as an interesting postscript to what has come before. The findings that have already been made were made without any need to rely on the conclusions of IIAC and therefore it is unnecessary to make express findings in relation to the above submissions. It is reassuring to find that IIAC have reached the same conclusions albeit they followed a substantially different intellectual, procedural and legal path in so doing.

Asthma

That asthma can be a potent source of loss of ventilatory function is not in issue in this case. What the contest has represented has been the contention that long exposure to a low dose irritant can lead to the development of asthma and its refutation by Dr Pearson who went only so far as to agree that there may be instances of temporary exacerbation, with the emphasis on temporary, while hotly contesting that chronic exposure at low dose can have any long term or lasting effect. There is an additional complicating factor which originates from the undoubted occurrence of what is termed 'late onset asthma' in which the condition will manifest itself, not in childhood as is the most frequent case, but in adulthood.

Only one of the individual plaintiffs (Griffiths) has been diagnosed as suffering from asthma. Dr Rudd was cautious about expressing any views on causation in relation to exposure to coal mine dust and preferred to leave the subject of asthma to Dr Howard who had examined a number of the individual plaintiffs and had made a contribution to the Generic Medical Report.

Dr Howard's evidence was to a large extent empirical and based on his personal experience working as a chest physician in Sheffield (workers exposed to steel working as well as coal mining). But this is not to say that he did not also refer to and rely upon a number of studies to support his opinion. It became manifest that he was greatly influenced by the results of his own clinical observation carried out over a period of nearly 35 years. Dr Howard thought that occupational asthma could be caused either by sensitisers which will provoke an allergic response or by irritants. There is no evidence in this case to support a non-irritant agent as a potential cause of occupational asthma. His understanding of the learned papers on this topic was that their authors were cautious about the possibility whether or not the existence of the low dose lung disease resulting from particular occupational conditions could properly be made. However, the main review paper by Kipen was reviewing only 10 cases of the low dose irritant type. The authors recognised that further prospective studies would be required to "examine the significance of the association for the development of occupational asthma. " Such is awaited.

Dr Howard would not accept that the Kipen paper was merely anecdotal and thought that it was based on clinical observation. It became apparent that Dr Howard's approach to the topic was, understandably, heavily conditioned by his clinical experience for which there was little scientific literature to support.

On the evidence to which I listened, not enough is known about the causes of occupationally induced asthma to justify a finding that there is a type which, as distinct from other respiratory conditions, results from exposure to chronic low dose irritants.

The Law

The magnitude of effect of dust on lung function is a subject much debated in evidence and argument. If, as is my finding, men are not only susceptible to but also show variability of response, there remains the problem what is the range of that response and whether or not it is possible to ascertain the limits of what that response might be in an individual. There is the further point as to the extent to which it may give rise to clinical disability. It is only in relation to this last point that, in a sense, this case is concerned. Given that tobacco smoke and dust induced obstructive disease may both lead to decrement in FEV₁, the problem can be seen to be a difficult one to resolve but whether it is the one or the other or both and in what proportions is what gives rise to the principal legal difficulty in the case. The problem is not special to coal miners, it is inherent in cases where occupational hygiene is involved and claims for damages are made where exposure has been to more than one agent of the disease in question, but in respect of one only of which a claim may lie. For the purposes of the present discussion it must be assumed, as I have found, that British Coal, in general failed, throughout the greater part of its life to do what it reasonably should in the way of reducing the exposure of miners to coal mine dust. The evidence has also shown that, at one stage at least, more than 80 per cent of working miners were also tobacco smokers. The majority of the individual plaintiffs in this litigation have also been tobacco smokers. For present purposes, it will be assumed that the causes of their ventilatory deficiency were tobacco smoke, non-tortious as well as tortious exposure to mine dust. By non-tortious exposure is meant that exposure which could not have been avoided if reasonable care had been exercised. How is the court to decide the answer to the problem given that a plaintiff has to prove, on balance of probabilities, that the injury of which he complains was caused by one or the other or both possible concurrent causes? The position where the cause is exclusively one. rather than another or others, is different and, as will be seen, more easily solved.

The disparate nature as well as the number of different factors present in most of the individual cases in this litigation means that any precision in seeking to apportion loss of lung function between tortious / non-tortious / time barred and tobacco is a most difficult exercise which, if it can, should only be approached on a very broad basis.

The basic submission of British Coal was that loss of lung function is one continuous process with numerous pathogenic causes from which, according to the evidence, the Court had to choose. Hence, whereas dust, smoking and other causes may contribute to the overall deterioration by a variety of mechanisms their contributions are distinct and additive. In summary British Coal's submissions may be simplified and reformulated in terms that as a matter of law the defendants may only be found liable to an individual plaintiff if:

Any smoking plaintiff (past or current) can prove that dust exposure has caused him to suffer deficiency of lung function. Since, in any such individual case there are no biological markers to indicate susceptibility, let alone variability those cases must fail.

The plaintiffs' submissions while recognising and adopting the principle in Bonnington Castings v. Wardlaw [1956] AC 613, relied heavily on McGhee v. National Coal Board [1973] 1 WLR 1 and, in particular a passage in the speech of Lord Simon of Glaisdale in which he said:

... that where an injury is caused by two (or more) factors operating cumulatively, one (or more) of which factors is a breach of duty and one (or more) is not so, in such a way that it is impossible to ascertain the proportion in which the factors were effective in producing the injury or which factor was decisive the law does not require the Plaintiff to prove the impossible, but holds that he is entitled to damages for the injury if he proves on a balance of probabilities that the breach or breaches of duty contributed substantially to causing the injury. If such factors so operate cumulatively, it is, in my judgment, immaterial whether they do so concurrently or successively

It may be important, however to note the words of qualification, underlined for this purpose in the above passage, for the question at issue in this litigation may be just that - whether coal dust exposure and tobacco smoking did operate cumulatively. It will be remembered that in only a minority of smokers and of miners will susceptibility to the adverse effects of either or both be found to exist. The plaintiffs then submitted that

Where the relevant exposure had increased the risk of contracting a disease but medical science does not enable the experts to identify the process of causation then a Court is entitled to infer that increasing the risk of a disease is equivalent to causing the disease, McGhee.

The plaintiffs' main submissions were that in each individual case there is sufficient expert evidence to enable the court to find that tortious exposure has made a material contribution to injury. Their submission was put in broad terms and was to the effect that all that any individual had to show was that he suffered a diminution of lung function by reason of COAD (to which exposure to coal dust had made a more than minimal contribution). In contrast British Coal's developed submission was that the litigation was not only dealing with causes which result in a single disease but also was dealing with a variety of causes which have a number of different physiological effects, albeit in the end result it came under the umbrella of COAD or 'breathlessness'. That said, the plaintiffs' was a restricted (?unrealistic) position. What the court was concerned with was damage and function, not physiology. It was submitted by Mr Brown, in particular, that assistance could yet be obtained from McGhee since those parts of it which survived Wilsher v. Essex AHA [1988] AC 1074 suggest that what it decided, in its robust common sense way, was that, given the increased risk (of the development) of dermatitis from the delayed washing, the court was entitled to infer that that delay did in fact cause dermatitis.

Lord Kilbrandon in McGhee said:

My Lords, the facts relating to the nature and conditions of the pursuer's work, to the facilities provided by the defenders and to the pursuer's having contracted an industrial dermatitis in consequence of those conditions or work, are undisputed. Medical science has, however, not yet been able to provide an indubitable account of how those conditions actually give rise to that disease, although the fact of causation is, according to the evidence in this case, unanimously accepted.

It is, in the present state of medical knowledge, impossible to say that if the pursuer had taken a shower he would certainly not have got the disease, and it is equally impossible to say that another man, in exactly the same case as the pursuer, would on the contrary certainly have got it.

In that state of facts, what the pursuer has to establish, as a condition of his substantiating a claim against the defenders, is that their admitted breach of the duty which they owed to him caused or materially contributed to the damage which he has suffered. He has proved that there was a precaution, neglected by the defenders, which, if adopted by them, as their duty in law demanded, would have made it less likely that he would have suffered that damage. The argument against him, as I follow it, is that that only shows that the provision of a shower bath would have reduced the risk of injury: it does not show that in his case he would more probably not have contracted the disease had the bath been provided.

It would have been possible to state the argument in this way: "The pursuer cannot show that it is more probable than not that, if a shower had been provided, he as an individual would not have contracted dermatitis. Therefore it is impossible to say that the defenders were under a duty to him as an individual to supply a shower; A cannot have owed to B a duty to take a precaution the absence of which B fails to show probably caused him injury. " The duty can only be examined in relation to the individual who complains of the breach of it; it is not owed to him as a mere potential victim of dermatitis; and this is unaffected by the fact that other men, for reasons we do not understand would not have required the benefit of the precaution.

But once the breach of duty to the pursuer has been accepted, this argument seems to me to become untenable. It depends on drawing a distinction between the possibility and the probability of the efficacy of the precautions. I do not find it easy to say in the abstract where one shades into the other; it seems to me to depend very much upon the nature of the case. This is a case in which the actual chain of events in the man's body leading up to the injury is not clearly known. But there are effective precautions which ought to be taken in order to prevent it. When you find it proved (a) that the defenders knew that to take the precaution reduces the risk, chance, possibility or probability of the contracting of a disease, (b) that the precaution has not been taken, and (c) that the disease has supervened, it is difficult to see how those defenders can demand more by way of proof of the probability that the failure caused or contributed to the physical breakdown.

It can be said that the injury in McGhee, which was dermatitis, was one and indivisible. But there were two possible and non-exclusive causes for its occurrence, one non-tortious one tortious. In the present case, on one footing it may be said that there was one injury, namely breathlessness, the physiological basis of which was emphysema or small airways disease either of which was the cause of the breathlessness. The risk, chance, possibility or probability of a plaintiff developing the condition of breathlessness would have been reduced had the relevant precaution been taken which it was the defendants duty to have done. On this analysis the present case falls precisely within the contemplation of Lord Kilbrandon as one in which it is difficult to see how those defendants could demand more by way of proof and which precisely echoes Dr Rudd's pragmatic approach:

A. on the basis of epidemiological evidence about the risk in groups of subjects who smoke, we do not hesitate to say the balance of probabilities strongly favours this man's cancer having been caused by smoking.

Q. But is that in the absence of any other findings? Suppose you had a smoker, if it is possible, who did not develop emphysema or bronchitis, but nevertheless dies of cancer. Would you then still hold that the probabilities were that his cancer death was related this smoking?

A. Certainly. Whether or not he had bronchitis or emphysema would be regarded as irrelevant to the association between smoking and his cancer.

as being appropriate in the context of the findings already made in this litigation from the epidemiological evidence in regard to susceptibility.

In his submissions for the plaintiffs Mr Allan chose as his starting point an answer given by Professor Berry towards the end of his evidence in chief when he was asked about the paragraph 10.3 in the Generic Medical Report where he had written:

The discussion above has been in terms of epidemiological evidence. This is, whether effects can be demonstrated on a group of miners. Since it is not established, by any conventionally accepted epidemiological standards, that dust exposure leads to any disablement in a group of miners it follows that exposure cannot be implicated in any individual. Further, even if it were established that dust exposure may result in a small minority of miners becoming respiratorily disabled, it would not in any way be possible to establish that any individual's disablement was wholly or in part a consequence of exposure because of the other possible causes of disablement and the fact that even in non-exposed men a proportion become disabled.

about which, at the conclusion of his evidence in chief, he said:

I think, my Lord, something could be added to it, to the effect that, since it is established that there is an effect of dust exposure on lung function, then there would be a contribution of exposure to coal mine dust, on the loss of FEV in an individual and, in particular, there would be a contribution of the coal mine dust to the total loss in individuals who may have suffered such a great loss as to be classified as disabled. But it would not be possible to identify for any individual what the extent of the coal mine dust was on that individual other than in average terms. Some individuals may have suffered a greater loss due to coal mine dust; some may have suffered a lesser loss, but it would not be possible to say which was which.

Q. That is an inherent consequence of any epidemiological study, that it considers the effects in a group that does not assist except in terms of probability, so far as the individual is concerned?

A. I think that is the point, my Lord. It only assists in terms of probability, yes.

The cases of Bonnington and McGhee make it clear that the identification of the pathological route from tortious exposure to causation is not a pre-requisite to recovery. It is tempting at this stage to resort to robustness and pragmatism to find the answer to the problem under consideration. Having listened to evidence over many days, in part anecdotal from miners themselves, in part epidemiological, it would be easy to accept the intuitive solution and arrive at the general conclusion that exposure to mine dust is a cause of the breathlessness suffered by miners with respiratory disability, whether they had been smokers or not. But the temptation should be resisted. The same result can, however, be reached by a jurisprudential and analytical approach which stands up to examination. This can most efficaciously be done by formulation of a number of propositions, always mindful that the feature which unites all present cases, other than the asthmatics, is that they are a selection of man who have all suffered both loss of lung function and have been exposed to tortious mine dust to greater or lesser extent. At its most favourable to British Coal's case:

1. Out of a cohort of miners only a proportion will suffer from breathlessness, in other words those who are not susceptible will all have been excluded from consideration since by definition they have demonstrated no loss of lung function.

2. The same can be said of smokers.

3. In the present litigation we are only concerned, therefore, with a selection of men who are susceptible to the effects of either or both tobacco smoke and dust.

4. It is in relation only to these susceptibles that the question is whether or not they have proved that tortious mine dust has made a more than minimal contribution to the cause of their breathlessness.

5. Consider:

a. the defendants' concession as above

b. Professor Berry's 'reformed' view on paragraph 10.3 of his original report

c. mine dust makes no distinction between smokers and non-smokers.

d. that the risk of becoming breathless would have been materially lessened had the defendants complied with their statutory duty

6. In these circumstances, applying the appropriate forensic standard of proof, the answer must be that in any case in which a smoking miner who has been subject to heavy dust he is more likely than not to have had a significant contribution to his breathlessness made by that exposure.

7. In the case of non smokers, their position is a fortiori.

8. Recognition that there will be some miners who will have started life with a below average lung function does not weaken the argument. It should be assumed, unless there is evidence to controvert it, that all individuals will have started with average lung function. Whether this is so or not will not affect the issue, since if a man started with low lung function, he will finish with an even lower function due to the effects of dust or smoking.

In narrative terms, then, an individual miner who can prove that he has been exposed to tortious as well as non-tortious mine dust and suffers from breathlessness the law will not demand more by way of proof than that that breathlessness has been, at least in part, caused by his exposure. In this way the common law demonstrated how it has been able to adapt to modern conditions where circumstances, such as those which occur in cases of occupational hygiene, have arisen and were not foreseen when the origins of tort based recovery were developed.

Apportionment:

The consequence of this analysis is that the question of apportionment has now to be addressed. Just as in the cases of Thompson v Smiths Shiprepairers (North Shields) [1984] 1 QB 405 and Knox v. Cammell Laird Shipbuilders [unreported transcript 30^th July 1990] there arc here many imponderables which defy any precise attribution of effect to one cause or another. These variable can be listed:

1. Non tortious exposure)

2. Tortious exposure)

how much and for what period?

3. Smoking)

4. Exposure prior to expiry of limitation )

5. How should the marginal impact of tortious dust on lung function be reflected in the award of damages? This is the eggshell skull factor.

What is I believe, beyond question or serious argument is the fact that apportionment cannot be satisfactorily achieved by reliance on numbers, whether they be of the exposure to dust from day to day, to year to year, or over the whole period of employment. No more can numbers suggest, let alone dictate, what impact a known, and tortious unquantified dust exposure will have on the ventilatory capacity of any individual. Nor yet is it possible to arrive at any measured extent by which dust at any given moment or over an extended period exceeded the non-tortious quantity - whatever amount that might be. All these considerations must ineluctably impose on the court the solution sometimes praised, sometimes vilified and most often not fully understood that the solution is to be found as an answer to a 'jury question".

In reaching the conclusion that this is a case for apportionment I do so only in those individual cases in which the evidence has been sufficiently probative to satisfy me that:

1. An individual was exposed to tortious dust to a material extent;

2. Such individual was susceptible, in the sense discussed above.

3. Such individual has suffered from breathlessness where the underlying pathology was emphysema;

But there has to be excluded from the total impact of these factors on the individual, the effccts of:

A. tortious but non actionable (as excluded by limitation) exposure prior to 6th June, 1954

B. non-tortious exposure

C. smoking.

In any given case there will be variables of 1, 2, 3 as well as A., B., and C. The result must be one which fairly reflects the circumstances of any individual plaintiff. Where it is possible provide any indication of a factor which the evidence shows to have been of particular importance in the assessment in the case of an individual, that will be shown. What is important to recognise in all cases is that anything approaching mathematical precision is beyond the grasp of a trial process which has extended its enquiry at its longest to events as they occurred over 60 years, on some occasions, and between 40 to 50 years in many instances and long before precise methods of measurement were available and reliable records were made.

What constitutes actionable personal injury?

The relevance of the answer to this question for the purposes of this litigation is twofold. (1) First it goes to the issue much pressed by British Coal, whether chronic bronchitis according to the MRC definition is properly compensatable or not. (2) Secondly, it goes to the proper application of the Limitation Acts.

(1) Chronic bronchitis:

The MRC definition need not be repeated, although should be kept near at hand. Throughout the trial, British Coal's position was that the hypersecretion of mucus and expectoration (a necessary ingredient of the definition) are natural defensive bodily functions arising in response to a given stimulus - dust. Just as it was said sweating is the response of the body to heat or hard exercise. The dust which is the cause of the mucus hypersecretion is expelled from the body by a natural process, the condition is transitory so that when no longer exposed to insult and expectoration is complete, the body is returned to the condition in which it was before the insult (coal dust) was applied. Just as with breathlessness, so with chronic bronchitis. It was further contended that even if chronic bronchitis is a compensatable injury, the evidence is insufficient to enable the court to make the determination that it is mine dust not, rather than, smoking which is a cause of the condition. This argument only applies in relation to dust for there is abundant, unchallenged, evidence that smoking can be a cause of chronic bronchitis.

British Coal's argument rests on the premise that the MRC definition of chronic bronchitis is an artificial functional description and not directly related to whatever the true underlying pathology may be.

The argument proceeds that in chronic bronchitis the effects of dust and smoking, unlike in emphysema, are not necessarily additive, in that chronic bronchitis may reach the end state simply by exposure to one insult, in which case, the imposition of a separate potential and causative mechanism can be of no further effect. British Coal founded themselves on the evidence of Dr Morgan for the argument that chronic bronchitis is a condition of rapid onset (two years, or so) followed by only modest worsening over the succeeding years. Dr Morgan's evidence was such, as upon which, I have said, I am not prepared, to base my decision unless there be other evidence to support it. I reject it for this intrinsic reason, and also because it is inconsistent with other evidence which I can accept notably Dr Rudd, see later. British Coal then resort to the case of Jobling Associated Dairies [1982] AC 794 for the submission that a smoking miner:

would have developed the same or similar response as a consequence of his smoking even if he had not been exposed to the dust, in which case.....either the claim should fail altogether or recovery should be on the limited basis that the condition occurred slightly earlier than it would otherwise have done.

Since British Coal have made a parallel submission in respect of emphysema, this is a convenient moment to examine the decision of the House of Lords in Jobling. In my judgment Jobling's Case does no more than establish for the defendants that, where a supervening event would in any event have curtailed a claim for loss of future earnings arising from a compensatable tort, the court must reflect that in the basis upon which it assesses damages for future loss, no more and no less. If and to the extent that chronic bronchitis may be attributed to mine dust or smoking, subject to the major consideration whether it is compensatable at all, the court's approach to the award of compensation should be by way either of apportionment or that adopted in Bonnington.

The plaintiffs submitted that the defendants' reliance on Rae (1971) table 4, did not support the case which the defendants were seeking to make and also ignored what appeared clearly appeared in table 5, (see the main judgment). Table 4 showed the percentage of men with bronchitis by dust exposure, age and smoking habits. It can be seen that it is only in the highest age and dust exposed groups that there is any flattening of effect from increasing dust. In table 5 which shows the incidence (new cases) of bronchitis, it is demonstrable that it continues at much the same rate in all dust and age groups. It was further submitted on the plaintiffs' behalf that the argument that there was any burden resting on the plaintiffs to quantify and separately apportion the effects of mine dust and smoking was wholly unrealistic. I would merely add that any such submission was at variance with the approach of the two first instance decisions of Thompson and Knox. While plainly not accepting that the court should rely on Dr Morgan's evidence that chronic bronchitis being a phenomenon of "early effect" the plaintiffs rely upon two passages in the evidence of Dr Rudd. On day 38, Dr Rudd said:

those with heavier dust exposure develop their bronchitis earlier than those with lower levels of dust exposure on average.

When pressed further about the so called "earlier effect of dust". Dr Rudd was asked

Q. But it is an early trend, is it not, in the sense that it affects these particular age groups; "earlyish" perhaps is a fair way of putting it?

A. It depends how one defines "early", does it not? We are talking about the 35-44 age group, if that refers to, for example, a Welsh miner, he may have been underground for 25 or 30 years which is not particularly early in the terms of a working lifetime.

Table 4 showed that prevalence of chronic bronchitis in both smokers and non smokers doubles between the youngest and oldest age groups. Not only has Dr Morgan's evidence in general been seen to be unreliable, here, in particular, it has been seen to be at odds with what is clearly shown in Rae (1971) and Dr Rudd's sensible interpretation of it. This part of the defendants' proposition is as unrealistic as it is untenable.

The defendants sought to rely upon selected passages from the evidence of Dr Rudd in the context of the argument whether chronic bronchitis can constitute actionable damage. I am moved to say that this was not an argument which embraced cogency or realism. On day 37, Dr Rudd said in answer to the questions:

Is that developing a point that we touched on previously, the fact that you can have mucus production which does not manifest itself in expectoration?

A. That is the point they are making.

Q. Is that a point you agree with?

A. It is a point which I would accept, yes, although I would suspect that there is a good correlation between mucus production and expectoration.

Q. As expected --

MR JUSTICE TURNER: In the ordinary way you would expect that with excess mucus production you would get expectoration?

A. Yes.

Q It is the body acting as it is intended to act.

A. Yes.

In the course of submissions I was emboldened to offer a definition of what should be held to constitute personal injury which takes into account both medical 'lore' and the requirements of the law relating to personal injury - illustrating that although the two systems make use of the same words, they do not always use the same language. But there is, or may be, more to the condition than simple mucus hypersecretion and expectoration.

The plaintiffs did not seek to improve upon the proffered definition of actionable 'personal injury' as a being a condition of the body that:

represented more than passing and minimal discomfort as the result of tortious conduct.

Such, I believe is not only consistent with previous authority, but also meets the juridical needs of the present case. Since the leading case of Phillips v. London and South Western Rly Co (1879) 4 QBD 406 the concept of what constitutes injury sufficient to qualify as an accrual of a cause of action has been consistently held to be:

The bodily injury sustained; the pain undergone; the effect on health of the sufferer. according to its degree and probable duration as likely to be temporary or permanent.

Such a proposition is also consistent with that class of case, which is not easily classifiable as 'personal injury' but recognisable as such under the generic description applicable to the holiday type of case - discomfort and inconvenience.

In my judgment, the production of excessive quantities of mucus with associated frequent bouts of coughing or expectoration as the result of exposure to dust or other irritant if "more than trivial" is capable of constituting personal injury sufficient to found a cause of action. I hold, therefore, that subject to these qualifications chronic bronchitis is capable of constituting injury, in respect of which an action may properly lie. This decision is consonant with that reached by the Court of Appeal in Tanner's Case above, although I respectfully think that it is not so predicated.

(2) Limitation

There is first an historical context. Under the Coal Industry Nationalisation Act, 1947 provision was made for the liabilities of the independent colliery companies to become vested in the defendants. For a reason that is difficult to fathom so long after the event, the necessary Order in Council which was needed to bring that provision into legal effect was either not drawn up or not laid before Parliament. In the result no liability exists in the defendants in respect of any of the present claims for any act or omission of the defendants' predecessors before 1^st January 1948.

British Coal's position was that since it is not possible to reach with any confidence the conclusion that mine dust inhaled before 4th June 1954 caused injury only on or after that date, any cause of action based upon excess dust exposure prior to 4^th June 1954 is therefore time barred. It was for the plaintiffs to prove that the damage of which he complained occurred within the relevant period. The origins of the significance of the 4th June 1954 are to be found in the Limitation Acts passed successively in 1939, 1954, 1963 and 1975 and in the decision in Arnold v. CEGB [1988] 1 AC 228. There, as the head note shows, it was held per curiam:

(ii) The Limitation Act 1963 does not deprive any defendant of a time bar which has accrued on the expiry of the six-year limitation period prescribed by section 2(1) of the Limitation Act 1939 in its original form which, by virtue of section 7 of the Act of 1954, continues to govern any cause of action in a personal injury case accruing before 4 June 1954 (post, p. 271D-E).

British Coal have not taken, or do not press, the point that any should fail because injury or relevant injury was caused more than three years before the date of the issue of the writ. The point which British Coal have made is that, if it be accepted that mine dust can be a cause of respiratory dysfunction, the process which leads to disability is cumulative from the day upon which the first particle of mine dust settles in the lung and which the natural responses of the body are unable to repair. The process being cumulative, the lung starting off with ample reserve (from age about 25 onwards when most have achieved maximum capacity) it takes time for the reserve to be eroded and for symptoms to appear. But in Cartledge v. Jopling [1963] AC 758 it was held that lack of knowledge of damage did not mean that damage or, more precisely, accrual of cause of action for the purposes of Limitation Acts, had not occurred.

There is no evidence from any doctor or medical record that any of the plaintiffs (which for this purpose are taken to include the deceased) had ever shown symptoms or signs of disease before the cut-off date. 'Not good enough' said British Coal since the plaintiffs' whole case is that the effect of dust is cumulative. Given that this was, indeed, the case made on the plaintiffs' behalf and amply demonstrated by the impressive evidence led on their behalf, the applicable law as to the burden of proof in such circumstances is as set out by Lord Pearce in Cartledge:

I agree that when a defendant raises the Statute of Limitations the initial onus is on the plaintiff to prove that his cause of action accrued within the statutory period. When, however, a plaintiff has proved an accrual of damage within the six years (for instance, the diagnosis by X-ray in 1953 of hitherto unsuspected pneumoconiosis), the burden passes to the defendants to show that the apparent accrual of a cause of action is misleading and that in reality the causes of action accrued at an earlier date. As, however, the judge found that [Mr] South was in fact suffering from pneumoconiosis in 1950, the question of onus was not a deciding factor.

There has to be some apportionment in relation to dust exposure prior to the cut-off date. Such apportionment will reflect the fact that, in the now accepted state of the evidence, no plaintiff actually suffered from the effects of incapacity for which such exposure had conditioned him. It follows that although at the cut-off date there was no way in which clinical or X-ray examination could have revealed injury or provided direct evidence that such had occurred, the overwhelming inference is that the injury or disease process had in fact already begun at or shortly after the time when the men were first exposed to dust burdens underground.

The Individual Plaintiffs

The full judgment runs to a further one hundred and fifty pages. For a description of the working conditions in the various collieries where they were employed reference should be made to page 322 onwards. Likewise for a full description of their individual medical complaints reference should be made to the same section of the judgment. For the purposes of this summary a schedule has been prepared which shows my key findings:

Plaintiff	d. o. b.	Employed by British Coal	Suffers from due to exposure to coal dust	Dust exposure Category	Smoker	General Damages (£)[1]	Apportioned sum (£)
A.C. Griffiths	12.02.44	1960-1989	-	-	Non	5, 000	-
M. A. Rees	03.04.41	1956-1985	emphysema symptomless pneumoconiosis chronic bronchitis	245 ghm-3 is a serious under-estimate	Average - gave up 1977	30, 000	8, 750
E. G. Jones	17.08.26	1941-1977	emphysema pneumoconiosis	High	Non	32, 500	9, 000
E. Jones	05.12.16	1930-1978 undergroun d 1935-	emphysema chronic bronchitis pneumoconiosis	High	20 a day until 1984, since then an average of 10 a day	40, 000	3, 200
S. R. Wells	18.08.23, died 10.08.94	1937-1980	emphysema chronic bronchitis pneumoconiosis	Very high	50 yrs at 10 cig/day	32, 500	4, 875
R. Liddle	07.09.29 died 22.09.96	1943-1977	emphysema chronic bronchitis pneumoconiosis	Exceptionally high	5 cig/day, occasionally 10.	35, 000	12, 600
K. Williams	24.05.38	1955-1985	chronic bronchitis pneumoconiosis (borderline) emphysema	Thurcroft: Very high Treeton: No finding	20 cig/day, until 1983, then reduced consumption, finishing in 1985	40, 000	7, 000
R. Clay	28.07.16	1932-1978	-	Average	5-8 cig/day	8, 000	-

Note 1   if British Coal had been held liable for all injury. Note: special damages await computation.    [Back]