Bannister v Freemans Plc [2020] EWHC 1256 (QB) (Part 3 of 3)

This is the third and final post on Bannister v Freemans Plc, written by Michael Rawlinson QC with the assistance of Samuel Cuthbert. This post deals with the topic of epidemiology.

The three parts of this blog series can be viewed and downloaded in one PDF by clicking here.

The test promulgated by the medic

Dr Rudd is immensely experienced. The test which was adopted by the Court had been first put to him in cross examination by Mr Platt QC in the case of Sloper. He agreed with the formulation. The same happened again in Bannister. I will deal with the test in three stages:

(a) As a proposition of law;

(b) As a matter of practicality;

(c) The use of epidemiology.

The difficulty in adopting the test can swiftly be put: it is no more permissible to tie the what is de minimis question (which is, after all, an issue relevant to both breach and causation) to the notion of ‘an average response to worrying news’ than it is to assume an average strength and thickness of a skull where the skull has been negligently struck. The relevant passage from Clerk & Lindsell (22nd Ed – 2nd Cum. Supp) 2-166 to 2-170), viz.

“2-166 The Eggshell Skull Rule Long before Wagon Mound, it was an established doctrine that a defendant has to take his victim as he finds him, which means that if it was reasonable to foresee some injury, however slight, to the claimant, assuming him to be a normal person, then the defendant is answerable for the full extent of the injury which the claimant may sustain owing to some peculiar susceptibility. The rule applies only when the claimant’s pre-existing hypersensitivity is triggered into inflicting the injury complained of…2-169….The Canadian courts refer to such cases as “crumbling skull” cases. In Athey v Leonati571 the Supreme Court of Canada observed that: “As long as a defendant is part of the cause of an injury, the defendant is liable, even though his act alone was not enough to create the injury. There is no basis for a reduction of liability because of the existence of other preconditions: defendants remain liable for all injuries caused or contributed to by their negligence.” 

(a) The analogy is precise: since there is no known limit of exposure below which mesothelioma cannot be caused, every exposure must be deemed capable of being a cause. Thus in every low exposure case in which mesothelioma arises out of individual susceptibility (whereas in other persons such exposure would be tolerated) D cannot be heard to say ‘but my exposure would not have caused disease in some others’: D takes the victim’s body as he finds it. Therefore must he take the victim’s reaction to information imparted by the medic.

(b) I respectfully suggest that a test relying on what the average patient should worry about is wrong in law. If it were ever capable of being the test (and it isn’t because it is an overall impermissible attempt to create an objective shining path as we have already seen), then it would have to be cast in subjective terms: what would this victim have worried about?

(c) Now, it might be argued that I have misunderstood the role of words ‘should not’ within Dr Rudd’s formulation of the test. Let us remind ourselves again of the wording:

“..[de miminis could be] defined as a dose which a medical practitioner who is aware of the medical risks would define as something that the average patient should not worry about”.

Ds may argue ‘well, the role of ‘should not’ in that sentence means ‘should not worry about because objectively there is nothing to worry about’. But that cannot be right for two reasons:

  • Since there is no dose which can be excluded as being small enough as not to be physically capable of causing mesothelioma, then as a matter of strict fact, there is no dose which should not be worried because there is objectively nothing to worry about.
  • This reality was adverted to by Underhill LJ in Bussey

“I say ‘significant’ only so as to exclude risks which are purely fanciful: any real risk, albeit statistically small, of a fatal illness is significant”.

Until medicine can set a dose below which mesothelioma simply cannot be caused, then what dose, I ask rhetorically, can properly be called ‘fanciful?’

As a matter of practicality, how could the test ever operate?

(a) The test would quickly break down into one which was personal to the victim before the medic and not some notional ‘average’:

  • Age makes a difference: a person exposed at 20 has many decades of the fibre burden on their lungs. A person at 90 would almost certainly be dead before clinical manifestation of mesothelioma arising from such exposure. Thus the approach to what they should worry about would differ;
  • The same can be said for antecedent family history: a person might well be entitled to worry more if their father and grandfather had died from mesothelioma following asbestos exposure;
  • The same can be said for antecedent fibre history before the index exposure: a man aged 50 who had just had 1 day’s exposure and no other might very well be less ‘entitled’ to worry than one who was 60 but had suffered 10 fibre/ml exposure prior to the index exposure;
  • The same can be said for gender since the Darnton & Hodgson paper relied upon by Dr Moore-Gillon – which was the same as the one he relied upon for de minimis – states that up 1/3 women have idiopathic mesothelioma.

Thus the test would have to be formulated in subjective terms ‘De minimis is the level below which an informed medic would consider a person of the victim’s own gender and age and exposure and family history should be worried about’.

(b) In fact there are multi – layers of subjectivity in this test:

  • What does the Judge consider that;
  • The medic should have considered that the;
  • Victim should have worried about.

Thus, as a shining bright line, it is quickly rendered lost to the subjective undergrowth of weeds.

(c) Finally, when would the test be being administered? The day after the exposure? The day after a sinister cough developed decades after the exposure? Some intermediate point? If it is the day after symptoms commenced then which medic would ever say ‘well I would have told him not to worry had he asked me the day after the exposure, but now I know he has a cough and a shadow on the lung, I think he should worry’? It would quickly then be seen that the test simply demonstrated that no medic can ever inform safely a victim that they have no chance of developing mesothelioma after an exposure.


(a) My respectful criticism of the Judgment is not that the Court failed to note that epidemiology was capable of being a false guide [173-175] but that it relied upon epidemiology at all to seek to answer what constitutes ‘de minimis’. This is because epidemiology, being the study of cohorts, cannot inform in an individual case whether or not a genetic factor has been at play. Thus it cannot be known in the low exposure cases, whether or not a person developed mesothelioma having inhaled (let us say) 1,000 fibres because that is an amount which might cause mesothelioma in anyone. Equally, owing to a genetic risk factor being present, 1,000 fibres will be sufficient in some whereas in those without the risk factor 5,000 fibres would otherwise be necessary.

(b) Let me take an analogy across 2 scenarios:

First Scenario:

  • Sam and I each buy a single lottery ticket with a single line on Sunday.
  • On Monday at 9 00 am, each brandishing our ticket, we attend at our mutual accountant and ask him ‘how will we account to HMRC for our winnings at the next lottery? Is it capital gains or income – a lot rides on this for the next tax bill’. Our accountant looks at us both and says ‘Gents, since the chance of either of you winning is 14 million to 1, you have nothing to worry about’.

Second Scenario:

  • This scenario is identical to the first, but this time our accountant has heard a rumour that one barrister at 12 KBW has struck a secret deal with the Lottery – namely that for each ticket bought, the lottery will print another million tickets for that barrister each with their own unique number sequence.
  • Now, when Sam and I attend, the accountant cannot know whether the ticket we are each waving represents 1 line or 1 million and 1 lines. He does not know if either of us have struck the secret deal and if so, which?
  • Now when we ask him our question, he must answer differently because there is a risk that one of us is actually very much more likely than is obvious to win.

It is statistically valid to add up lots and lots of independent chances and see overall what the combined risk is. Test the matter in your mind in this way: if I toss one coin and ask myself the question: what are the chances that I will turn up a head, then the answer is 50:50. But if I toss 2 coins (either together or separately) then the chance of my turning up a head is 75:25.

And so it is with asbestos fibres. Each individual fibre is very, very unlikely to cause mesothelioma, but the risk is cumulative with each extra fibre ingested. And hence why the medical position given is that the risk of mesothelioma is proportionate to the dose.

The analogy with genetic susceptibility is a close one. Science cannot say who has it and who has not; science cannot say how the susceptibility works or at which stage – whether it renders 1 fibre as potent as it were 50 fibres or whether it makes the usual limit of 50 fibres to cause mesothelioma drop to 1 fibre or any combination in between.

(d) It was this failure to analyse the role of the genetic factor, notwithstanding that it was raised in submissions and in cross examination of the Defendant’s expert who, perfectly reasonably, could not say from the medical perspective what the safe limit of exposure was to someone with a genetic susceptibility, that led the Court to accept evidence which was an exercise in comparing apples with pears. The Court accepted that the Deceased’s dose would, had it been asbestos, have been insufficient to raise the risk of developing mesothelioma above 0.2 deaths per 100,000 and amount to a risk 3,000 times lower than the annual risk of being in a road traffic accident. The criticisms here are several:

  • First, as a matter of law, this is an analysis that the increased risk was ‘acceptable’. Why else draw the analogy with the risk of road traffic accidents? But, in this, the Court accepted a line of logic expressly rejected by the majority in Bussey. There is no test of the creation of ‘acceptable risk’ which is not actually ‘de minimis’. Thus de minimis remains the only measure of actionability (ie if the exposure is above it);
  • Second the risk of road traffic accident death is not uniform. My copy of ‘The Grim Reaper’s Road Map’ (2008) shows that the risk of dying in an RTA is three times greater for men than for women; greater for men in their teens to 30s; and greatest still in rural areas where cars are the only way of travelling, pavements absent, lighting poor and, in Scotland where the highest rate of deaths occur, the nights are long. The standard mortality rate in northern Scotland approaches 400 (as compared to the national average of 100). Thus comparing mesothelioma in a susceptible individual with the risk of an octogenarian lady living in well-lit Surrey suburbia is far greater than being 1/3000th;
  • Third, and with profound respect, he criticised Dr Rudd for expressing the orthodoxy which I have set out so exhaustively above:

“187.  By contrast, Dr Rudd conceded that there were some cases where exposure was so trivial that he would regard them as not material but he could not explain on what principled basis I could assess whether there was a material increase in risk. Moreover, his evidence made no attempt to assess what level of risk, if any, was created by any exposure to asbestos whilst the Deceased was in the employment of the Defendant or whether such risk was more than de minimis…. do not accept Dr Rudd`s evidence and I felt that he was straining logic and common sense to regard an annual risk of 1 in 50 million as a material increase in risk and I am satisfied that in making any such assertion that there was no material increase in risk, Dr Rudd was hoping that I would rely on his consummate experience to justify an assertion which he realised could not properly be made.”

It is right that what is material is a matter for the Court and not for medics as materiality is a purely legal concept.

It is right that he could not provide an objective measure for materiality – the appellate Courts have rejected such measures.

It is right that the level of materiality could not be measured in any one case because the effects of genetics (and the stochastic nature of carcinogenesis generally) rendered such an exercise impossible.

It was wrong for the Learned Judge to first caution himself on the ‘dangers’ of the epidemiology and then to apparently rely on it entirely when rejecting Dr Rudd’s evidence on the basis that the risk was only 1 in 50 million (not least because that was, at best, the excess risk beyond that which we all face).

It may be that it will be necessary for these matters to be considered again by the Appellate Courts. Full and proper consideration would require epidemiology, the evidence of chest physicians and evidence in respect of carcinogenesis. With profound respect to the engineers, their evidence would be of marginal utility at best in such a case.

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