Mr Justice Jay:
INTRODUCTION
1.
This group litigation involves numerous similar claims for damages for
personal injuries, in the torts of negligence and public nuisance, brought by
16,626 Claimants arising out of a major fire at the Defendant’s particle board
manufacturing plant at Knowsley Industrial Park, Kirkby commencing on Thursday
9th June 2011, at approximately 17:30. The seat of the fire was
bunker no. 1 in the Woodyard building at the plant, but the fire spread to all
six bunkers in the building, causing a very substantial plume of smoke, fumes, associated
chemicals, and particulate matter to issue forth into the surrounding area. In
due course, most of the flammable contents of the building were consumed in the
fire. The Claimants, all of whom either lived or worked in the neighbouring
area or near the plant, say that they were exposed to quantities of smoke
sufficient to cause them personal injuries: in particular, a range of symptoms variously
involving the respiratory tract, the eye, and the skin; and in some cases
headache and more general debility. Fortunately, no one has alleged symptoms of
any permanence, and it is accepted that these are low-value claims.
2.
Since a Group Litigation Order was made in this case by Hamblen J on 12th
July 2012, the issues between the parties have narrowed considerably. By its
Group Defence filed on 25th January 2013, the Defendant admitted
breach of duty in respect of those who might foreseeably suffer injury in
consequence of exposure to the smoke. This admission has removed a layer of
evidential exploration, and concomitant potential complexity, from the scope of
the litigation. Both the existence and causation of actionable injury remain
hotly disputed.
3.
By Order dated 17th June 2014 the court directed that there
be a trial of common issues and of 40 test cases (at a pre-trial review which
took place on 5th May 2015 I reduced the number of test cases to 20).
The issues scheduled to that Order (being the varied GLO issues for the purpose
of CPR Part 19.13) are:
“1. When did the fire start and how did it spread?
2. What part of the site in addition to the Woodyard
Building was affected by the fire?
3. What was the quantity of recycled wood in the Woodyard
Building and any other part of the site affected by the fire when the fire
started?
4. What was the composition of such recycled wood when the
fire started?
5. What other materials were in the Woodyard Building
and any other part of the site affected by the fire when the fire started?
6. For how long did the fire burn/smoulder?
7. When did the recycled wood/other materials burn in the
fire?
8. What was the heat output of the fire over time?
9. What were the meteorological conditions during the fire?
10. What was the geographical spread of the smoke plume
during the various stages of the fire?
11. What was the chemical composition and concentration of
the smoke, in the geographical area in which exposure is alleged, during the various
stages of the fire?
12. What air quality or equivalent standards apply to
exposure to the smoke?
13. What, if any, air quality or equivalent standards apply
to short term exposure to the smoke?
14. What is the relevance of such air quality or equivalent
standards that exist to short term exposure?
15. Does Rylands v Fletcher apply?
16. What are the findings from the 40 test cases and how
should those findings apply to the issues in the individual cases, including:
(i) the extent of the Claimants’
smoke exposure.
(ii) the nature of any injury
suffered by the Claimants.
(iii) the diagnostic criteria for
any such injury.
(iv) the duration of symptoms
attributable to any injury suffered by the Claimants.
(v) the cause of any such injury.
(vi) whether such injury was
foreseeable.
(vii) whether such injury was
actionable in law.
(viii) the relevance of
pre-existing medical conditions.
(ix) the relevance of other
environmental factors such as cigarette smoke.
(x) Damages (if any)”
4.
Since this Order was made, it is apparent that (a) a number of issues
have fallen away, either through redundancy (e.g. issue 15) or agreement (e.g.
issue 9), and (b) some of the issues require refinement in the light of the
parties’ greater understanding of the case and/or the Joint Statements of the
experts. It is unnecessary to take time in the reformulation of the common
issues in this introductory section of my judgment. The Skeleton Arguments
filed at the beginning of this trial have served to stake out the battleground,
and indeed during the course of the 18 day hearing a number of issues either
disappeared altogether or the parties’ respective positions in relation to them
converged. I should also record that at a late stage in this litigation an
application was made to vary the GLO issues to enable the Claimants to pursue
nuisance and annoyance claims which differed from, or fell short of being,
claims for damages for personal injuries, but I refused that application
because it came far too late and the Defendant had all along been meeting these
claims on the basis that they were solely claims for personal injury damages –
see, for example, the original GLO issues as set out in the Order of Hamblen J.
5.
My judgment will set out the essential factual background in order to
provide sense and context to readers unfamiliar with this litigation, but the
main focus of what follows will be on what remains in dispute. In truth, not
all of the voluminous evidence I received, either orally or in writing, has
been entirely relevant to the matters remaining in issue. Moreover, the oral
evidence has been transcribed by Livenote, which may readily be referred to if
this case goes further.
THE
DEFENDANT’S PLANT AND MODUS OPERANDI
6.
The parent company of the Defendant is Sonae Industria SGPS SA, incorporated
in Portugal and a global producer of wood-based products. The Kirkby plant
opened in July 2000 and ceased production on 14th September 2012. At
the time of the fire, the plant operated for 24 hours a day, 7 days a week, and
produced approximately 400,000m³ of chipboard product a year. Back in 2000,
virgin wood was mainly used, but by 2011 the Defendant’s evidence was that 99%
of the raw material was recycled wood – with a lesser moisture content and a
greater degree of contamination from sundry extraneous matter such as plastic,
metal, glass, concrete and general detritus. The use of recycled wood also magnified
the inherent fire risk consequent on the storage of a dry, dusty product in a
relatively closed environment, and I heard evidence of a significant number of
fires before the incident presently under scrutiny. In my view, it is
unnecessary to examine the quantum of that risk, and the reasonableness of the
Defendant’s steps to minimise it, because breach of duty is not in issue.
7.
The parties called a number of witnesses to explain the workings and
operation of the plant. By way of summary, and avoiding matters of controversy
at this stage, external suppliers delivered the recycled woodchips to the plant
in vehicles variously described as lorries, trucks or wagons. The capacity of
these vehicles was up to 25 tonnes, but on average was in the region of 22
tonnes. Although the plant maintained a continuous operation throughout the
week, the vast majority of deliveries took place during normal working hours
with only around 4% of the total of 386 deliveries a week at weekends. According
to the evidence of the Defendant’s quality control manager, Mr Mark Callaghan,
incoming deliveries were weighed at the weighbridge and then directed to any
one of three areas where, after visual inspection and the possibility of rejecting
sub-standard consignments, the loads were taken off the vehicles to be
introduced in due course into the Defendant’s processes. Aside from the
external yard where considerable quantities of unprocessed woodchip may be seen
on a number of photographs, the loads were either removed from the vehicles
using massive hydraulic, tipping devices called Cometers, or were more
straightforwardly unloaded onto the walking floor of the woodyard building.
Thereafter, the loads underwent an initial cleaning process (the nature of
which varied depending on the pathway taken) before woodchips (by now measuring
between 1 and 80mm) were transferred, primarily by overhead conveyors, into any
one of six concrete bunkers which were in the same building. These bunkers were
contained in three separate silos aligned across the woodyard building in pairs
of two. Simultaneously with the deposit of woodchip into the bunkers, this
material was being withdrawn via a similar conveyor process (involving the use
of a large screw at the bottom of each bunker) to be subjected to further
cleansing and manufacturing processes “upstream”.
8.
The diagram appearing below clearly depicts the general layout of the
plant. The construct I am describing as the woodyard building comprises the
Cometer area and the Flaker Hall; the external yard is marked on the plan as
Chip Storage Areas 1 and 2. Given that the fire started in one of the concrete
bunkers in the woodyard building, it is unnecessary to describe later stages in
the Defendant’s processes culminating in the manufacture of the finished
product, namely sheets of chipboard.
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.gif)
A labelled
photograph appearing below shows the external configuration of the plant more
naturalistically, although the position and layout of the woodyard building is
less clearly depicted. This photograph will be better seen on an electronic
version of this judgment.
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9.
I heard a considerable amount of evidence about the Defendant’s quality
controls (the efficacy of which was hotly disputed by the Claimants’
witnesses), cleaning procedures and quantities of dust. Given the evidence of
Mr Gregory Butler, which I consider in more detail below, it is unnecessary for
me to address these peripheral disputes. I certainly have the impression of a
plant which, at times, was dry and dusty, and the management of which may well
have failed to take proactive steps to analyse the fire risk and to address it.
However, these issues do not warrant close analysis, nor does the quite general
and unspecific evidence about “dressed” loads and degree of contamination.
Ultimately, there is convincing quantitative evidence upon which I am able
safely to rely.
10.
Returning to the layout of the woodyard building, the diagram appearing
below, drawn by Dr Jowett, provides a basic schematic pictorial of the position
of the silos and bunkers in relation to the Cometer area and the Flaker hall:
.gif)
Each bunker was 25m in length, 12m
wide and 12m high. Each silo was 50m long and was split into two by means of a
400mm thick dividing wall, made of reinforced concrete. Along the base of each
bunker were “letterbox” or slot openings each 970mm deep.
11.
The overhead conveyor system was largely automated, and was controlled
by a SCADA system running on computer screens in various locations in the
plant. There was also a spark detection or “fire-fly” system intended to
provide early warning of combustion within the bunkers, and elsewhere.
12.
Appearing below is a diagram, furnished by the Defendant in late April
2015, illustrating the deposit of wood into the bunkers:
.jpg)
The legend explains the position
but further explanation is required. The ultrasound level detector (the
existence of which was revealed to the Claimants only very late in this
litigation) was designed to measure the distance between the conveyor and the
level of woodchip directly underneath. When the sensor detected that the level
had attained a pre-set value, the conveyor moved along the bunker to another
position before further deposits were effected. In this way the bunkers were
filled, but not in such a manner that the woodchips were ever horizontally
aligned within the plane formed by the tops of bunkers. The woodchips formed
peaks and troughs. Had an experiment been carried out to ascertain the maximum
capacity of the bunkers through this filling system, one would culminate with a
pile of woodchips describing a “Toblerone” shape, with the peak at a level
which matched the pre-set value on the sensor. Subject to some doubt as to the
angle of incline of this tent shape, the maximum tonnage of each bunker
calculated on this basis would have been in the region of 3,600 Te (the
Claimant proposes 3,696 Te). However, this theoretical perfection could never
be attained in practice, for several reasons. First, operational reasons within
the plant would dictate the state of the bunkers, and there was no need for the
bunkers to be as full as possible: as the operators all told me, they needed to
be “healthy”. Secondly, it is apparent from the schematic at paragraph
12 as above that the system was not designed to create a uniform, even peak –
hence the troughs to which a number of witnesses referred. Lastly, the process
was dynamic in the sense that the bunkers were constantly being emptied via
separate conveyors to enable the woodchips to enter the next stage in the
process.
13.
The SCADA system recorded the data sent back from the bunker sensors
(there was one sensor per bunker) on temporary log files, by definition for a
limited period. These files are no longer available. Two issues arise: first,
whether the data would in any event have thrown valuable light on the content
of the bunkers, as opposed to the distance between the sensor and the “drop
area” immediately below; and secondly, whether I should draw an inference
adverse to the Defendant flowing from the non-retention of these data. I will
be returning to these issues under the heading, “The Quantity of Woodchip in
the Bunkers”.
14.
Until a late stage in this litigation, the moisture content and degree
of contamination of the woodchips in the bunkers were in issue, and various
parameter values were suggested by the Claimants. However, the supplementary
witness statement of Mr Gregory Butler, the Defendant’s quality manager,
supplies an analysis, via sampling data, of the average moisture and
contamination levels over a five month period between January and May 2011; and
his evidence, although tested, was not seriously challenged under
cross-examination. Moreover, although the moisture values must be envisaged as
reasonably accurate, I accept the Defendant’s contention that the recorded
contamination levels in fact overstate the actual levels within the
bunkers, because the samples were taken before the first cleaning process. In
short, I proceed on the basis of data which cannot be significantly impugned,
namely a moisture level of 20% and a contamination level of 0.8%.
A SYNOPSIS OF
THE COURSE OF THE FIRE
15.
It has been estimated that the fire started at approximately 17:30 on
Thursday 9th June in bunker no. 1. The initial activation of the
“fire-fly” detection system occurred at 18:57, but the processes were not shut
down until just before 19:35. Employees smelled smoke, which slightly later was
seen to rise from an area towards the south-western corner of the bunker, and
attempts were made to douse the nascent fire using a hose. The Merseyside Fire
and Rescue Service (“MFRS”) was telephoned at 20:03, and fire-fighting
personnel soon arrived at the plant. Apart from spraying water into the bunker,
the strategy adopted was to remove as much woodchip material from the bunker as
possible in order to reduce the actual and potential fire load. At
approximately 03:40 on Friday 10th June a flame was seen to rise, or
shoot, from the south-western corner of bunker no. 1, fanning in all
directions. The flame was dark in appearance, and was lacking oxygen. Within a
rapid space of time flames were shooting out of the top of the bunker, and a
MFRS evacuation whistle was blown.
16.
Thereafter, the development of the fire was sudden. The amount of smoke
increased and the fire was soon spreading along the conveyors at a high level
in the building. The senior fire officer within the woodyard building described
the event as a “conflagration”. By 04:00, although the timings cannot be
altogether precise, it seems from the evidence of the fire-fighting
professionals on the ground that the fire had spread throughout the whole of
the woodyard building. By 06:05, all six bunkers were recorded as being on
fire, although it is possible that the ferocity of the fire had already
encompassed these structures. At that stage the fire was a raging inferno and
thick, black smoke was spewing from the roof of the woodyard building in
substantial quantities.
17.
According to Dr Jowett’s report dated 20th June 2011,
frictional heating within bunker no. 1 was the most likely cause of the fire.
The sudden escalation of the fire was caused by the collapse or slippage of
bulk material within the bunker, leading to the ignition of accumulated
pyrolysis products formed in the preceding hours.
18.
It is common ground that the fire went through three distinct stages or
phases. The first stage started at about 17:30 on 9th June (the
precise time matters not) and entailed a smouldering fire propagating slowly
outwards from the origin, creating a “nest” of burnt and smouldering material.
During this stage the heat that was generated by the process of combustion was
sufficient to pre-heat woodchips in the vicinity, but insufficient to ignite
the resulting pyrolysis products and cause flame. The first stage concluded
between 03:35 and 03:40 on Friday 10th June. The transition between
the first and the second stages occupied a number of minutes, and the second
stage commenced at about 04:00. This was the fully developed, substantial fire
involving in due course all six bunkers and other combustible materials within
the woodyard building. Amongst the characteristics of this second stage were
flame and black smoke. The fire transitioned into the third stage when the
appearance and quantity of smoke reduced, and the residue materials were
gradually consumed in a smouldering process characterised by “reverse
propagation”. The parties are not in agreement as to the timing of this
transition (which on any view must be somewhat imprecise), the Defendant
averring that it occurred by about 10:00 on 10th June, the Claimants
by 14:30. Thereafter, the fire diminished in intensity as the residue within
the bunkers was gradually consumed within the smoulder, with the MFRS permitting
it to burn out in a controlled manner and not declaring the incident officially
“closed” until 7th July 2011. By that point, there was very little
left in the bunkers except for ash and similar residue. Despite the extent and
intensity of the fire, only the woodyard building was involved.
THE ISSUES
ARISING FROM OR TOUCHING ON THE NATURE AND EXTENT OF THE FIRE
19.
At this stage, it is convenient to identify with greater salience and
precision than was achieved on 17th June 2014 (when the parties’
knowledge and understanding of the case and what really divided them was not as
great as it now appears) the issues which seem to me to arise for resolution in
relation to the matters I have ventured to summarise thus far. These are:
(1) the
quantity of woodchips in the bunkers.
(2) the
remaining fire load, in terms of its constituents and its quantities.
(3) the timing
of the transition between stages 2 and 3.
(4) the heat
release rates for the three stages.
(5) the
emission factors which should be applied to this fire.
(6) ash and
dust generation.
20.
The relevance of the fourth and fifth issues needs to be explained. In
order to achieve indicative values for the levels of exposure of the Test Claimants
to relevant chemicals and particles at various times, the plume modellers require
a range of data and information, including the relevant heat release rates and
emission factors. The concept of a heat release rate is self-explanatory –
other things being equal, the greater the rate, the higher the smoke plume travels
and the more widely it disperses. The concept of an emission factor is less
straightforward, and a full explanation appears under paragraph 92 below. The
basic point is that these variables are fed into the computer programme used by
the plume modellers. They also need to know the wind speeds and directions at
all material times (these are agreed), and finally they factor into their model
other variables such as exit velocities, temperature, diameter and number of
buildings (all of which variables are now also agreed). The parties are agreed
that emission factors constitute the most important scientific issue in this
litigation because they are so far apart in relation to it.
21.
Once the plume modellers have run their computer model on the basis of
the correct heat release rates, emission factors and other variables, the Test Claimants’
levels of exposure to chemicals and particles of interest can be evaluated. In
order to ascertain whether any individual Test Claimant may have suffered a
potentially injurious exposure, a scientific approach would mandate that the
raw exposure level predicted or indicated by the model be compared against
known toxicological data for the chemicals and particles of interest. These
data, to the extent that they are scientifically robust and substantiated at
relatively low levels of exposure, will serve as a guide in determining whether
any individual Test Claimant’s modelled exposure was above or below what might
be described as a threshold level for potentially deleterious health effects.
22.
I should make clear that the application of scientific methods to
engineering, toxicological and modelling questions cannot be regarded as
exhaustively determinative of the key issue which arises further down the line,
namely whether, having regard to all the available evidence, I should be
satisfied on the balance of probabilities that any individual Test Claimant
suffered personal injury in consequence of exposure to the products of the
Sonae fire. Submissions were deployed as to the difference between the
scientific and legal standards of proof, and I will need to address these in
due course. However, at this stage of the analysis I should indicate that in my
view purely scientific questions (e.g. the ascertainment of the appropriate
heat release rates from given data by applying established formulae) can only
be answered by applying scientific methods, within the context always of a
civil trial: whereas science may require proximity to certainty, the law does
not. To the extent that the heat release rates depend on the quantity of
woodchips in the bunkers, I approach the issue by applying the traditional
probabilistic standards familiar in civil litigation. To the extent that there
is inherent uncertainty or imprecision in any given scientific method, this may
be reflected in the overall assessment of whether any individual Test
Claimant’s case is proved on the balance of probabilities.
23.
I have mentioned expert evidence in a number of disciplines, and at this
stage I should explain the position in slightly more detail. The Defendant has
filed and served three reports and one letter from an expert in mechanical and
fire engineering, Dr Alan Mitcheson. His evidence bears on the issues of the
transition between stages 2 and 3, heat release rates and deposition of dust
and ash. At a pre-trial review which took place on 5th May 2015, the
Claimants sought my permission to file and serve comparable evidence from Dr
Phylaktou (I understand that he would also have assisted me on the issue of
emission factors), but I refused permission and relief from sanctions, on the
ground that it was far too late to adduce such evidence, and the smooth running
of the trial would be seriously prejudiced. My detailed reasons appear in a
separate transcript. Accordingly, the Claimants have no expert evidence
addressing these issues, although they do rely on their modelling expert, Dr
David Carruthers of Cambridge Environmental Research Consultants Ltd, to
address emission factors and the issue of radiative heat loss away from the
smoke plume (if a valid point, this would reduce the relevant heat release
rates accordingly). Issues arise as to Dr Carruthers’ qualifications to deal
with some of these issues. The Defendant has its own modelling expert, Mrs
Angela Spanton of Envirobods, and the parties have experts in meteorology (as I
have said, their evidence is agreed) and toxicology. In relation to this last
discipline, the Claimants rely on the evidence of Professor Alastair Hay, who
is an international authority in his subject, whereas the Defendant has called
Mr David Shillito, who is not a toxicologist but a chemical engineer with,
amongst other things, an environmental background. Mr Michael Redfern QC for
the Claimants did not object to Mr Shillito’s contributions in this regard, nor
did he object to him assisting the court on the issue of emission factors – a
matter on which he is qualified to opine, although it might be said that the Defendant
has exceeded its permitted quota of one engineer.
24.
I have to say that the state of the expert evidence in these technical
disciplines is not wholly satisfactory. In particular, I consider that I would
have benefitted from more evidence on the issue of emission factors. However, I
am not conducting a public inquiry, and I have to do the best I can on the
available evidence, remaining loyal to Mr Redfern’s warning, albeit delivered
in a different context, that judges are not “super-scientists”.
The Quantity
of Woodchips in the Bunkers
25.
I heard a range of evidence of variable quality and precision relating
to this issue. The theoretical maximum capacity of the six bunkers was in the
region of 4,200 Te (i.e. full to the brim), and the theoretical maximum achievable
in deployment of the sensor system was 3,696 Te (the “Toblerone” shape I have
previously explained). The Claimants’ case is that I should favour a figure in
the region of 3,000 Te, making allowances for what was practically attainable;
the Defendant’s case is that there were 1,550 Te of woodchips in the six
bunkers.
26.
The vast majority of the evidence bearing on this issue was of a lay,
not an expert, nature. The Defendant’s mechanical and fire engineer, Dr Mitcheson,
has contributed to the issue to a minor extent.
27.
The majority of the Claimants’ generic witnesses gave somewhat vague,
inconsistent evidence on this issue. According to paragraph 26 of the witness
statement of Mr Brian Beardwood, his belief was that for reasons of production
the bunkers were nearly full at the time of the fire. In oral evidence,
however, he could not say how much was in the bunkers, save that the levels
were “healthy”, which to him meant at least half full. Mr Brian Hoyles
told me that the bunkers were almost always full during the week, and fuller
during the week than at weekends. According to paragraph 33 of the witness
statement of Mr Michael McNamara, his belief was that bunker no. 1 was totally
full at the time of the fire. He was not certain, but believed that the
remaining bunkers must have been at least half full “because they tried to
keep them full all the time”. In his supplemental witness statement Mr
McNamara told me that one could view two months’ worth of data on the SCADA
system, and there were sensors on the bunkers which “definitely did measure
the quantity of woodchips in the bunkers”. He agreed in cross-examination
that his priority was the wet silos (further down the production line) and not
the bunkers, and accepted in relation to the latter that he was not sure
whether the sensors just measured the height of the drop immediately below
them. In re-examination, Mr McNamara said that as far as he could recall, when
he was reviewing the SCADA data for past trends, he was looking at the data
relating to the mixed-chip silos (i.e. not the bunkers).
28.
Mr John Rimmer, a maintenance technician, said in a statement introduced
as hearsay evidence under the Civil Evidence Act 1995 that the bunkers were “pretty
full, 65% at least at the relevant time”. The weight to be given to this
somewhat generalised and unspecific evidence can only be very slight.
29.
Impressionistic and inconsistent evidence of this nature from witnesses
who I would assess as not being particularly reliable falls a long way short of
being sufficient to prove the Claimants’ case that there was as much as 3,000
Te in the six bunkers. Further, I have already explained why operational
reasons would not require the bunkers to be so full, and that the process was
dynamic. In any event, other evidence called by the Claimants solidifies my
conclusion that the 3,000 Te figure cannot be right.
30.
Mr Terence Poulson, who I regret to say was a very poor witness, told me
that in the weeks before the fire the bunkers were 85% full to his knowledge.
On the night of the fire, he could see what was in the bunkers, and they were
85%, maybe 90% full. Under cross-examination, Mr Poulson expanded on this
evidence and said that he checked the level of the bunkers from the top of the
gantry, because he was trying to find out the source of the fire. Yet, at
paragraph 19 of his witness statement, Mr Poulson clearly stated that he was
not on the overhead gantry on the night of the fire, but was there the day
before. This is consistent with an earlier draft witness statement which was
put to him in cross-examination. Mr Poulson tried to persuade me that he was “at
the top of the stairs” rather than on the gantry itself. I did not believe
him. Another point which weighs heavily against him is that the evidence he
adduced to support his claim for damages for personal injuries was
inconsistent, exaggerated and in some respects (e.g. the reference in his
questionnaire to GP attendances) clearly untrue. I cannot accept Mr Redfern’s
submission that issues of credibility bearing on Mr Poulson’s symptoms must be
hermetically sealed from the credibility of his evidence relating to the bunker
levels. Mr Poulson well knew that the greater the contents of the bunkers, the
greater his prospects of succeeding on his damages claim.
31.
Another very poor witness was Mr Michael Moorcroft, who probably started
working at the plant as an industrial cleaner and occasional FLT operator on 22nd
May 2011. In his evidence in chief, he said “every time I visited the
bunkers, I would say that they were at least 85% full”. According to
paragraph 7 of his witness statement, “I can definitely say that they were
full”. However, it emerged in cross-examination that this witness did not
know that there were six bunkers in all. Further, his personal injuries’ claim,
although only cursorily examined because the whole picture was not available,
appeared extremely tenuous on the basis of the probable exposures to which Mr
Moorcroft was able to attest, and moreover his diagnosis of conjunctivitis on
10th May 2011 could have had nothing to do with the fire or his work
at this plant.
32.
I cannot conclude that because these two witnesses gave at best
unreliable, at worse untruthful, evidence it must follow that the Defendant’s
case is right. However, evidence of this quality has the tendency to undermine
the Claimants’ case that the levels were as high as 3,000 Te, or even 85% of
that figure.
33.
On 14th June 2011 Dr Paul Jowett of Dr J.H. Burgoyne and
Partners LLP, appointed to investigate the causes and circumstances of the fire
by the Defendant’s insurers, held a preliminary meeting with Rodney Mitchell,
its Chief Technical Officer, Nigel Graham, its Managing Director, and other
senior employees of the company. Dr Jowett was given contradictory information
as to the contents of the bunkers. The Defendant disclosed Dr Jowett’s notes of
this meeting, and others, extremely late in the day but ultimately I conclude
that nothing turns on that. His notes are a Curate’s egg from the Claimants’
perspective; and, more importantly, they are reliable. Dr Jowett was informed
of the identity of employees he might interview in the course of his
investigation. One of those employees was Mr Thomas Pybis.
34.
The Claimants called Mr Pybis to support their case on this issue. He
had been working as a Cometer operator in the woodyard building since
approximately June 2008. It is highly relevant that he was not asked to provide
a witness statement until this year. On 16th June 2011 he was
interviewed by Dr Jowett in relation to what he knew about the possible causes
of the fire and the quantities in the bunkers. Dr Jowett kept a contemporaneous
manuscript note and in my judgment was a particularly impressive witness:
moderate, measured, and astute to answer the questions put to him. The reason
why Dr Jowett took the trouble to speak to Mr Pybis was because he was the last
person to check the contents of the bunkers at approximately 18:50 on 9th
June. Mr Pybis gave Dr Jowett valuable information as to the profile of the
woodchips in bunker no. 1, and the manuscript diagram Dr Jowett was able to
draw was clearly based solely on that intelligence. When Dr Jowett’s detailed
notes were put to Mr Pybis in cross-examination, he agreed that they were
largely accurate, save as to the timing of the last inspection (in relation to
his dinner break) and the tonnages Dr Jowett recorded in relation to the
bunkers. The relevant section of Dr Jowett’s notes reads as follows:
“Bunker 1 I
estimate 200-250 tonnes a.t.o.f. [at time of fire] (i.e. about ½ full)
2 been
out of use – prob[lem]s with screw ∴ ~ 100 tonne
(sawdust) ~ 200 T
(purchased chips) ~ 300-350 T
Recycled wood 1 (S) ~ 350 T
Recycled wood 2 (N) ~ 350 T”
35.
It should be explained that Mr Pybis was using the names or labels for
these bunkers which were a throwback to the days when the plant took in virgin
wood, sawdust, purchased chips and some recycled wood. The two recycled wood
bunkers are numbered 5 and 6 on the plan (see paragraph 10 above). The
aggregate of these tonnages is 1,500 – 1,600 Te, and Dr Jowett has taken the
mid-figure of 1,550. Subsequently, Dr Mitcheson has used the self-same metric
to base his heat release rate calculations.
36.
Mr Pybis’ oral evidence was that the bunkers were habitually kept at a “healthy”
level, which in his view was anything in excess of 50% of capacity. He said, as
did other witnesses, that the bunkers would tend to be full on Thursday and
Friday to support weekend production. In cross-examination, he agreed that the
SCADA system did not indicate whether a bunker was full; it would merely show
the operators what was happening directly below the drop level. It was for this
reason that visual assessment of the bunkers, which entailed climbing up the
stairs onto the gantry, was the best way to evaluate the position, and was
therefore habitually undertaken. As regards Dr Jowett’s notes, Mr Pybis did not
accept that he would have told him the levels in terms of tonnages. He did not
in fact know these. Instead, he would have told him what the levels were in
terms of fractions or percentages. Mr Pybis agreed that he might have said that
bunker no. 1 was half full, but he would not have said that there was less in
bunker no. 2. In fact, his recollection was that bunker no. 2 was 75-85% full. He
was less sure about that in cross-examination. In his opinion, all the bunkers
had “healthy” levels, although there were different levels in each of
the bins.
37.
Mr Redfern urged me to treat Dr Jowett’s hearsay evidence, both that
contained in his notes and his oral account from the witness box, with
considerable caution. The notes were not checked for accuracy by Mr Pybis, and
the possibility for misunderstanding arises. In principle, I am content to
adopt that cautious approach in reaching appropriate conclusions about this
important seam of testimony. However, having seen and heard both Dr Jowett and
Mr Pybis, I am confident that the former’s notes are accurate.
38.
Mr Pybis gave the impression of trying too hard to persuade his
listeners that he would not have mentioned tonnages to Dr Jowett. I am sure
that he did, for a number of reasons. He was a reasonably able witness who told
me that he was passionate about his work. He had been working in the Cometer
hall for a number of years, and must have known the capacities of these bunkers
in terms of tonnages. In answer to my questions, he agreed that he heard others
mention 500 tonnes. When pressed in cross-examination, Mr Pybis let slip that
he rarely mentioned tonnages; he felt more confident using percentages. It
follows that he sometimes mentioned them. Finally, Dr Jowett’s unchallenged
evidence was that he simply wrote down what he was told. He had no reason to do
otherwise, and it is clear from other sections of his notes that he took care
to ensure that he had understood Mr Pybis’ explanations.
39.
My firm conclusion that Mr Pybis told Dr Jowett that there were
approximately 1,550 Te of woodchips in all six bunkers does not prove that the
former was right. Mr Redfern makes the points that the Defendant is relying on
the evidence of a labourer, and that an international company of this stature
should be able to adduce more cogent evidence in a case of this importance. I
will deal with Mr Redfern’s second argument later, but as for the first I
disagree with his somewhat dismissive assessment of his own witness. Mr Pybis
had worked his way up from being an industrial cleaner, and his competence and
experience are not in question. He was the last person who in fact witnessed
the levels in these bunkers. In my judgment, his experienced assessments were
reasonably reliable, and would have been at least as robust as anyone else’s. I
understand but cannot condone Mr Pybis’ reasons for wanting to backpedal. He
was not credible in that respect, but the reliability of what he told Dr Jowett
has not been undermined.
40.
Independent evidence as to the quantities in the bunkers comes from the
contemporaneous logs completed by fire officers of the MFRS. However, this
evidence is hearsay, somewhat contradictory and unreliable. MFRS’s sources are
unknown.
41.
The Defendant’s generic evidence of fact throws limited additional light
on this issue. Mr Mark Callaghan told me that the bunkers were usually
approximately 40-50% full (200-250 Te), which evidence is consistent with what
he told Dr Jowett in June 2011. Mr Callaghan said that the Defendant was
planning to stop production on Monday 13th June for at least three
weeks. This evidence came out the blue, and too late in the case for other
witnesses to be questioned about it. As I have said, other employees told me
that the bunkers would tend to be fuller towards the end of the week. I
understand Mr Redfern’s concern about the circumstances in which this evidence
has seeped into the case, but I believe that Mr Callaghan was a reliable and
impressive witness who did not enter the witness box in order to mislead me. Moreover,
in my view other former employees called by the Claimants were giving me, at
best, a generalised impression of the Defendant’s operation, not what was in
fact happening on this particular day.
42.
In any event, a shutdown on Monday 13th June might well have
precluded there being over 3,000 Te in the bunkers, but does not
necessarily contradict a total tonnage in the region of 2,500-3,000. I say this
because Mr Callaghan told me that approximately 700 Te were withdrawn per day.
On the basis of three days’ production (10th – 12th June
inclusive), and the necessity to leave the bunker screws safely covered, the
arithmetic speaks for itself. On the other hand, the impending close-down is a
pointer which slightly favours the Defendant and serves to neutralise the
Claimants’ point that as the weekend approached the bunkers tended to be
fuller.
43.
Mr Callaghan also assisted me with the workings of the SCADA system. He
explained that the purpose of the sensor was to monitor the height of the
woodchips so that they did not block the conveyor. The icon on the computer
screen would then give an indication in the form of a percentage of how much
was in the bunker overall. The temporary log files containing this information
were probably kept for around three months, but this witness was not sure. He
said that a “PLC engineer” would be needed to go back any further. However, he
was clear in his evidence that he never used the computer monitoring system to
evaluate levels, because there was no need to do so.
44.
Mr Callaghan also told me about a shift handover log which contained
information about the bunker levels; they were completed by the shift managers
on the basis of information from operatives. This was another evidential
revelation: no such logs have been disclosed, or mentioned in the Defendant’s
disclosure lists. Their purpose was to brief the oncoming shift, and the same
information would also be used at monthly meetings. In answer to my question,
Mr Callaghan told me that the shift manager on the night was Mr Steve Sharkey.
He would have ended his shift at 22:00, and would have “gone round the area”
maybe once during the course of the shift. I was given no explanation as to
why he was not called to give evidence about the bunker levels, but it is clear
that he did not speak to Dr Jowett about them and it is probable that what he
knew about bunker levels that night came from Mr Pybis. Furthermore, I draw the
reasonable inference that it is highly unlikely that any shift handover log
would have been prepared and completed on the night of the fire at or near to
22:00. There were other, more pressing concerns.
45.
Mr Alan Whitrow, the woodyard manager, told me that the bunker sensors
never worked, in the sense that they were never accurate. It was much easier to
check the levels visually, which was precisely the reason for operators and
managers doing so on a regular basis. Mr Whitrow did not agree with Mr
Callaghan’s assessment as to general practice in relation to levels within the
bunkers: he said that each week was different, and that it was difficult to
say.
46.
At the Claimants’ request, Mr Michael Kent QC for the Defendant called
Mr Brian Hayes, the company secretary of the Defendant since December 2012. At
the time of these events, he had been chief financial officer. He was responsible
for signing and declaring the truth of the Defendant’s disclosure statements in
this litigation. Mr Hayes was a somewhat cavalier witness who appeared to take
the view that because the Defendant had disclosed information relating to the
contents of the bunkers, viz. the Pybis data, that was the end of the matter. I
was not impressed by that attitude, or by certain features of his evidence. It
is unclear why no search for any electronic documents was made before the
Standard Disclosure Statement was signed on 28th March 2013. In
relation to the first Supplemental Disclosure Statement dated 25th
June 2014, Mr Hayes had ticked the box to the effect that no search had been
made for electronic data, but then it transpired that electronic meteorological
data had been disclosed. Mr Hayes told me that he had made a mistake about
this: that, in my view, evinced at best poor attention to detail. The further
Disclosure Statement dated 14th August 2014, again signed by Mr
Hayes, stated that a search had been made of the internal server in Portugal. On 17th June 2014 HHJ Gore QC had been told that a search would be
made of that server, and that it would take 4 months.
47.
The position in relation to the Sonae computer system was investigated
with Mr Hayes, but his evidence was not as clear as it might have been. He told
me that the SCADA data with which this case is concerned would not have been
backed up or saved on Sonae’s main server in Maia, Portugal. Those data were
retained on temporary log files which were deleted after 4 weeks. My
understanding of computer systems is imperfect, but I imagine that an expert
would have been able to retrieve these data from the systems in Liverpool notwithstanding their deletion. However, on 2nd November 2012 the
Sonae plant was sold to a competitor, along with its computers. Some data would
have been transferred to Portugal for financial and other obvious reasons, but even
if they still existed I see no reason for any of the SCADA data being preserved
in this way: their value was ephemeral.
48.
It follows that unless I reject Mr Hayes’ evidence about the SCADA data
not being transferred to Portugal at any stage, the data were deleted from the
system within 4 weeks (Mr Hayes’ figure) or 3 months (Mr Callaghan’s), could
not easily have been excavated from the hard drive after that, and were lost
forever on 2nd November 2012. I have asked myself why Mr Hayes took
the trouble to make any lengthy inquiries in Portugal if the true position was
that the data of interest did not exist by then. Upon reflection, and
considering Mr Hayes’ evidence as a whole, I cannot conclude that he was a
mendacious witness. It was necessary to undertake certain inquiries in Portugal
as to how the SCADA system functioned in relation to the bunkers, and the operation
of Sonae’s computer systems in general. Mr Hayes was an unsatisfactory witness,
but I do not reject his evidence wholesale.
49.
Mr Redfern also relied on the fact that in June 2011 Dr Jowett had
advised the Defendant by email to retain electronic data relating to the
firefly system, from which it should have been deduced that there was a need to
retain electronic documents generally. However, I do not draw that inference at
all: Dr Jowett was not interested in or impliedly referring to bunker sensor
data, and in June 2011 the Defendant could not have anticipated these claims,
or that the levels in the bunkers would be an issue.
50.
At this stage, it is convenient to address Mr Redfern’s submission that
I should draw inferences adverse to the Defendant regarding the contents of the
bunkers because it has lost or withheld relevant information, namely the records
from the SCADA system relating to the data sent back by the sensors. He relied
on the well-known case of Armory v Delamerie [1722] 1 Strange 505 which
has recently been considered by Mann J in Gulati and others v MGN Ltd
[2015] 1482 (Ch). In that case Mann J was considering breach of privacy claims
by victims of phone-hacking. He decided that the Armory principle was
relevant to his judicial task because on the facts of the case before him it
was germane to the scope of the Defendant’s wrongdoing, which was itself
relevant to the scope of the invasion of privacy, and concomitantly relevant to
damages [91]. Further, at [96] Mann J explained that Armory encapsulated
an evidential principle relating to how the court should assess and find facts
when that process has been obstructed by the acts of one of the parties.
51.
Mr Redfern submitted that the Defendant, both through Mr Hayes and more
generally, has acted reprehensively in failing to preserve the SCADA data
before deletion, and/or failed to interrogate the main server in Portugal. On that footing he invited me to draw the inference that the bunkers were in fact
at maximum operational capacity, which realistically (from the Claimants’
perspective) means 3,000 Te.
52.
Persuasively though they were presented, I cannot accept Mr Redfern’s
submissions. There are two answers to them. First, I do not accept that the
Defendant should have preserved the SCADA data before the temporary log files
were deleted, and/or before November 2012. Assuming that the Defendant’s
solicitors advised its client to retain relevant documents, including data,
when this claim was first intimated, the Defendant’s computer system in the UK
was sold at an early stage in the litigation. It would have required
considerable knowledge and “joined up thinking” to have concluded that these
systems should have been interrogated, and temporary log files reconstructed,
before they were transferred to the purchaser. By the time the Defendant should
reasonably have been alert to this recondite issue, it was too late. Overall,
the Claimants have fallen short of demonstrating the sort of reprehensible
conduct on the Defendant’s side which would justify the drawing of the adverse
inference sought; and, in any event, the requisite causative link between
conduct and the loss of electronic documents has not been established.
53.
Secondly, the SCADA data, even if available, would have thrown little
further light on the actual contents of the bunkers. The computer may have
generated a percentage figure from the sensor data but it was, at best, only
indicative. The clear evidence from Messrs Whitrow and Callaghan, which I
accept, is that these data were not relied on. The only reliable means of
establishing the bunker levels, and that was imprecise too, was to take a look.
Operators and managers would not have taken the trouble to do this if their
efforts were supererogatory. Furthermore, looking again at the diagram at paragraph
12 above, it is quite obvious that the inferences to be drawn from a series of
distances from sensor to individual peaks were likely to be imprecise and
inaccurate, in relation to a process which was dynamic. In the end, Mr Redfern
had to submit that I should “draw an inference from an imponderable”. The
philosophers might enjoy this sort of metaphysical conundrum, but it is lost on
the common lawyer.
54.
Mr Redfern advanced a separate submission regarding the Defendant’s
comportment in relation to its disclosure obligations generally. This was less
persuasive, given my judgment at the pre-trial review on 5th May
2015. Mr Redfern did not make sustained submissions about the shift managers’
logs, and unless the Defendant is wholly misleading the court, the position
must be that they are no longer available. I do accept, however, that the
Defendant – through Mr Hayes, is remiss in failing to include these logs, as well
as the temporary log files in its August 2014 Disclosure Statement, under the
rubric of documents no longer in existence.
55.
It is also convenient to deal with Mr Redfern’s yet broader point,
advanced more in cross-examination than at the end of the trial, that I should
draw general inferences adverse to the Defendant flowing from its poor safety record,
the number of fires, the inherent risk and the dryness of the work environment.
Mr Redfern submitted that this fire was reasonably foreseeable, and that issues
of foreseeability and causation are, by their nature, intrinsically
intertwined. I cannot accept this submission either. The Defendant does not
dispute that the Claimants’ alleged losses are reasonably foreseeable. I do not
accept that foreseeability and causation can be elided, or (to put the point
slightly differently) that the degree of the Defendant’s fault is capable of
being relevant to the issue of causation. These are, and remain, discrete
concepts. However badly the Defendant may have behaved, the Claimants still
have to prove their cases to the requisite standard, and their task is by no
means attenuated or abbreviated by the extent or quantum of breach of duty. The
instant case is wholly different from the situation analysed by Mann J in Gulati
(at [91] of his judgment) where the scope of wrongdoing bore on the quantum of
damages, and also differs from the context of Viscount Simonds’ dictum in Nicholson
v Atlas Steel Foundry & Engineering Co. Ltd [1957] 1 WLR 613, 618 (once
breach is admitted, it requires “little further to establish a causal link”).
56.
Mr Redfern advanced a separate submission on the drawing of adverse
inferences based on a case extremely familiar to him, Wisniewski v Central Manchester HA [1998] PIQR 324, 340. He submitted that I should draw inferences
adverse to the Defendant flowing from its failure to call relevant witnesses,
namely Mr Sharkey and Mr Mitchell. I cannot conclude that these men could have
given me no relevant evidence, but I do conclude that their evidence could
not have assisted me significantly. Mr Mitchell could have spoken to the
capacity of the bunkers, but this issue is no longer in dispute, pace Dr
Mitcheson’s arithmetical error in this second report. As I have already said, Mr
Sharkey could not improve on Mr Pybis’ evidence, particularly in circumstances
where the shift managers’ logs are no longer available.
57.
Returning to the quantity of woodchips in the bunkers, the final point
which places the seal on the Defendant’s case pertains to the separate
calculations Dr Mitcheson performed to ascertain the approximate tonnage within
the bunkers at the end of second stage of the fire. Paragraph 64 of Dr
Mitcheson’s first report dated January 2014 proceeded on the basis of an
initial tonnage of 1,550 and a heat release rate of 330 MW, leading to a burn
of 700 Te and a residue of 850 Te. In his report dated 12th
September 2014, Dr Mitcheson carried out a more straightforward calculation
based on the assumption that the bunkers were filled with unburnt woodchips up
to the level of the letter boxes. On this premise, the mass of the unburnt
woodchips was in the region of 900 Te, a figure not far off the 850 Te attained
by a different methodology altogether. Mr Redfern sought to persuade me through
cross-examination of Dr Mitcheson that the second method was either
self-evident or tautological, amounting in effect to the skinning of the same
cat by the same knife (my metaphor, not his), but I cannot agree. Somewhat
rough-and-ready though Dr Mitcheson might have been in his later report, I
consider that his methodology was different and the point he was seeking to make
is valid.
58.
Furthermore, Dr Mitcheson’s advice to the court is that if there had
been 3,000 Te in the six bunkers, then the heat release rate during stage 2 of
the fire would have been a staggeringly high 1,000 MW. I accept his evidence
that the degree of heat damage to the woodyard building tells against this
having been the case.
59.
It was put to Dr Mitcheson that an inference could be drawn from the
fact that the similar quantities of ash seen in the bunkers after the woodchips
had burned indicated that there were similar quantities ex ante. Dr
Mitcheson’s answers, which I accept, were that there was in fact less debris in
bunker no. 2; and, in any event, that post-fire ash levels cannot give a
reliable indication of the pre-fire load.
60.
Overall, I am satisfied on all the evidence that the total quantity of
woodchips in the bunkers was in the region of 1,550 Te. It might have been
slightly more, it might have been slightly less, but it is reasonable to
proceed on the basis of that figure.
The Remaining
Fire Load
61.
Dr Mitcheson has calculated the remaining fire load in the woodyard
building. In his estimation, there was approximately 20 Te of conveyor belting,
16 Te of foam insulation and 4.5 Te (or 5,000 litres) of hydraulic oil. The
combustion of these materials created dense black smoke. In addition, there
were unquantified accumulations of woodchip and associated dust outside the
bunkers which would not have materially contributed to the fire load but would
have accelerated the spread of the conflagration at or shortly before 04:00 on
10th June. Finally, Dr Mitcheson refers to electric cabling with
small amounts of plastic insulation, hydraulic hoses, miscellaneous painted
surfaces and other similar combustible materials. Again, these did not
contribute materially to the overall fire load.
62.
Dr Mitcheson has taken into account the conveyor belting and the
hydraulic oil in computing the heat release rate for stage 2 of the fire. In
that regard, he has not taken into account the foam insulation (more exactly,
the polyurethane foam filling the gap between the perimeter walls of the
building), on the basis that it pyrolised and absorbed heat to more or less the
same extent as it emitted heat. I do not understand that part of Dr Mitcheson’s
evidence to have been contradicted. In any event, the Claimants would not be
assisted by greater heat release rates.
63.
The Claimants dispute the quantity of foam insulation and contend for a
figure of approximately 40 Te. They also argue that 4-5 Te of perspex roof
sheeting was involved in the fire. Dr Mitcheson agreed that the total potential
fire load as regards the foam insulation was in the region of 40 Te, and on one
interpretation of his evidence in cross-examination he appeared to accept that
had it burned it would have added considerably to the heat release rate. It is
unclear to me why he made that concession (if indeed he made it) – logically, combustion
should have a neutral impact on the heat release rate regardless of the
quantity burnt – but his real point was that on his interpretation of the
photographic evidence no more than 16 Te could have been consumed in the fire. This
was on the footing that only the top 2m burned. Dr Jowett, who was in a better
position to assess this damage, said in cross-examination that “just the top
few metres were involved in the fire”. However, he also said that he had not
done the calculation. In my judgment, it is likely that more than 16 Te of foam
insulation was involved in the fire, but it is unclear how much more. I do not
accept that the whole potential fire load of 40 Te was entailed. My finding has
no impact on Dr Mitcheson’s heat release rate calculation for stage 2, but it
does serve to enhance the emissions of pollutants during that stage. Yet, how
much difference that made cannot be assessed, save in the general sense that
the enhancement could not have been that great in proportion to the quantity of
woodchips. Finally, I cannot accept Mr Redfern’s criticism of Dr Mitcheson that
he should have accounted for the foam insulation. This expert’s brief was to
evaluate heat release rates; he had no interest in emissions and pollutants.
64.
As for the perspex sheeting in the roof, it is clear that Dr Mitcheson
did not take these into account. They would have had a minimal impact on heat
release rates but would have contributed to some extent to the overall fugitive
escape of potentially toxic chemicals. This is extremely difficult to quantify,
not least because the dimensions of the roof spaces have never been measured,
and to the extent that they appear in photographs their size and weight cannot
be readily estimated. Mr Callaghan said that there were 3-4 pitches in the
roof, with a maximum of 2-3 thin perspex panels in each pitch. With reference
to furniture in the court room which Mr Callaghan used as his yardstick, I
formed the impression that each panel was about 2m x 1.5m. I would not wish to
speculate as to the total weight of all the panels, but the Claimants’ estimate
of 4-5 Te seems excessive. The panels melted at the outset of stage 2 and added
to the mélange of chemicals at that juncture.
The
Transition from Stage 2 to Stage 3
65.
Stage 2 of the fire was characterised by very considerable quantities of
thick, black smoke billowing forth from the roof of the woodyard building.
There are photographs and spectacular video footage which illustrate this quite
well, allowances being made for photograph quality, the play of light sources
across the lenses, and (at least in some cases) some doubt as to the exact
timing of certain, publicly available video footage. The black smoke was the
result of an oxygen-deprived fire, burning rich, producing incomplete products
of combustion. Dr Mitcheson agreed in cross-examination that the space both
immediately above and within the bunkers was heavily smoke-logged during stage
2, and that the richer the burn, the greater the pollutant content. Dr Jowett
was asked about smoke-logging, and in his view what mattered was not the
clogging smoke above the bunkers but within them. In my judgment, nothing
really turns on this nuance.
66.
In Dr Mitcheson’s opinion, the transition from stage 2 to stage 3
occurred at approximately 10:00 on Friday 10th June, although he
accepted that placing an exact timing on what was essentially a process rather
than an event was somewhat arbitrary. Dr Mitcheson based his opinion on the
MFRS log and what he considered to be reliable lay evidence (appended to his
first report), and on the photographic and video record. I have reviewed the
log very carefully but I am far from convinced that it provides much positive
support for Dr Mitcheson’s argument. Certainly by later on that afternoon there
is reasonably clear evidence of a significant reduction in the overall
quantities of smoke, and the Claimants propose a later time for the transition,
namely approximately 14:30 on Friday 10th June.
67.
There are two features of the evidence which require closer examination.
First, what may be described as the highlights of the photographic and video
evidence were considered by Dr Mitcheson, both in chief and in
cross-examination. I should add that when opening his case to me Mr Redfern
presented a 40 minute montage of the available evidence, and Dr Mitcheson
confirmed that he had seen it. A video available on Youtube, which is untimed
but Dr Mitcheson surmises was taken at around 10:00, shows lesser quantities of
smoke issuing from the plant, and a possible change in colour – blending from
white grey to a darker shade of grey. Photographic images taken at 10:28 and
10:29 that morning, showing the west and northwest aspects of the woodyard
building, appear to depict smoke of a light grey colour tinged with yellow.
There was some suggestion that the yellow might be a refraction or reflection of
light from the sun, but I doubt that. Dr Mitcheson agreed in cross-examination
that the yellow smoke was probably the product of something other than wood.
However, it remains unclear what this was or might have been, and ultimately smoke
of this hue does not really assist me in timing the transition from stage 2 to
stage 3. Another image timed at 11:04, but taken from a different angle, shows
what I would describe as grey, but not black, smoke. A further photograph taken
at 11:17 shows a significantly reduced amount of smoke.
68.
Dr Mitcheson agreed that the position changed at approximately 13:24 on
the Friday afternoon when there is a body of photographic and video footage
showing thick black smoke. By 14:49 the quantity had reduced but the colour was
still fairly black. Dr Mitcheson’s contention is that this represents the combustion
of approximately 2,500 litres or 2.25 Te of hydraulic oil which had entered the
immediate zone of the fire. There is some support for this explanation from a
MFRS log entry timed at 13:29 – it erroneously refers to “approximately 1,500
litres of hydraulic fuel” having entered the area of the fire, but nothing
turns on this quantitative error, or the mis-description of the substance.
69.
On the other hand, the Claimants contend with some conviction that it is
not easy to understand how 2,500 litres of hydraulic oil could have accounted
for densely copious quantities of black smoke which endured for at least 85
minutes. Interestingly, Mr Callaghan put the duration of this black smoke as
being only 10-15 minutes, which in my view is incorrect. I see the common sense
force of the Claimants’ point, but Dr Mitcheson explained in cross-examination
that the oil could have pooled on the ground. Dr Mitcheson did not accept the
force of the point that one would have expected both oil tanks to enter the
fire zone more or less simultaneously. In this regard he received some support
from the evidence of Mark Callaghan to the effect that the oil tanks were 8-10
metres apart.
70.
To my mind, there are two difficulties with the Claimants’ argument
hereabouts. First, they have no expert evidence with which to contradict Dr
Mitcheson, and overall I have concluded that he was a good witness. Secondly,
if this was not hydraulic oil burning, then the only competing hypothesis is
that there was some unexplained recrudescence in the fire involving the
woodchips, and what might be characterised as a temporary reversion from stage
3 back to stage 2. Although I fully accept the possibility that this fire waxed
and waned to some extent, I cannot agree that a flare-up of this magnitude might
have occurred. All six bunkers were heavily consumed in the fire by 06:00, and
I cannot accept Mr Redfern’s subsidiary point that more polyurethane foam might
have been involved after 13:30.
71.
For all these reasons, I have concluded on the balance of probabilities
that the transition from stage 2 to stage 3 occurred at approximately 10:00 on
Friday 10th June, and that at that point Dr Mitcheson is correct in
advising the court that around 700 Te of woodchips were consumed over the six
hour period from 04:00 to 10:00, leaving approximately 850 Te at the point of
transition. Dr Mitcheson derived this figure from the level of woodchips in
relation to the “letter box” or slot openings. In my view, this was a somewhat
rough-and-ready approach, but Mr Redfern did not take issue with it.
72.
Nor did Mr Redfern take issue with another calculation which appears at
paragraph 69 of Dr Mitcheson’s first report. There, Dr Mitcheson explains that
by 13th June the MFRS photographs show that the bunkers contained
ash and smouldering woodchips to a depth equivalent to about three-quarters of
each slot height, i.e. about 0.75 metres. This equates to a volume of about 225m³
in each bunker, suggesting an unburnt mass of about 22 Te per bunker and a
total mass of about 120 Te. Accordingly, the majority of the woodchips
remaining at the commencement of stage 3 were consumed by about midday on 13th
June. Subsequently, it is obvious that there was much less left to burn, and Dr
Mitcheson calculates that by 7th July only about 10 Te remained. Put
another way, by midday on 13th June there was much less left to
burn, much less smoke, and many fewer emissions of pollutants.
73.
In my judgment, the Claimants cannot escape from the logic of these
computations, nor did they try to. Dr Mitcheson was cross-examined on the basis
that if the figure of 1,550 Te which he was given by Dr Jowett was wrong, then
his report was wrong overall. As it happens, the figure he was given was – on
my findings - correct, but even if it had been erroneous Dr Mitcheson would
simply have had to revise his calculations on the basis of my finding; he would
not have had to revisit his methodology.
74.
Dr Mitcheson’s calculations receive further support in the lay evidence
from the Defendant’s side. I was not particularly impressed by the evidence of
Ms Joanne Ashton and Ms Gina Fitzgibbon – there were too partisan for my
liking, and overly disposed to downplay the extent of the fire on the Friday
morning. The evidence of Mr Alan Whitrow was very much more compelling.
According to paragraphs 39 and 40 of his witness statement:
“I returned to the site on Saturday 11th and
Sunday 12th June 2011. During these days, I walked around and
liaised with demolition contractors and the fire brigade. On a number of
occasions I was inside the woodyard building. I was able to see clearly and did
not experience any breathing difficulties. The fire fighters were not wearing
any breathing apparatus as we walked around the site or were inside the
woodyard building …
During the remaining period of the fire, I continued to be on
site during my normal working hours. By approximately Monday, the smoke from
the fire had decreased significantly and from then onwards, the smoke gradually
decreased.”
75.
Best of all from the Defendant’s perspective was the evidence of Dr Jowett.
Back in June 2011 he had no interest in matters such as the quantity, thickness
and colour of the smoke; these were wholly outside the ambit of his concerns. As
I have said, he went to the plant on 14th June in order to undertake
a preliminary inspection. His photographs taken at the time do not show copious
quantities of smoke, and when he inspected the woodyard building that afternoon
there was very little smoke at ground floor level. The position was the same
the following day. Dr Jowett returned to the site on 23rd June and
carried out a risk assessment for his own purposes. This assessment made
provision for wearing a personal gas monitor should the need arise, but
according to paragraph 22 of his witness statement the alarm levels on the
monitor were triggered at no point during his inspection. On that occasion, Dr
Jowett took what he called an “inspection movie” (his exhibit ‘PAJ-5’, lasting
40 minutes) which shows little smoulder or smoke emanating from the bunkers by
that stage.
76.
Finally in this regard, there is an illuminating photograph published in
a national newspaper showing the scene at 17:21 on 14th June. From
the woodyard building emerge relatively modest quantities of grey-white smoke.
The wind direction is towards the photographer. And between the photographer
and the plant we see a mother and child, apparently oblivious to the smoke or
its immediate consequences. True, one possible inference is that the woman in
question was acting in reckless disregard of her own and her child’s health. My
preferred inference, having considered all the available evidence, is that the
smoke was not causing any obvious, immediate ill-health effects.
77.
Of course, the weight to be given to this corpus of evidence should not
be exaggerated. It is far from being quantitative; it merely creates a general
impression. On the other hand, it needs to be recognised that aspects of the
Claimants’ case depended on the making of a favourable impression from their
perspective. That aside, I appreciate that from a more scientific viewpoint
greater emphasis should be placed on considerations such as the applicable
emission factors, the meteorological variables and health thresholds to be
drawn from the toxicology, all being matters which remain to be addressed in
this judgment.
Heat Release
Rates
78.
The only evidence available to assist me on this issue came from Dr
Mitcheson. Apart from a major attack on Dr Mitcheson’s factual premises (e.g.
initial tonnage of woodchips in the bunkers; amount of foam insulation), and a
strand of cross-examination intended to reinforce his case in relation to
emission factors, Mr Redfern did little to impugn Dr Mitcheson’s methodology in
this somewhat technical and recondite domain. In these circumstances, I am able
to be quite brief.
79.
As its name might suggest, the heat release rate is the heat generated
by a fire measured in watts. In a case such as the present where any empirical
evaluation would have been close to impossible, heat release rates can be
computed from the product of the mass burning rate (measured in m¹ kg/s) and
the heat of consumption, ΔH, expressed in MJ/kg.
80.
Dr Mitcheson has computed heat release rates for the various stages of
the fire, as follows:
·
Stage 1, from about 17:30 on 9th June to about 03:35
on 10th June: q¹ = 0.01 x t² MW (t being measured in hours).
·
Stage 2, from about 04:00 to 10:00 on 10th June: q¹ =
330 MW (for the woodchips), + 28 MW between 04:00 and 06:00 (for the conveyor
belts) + 12.5 MW between 06:00 and 07:00 (for the hydraulic oil).
·
Stage 3A, from about 10:00 on 10th June to about 12:00
on 13th June: q¹ = 64 x exp (-0.65 x t) MW (where t is the time in
days after reverse smouldering became predominant, on 10th June, at
which time t = 0).
·
Stage 3B, from about 12:00 on 13th June to 7th
July: q¹ = 1.4 x exp {-0.1 x (t-3)} MW (where t is the time in days after
reverse smouldering became predominant, on 10th June, at which time
t = 0).
81.
In reaching these conclusions, Dr Mitcheson made a number of assumptions
about the nature of the fire at various stages, its levels of oxygenation, the
calorific value of wood, its moisture content, and other matters. These were
necessarily imprecise, and the resultant heat release rates cannot be regarded
as entirely robust. Given the absence of an expert instructed by the Claimants
who might have advanced different heat release rates, following which there
might have been room for an element of compromise at a joint experts’ meeting, at
the conclusion of his evidence I invited Dr Mitcheson to reconsider his
conclusions and advise me as to whether there might be respects in which a
different opinion might be accommodated. Dr Mitcheson declined my invitation.
82.
On my understanding of his cross-examination, Mr Redfern sought to
undermine one of the assumptions made by Dr Mitcheson, namely that “the
combustion of the woodchips in the bunkers would be expected to resemble that
of an under-ventilated, close packed crib within an enclosure” (see
paragraph 63 of his first report). Shortly after lunch on the day Dr Mitcheson
was giving evidence (Friday 5th June), Mr Redfern cross-examined him
at length on the quantity of oxygen likely to reach the fire on account of the
degree of smoke-logging within and above the bunkers. Mr Redfern’s objective
was to ensnare the witness into a debate about emission factors, not heat
release rates, but Dr Mitcheson was unwilling to express a view about these. I
suspect that he might have been qualified to do so, but it was clear that he
had performed neither the calculations nor the degree of deep cogitation
required to express a properly tutored view. Mr Redfern made some headway on
this topic, in the sense that he was able to persuade me that certainly during
the earlier hours of stage 2 there were very considerable quantities of black
smoke and this fire was severely under-ventilated. However, I need to store
this evidence away for use at a slightly later stage in this judgment, under
the rubric of emission factors.
83.
Although Mr Redfern was far more concerned to develop his point in
relation to emission factors than to heat release rates, I pressed Dr Mitcheson
on the issue at the very end of his evidence. Given that Dr Mitcheson had
derived his mass burning rate set out at paragraph 63 of his first report from
the SFPE Handbook and a situation which is there described as apt for a “room
fire with one or more vertical openings”, I was concerned whether the
particular features of this fire might displace or undermine this model. Dr
Mitcheson had agreed in cross-examination that the simile was not exact, but he
told me that he had taken proper account of the ventilation of this fire in
arriving at his final heat release rate for stage 2. When I examine Dr
Mitcheson’s oral evidence against paragraph 64 of his report, I am not wholly
persuaded that his analysis is correct. In particular:
“The mid-heights of the slots were about 0.5m above the base
of the bunkers and the openings measured approximately 25m x 1m each side,
giving an area of 50m² per bunker. On this basis, the mass consumption rate is
predicted to have been about 4.25 kg/s per bunker. However, this ignores the
open top through which air would have entered and products would have escaped,
both of which would increase the burning rate. For this exercise I have
estimated that the burning rate during stage 2 would have been about 6 kg/s per
bunker, or 33 kg/s overall.”
84.
No one has spotted the arithmetical, or more likely typographical, error
in the final line of the foregoing quotation, and I have not redone the heat
release rate calculation to fathom this issue. Given the ubiquity of dense
black smoke and consequent under-ventilation of the fire during certainly the
early hours of stage 2, I suspect that Dr Mitcheson has increased the burning
rate by too high a factor in all the circumstances of this case. A slightly
lower burning rate, and a concomitantly depressed heat release rate, might make
a relatively small difference to the plume modelling, no doubt in the
Claimants’ favour – the higher the heat release rate, the higher the apex and
range of dispersal of the plume. However, Dr Mitcheson’s evidence has not been contradicted,
it is not obviously illogical or implausible, and I have simply no evidential
basis on which to reduce his estimated burning rate during stage 2.
85.
A separate issue arises as to whether a deduction should be made for
loss through heat radiation outwards from the smoke plume. Dr David Carruthers,
the Claimants’ modelling expert, assumed that 30% of the convective heat would
have been lost through radiation. In his evidence in chief, he explained that
it was “pretty standard in fire models to account for loss due to radiation
- it is heat lost through the buoyancy of the plume”. I appreciate that
this is Dr Carruthers’ standard practice, but his expertise in this area is
questionable. Although he has a doctorate in atmospheric physics, he is not a
fire engineer. Even so, I am prepared to accept that Dr Carruthers is qualified
to speak in broad terms about the natural propensity of a hot body to lose heat
to a cooler surface. That is basic physics.
86.
Mrs Angela Spanton of Envirobods did not make any allowance for heat
loss through radiation. Her evidence on this topic was not altogether clear,
but she appeared to be saying that the ADMS fire document takes radiative loss
into account, the radiative heat would have been retained or entrained within
the smoke, and in any event “the smoke would absorb some heat, but not 30%”.
I fail to understand her reference to absorption of heat within the smoke: the
issue is whether heat would have radiated away from the smoke plume. Mr David
Shillito, the Defendant’s chemical engineer, was qualified to comment on this
issue, but was not particularly helpful in giving me a figure upon which I
could proceed. He refused to accept that 30% might be lost through radiation;
he accepted that some might be dissipated that way, but he would not quantify
it.
87.
I am critical of the Claimants for not cross-examining Dr Mitcheson on
this issue. He was the expert best placed to deal with it, and it is clear from
paragraph 24 of his first report that he had factors such as “incident
radiant heat flux” in mind. What is entirely unclear is whether Dr
Mitcheson made any allowance for this in his computations, although I believe
not because there is no further mention of the issue. Doing the best I can in
these unsatisfactory circumstances, I am prepared to accept the probability
that some heat would have been lost through radiation, but I am completely
disinclined to embrace Dr Carruthers’ 30%, which is based on little more than
assertion. My deduction has to be somewhat intuitive and less than wholly
evidence-based, but in my judgment, applying the probabilistic standard of
proof, the correct deduction in this case is one of 10%.
88.
It follows that I am accepting Dr Mitcheson’s methodology and
computations in relation to heat release rates (see paragraph 80 above), and am
deducting 10% across the board for radiative heat loss. Overall, Dr Mitcheson
was a good witness, although the chemistry between him and Mr Redfern was at times
antagonistic. No blame for this slightly combustible situation needs to be
apportioned. It would have been preferable had Dr Mitcheson been required to
grapple during the forensic process with an expert in like discipline called by
the Claimants, but the state of affairs which obtained has absolutely nothing
to do with him.
Emission
Factors
89.
This was the most hotly contested scientific issue in this case, and by
far the most difficult. The expert antagonists were Dr David Carruthers for the
Claimants and Mr David Shillito for the Defendant. Dr Carruthers was involved
in the development of the ADMS plume model which both parties’ experts have
used to provide the court with an indication of the locations and wanderings of
the smoke plume over the relevant period. I have already alluded to the fact
that he is not an engineer, and emission factors fall within the discipline of
chemical engineering. Mr David Shillito brings precisely that expertise to the
forensic table. However, Mr Kent did not object to Dr Carruthers expressing
opinions on this issue. He was quite right not to do so. Dr Carruthers’
scientific background as a physicist, and his vast experience in the use of
emission factors in numerous situations, enables him to speak authoritatively
on the matter.
90.
Dr Mitcheson and Mrs Spanton declined to express an opinion on the issue
of emission factors. I have already observed that Dr Mitcheson was probably
qualified to do so, but the topic did not fall within the ambit of his
instructions. Mrs Spanton was less well-placed than Dr Carruthers to assist,
and from her perspective she was doubtless well aware that the Defendant’s
nominated expert in this regard was Mr Shillito. I draw no inferences adverse
to the Defendant from their silence.
91.
Throughout the trial, expert witnesses used the terms “emission factors”
and “emission rates” almost interchangeably. No confusion was created in their
minds by this approach, but I felt that this terminological schizophrenia
created the risk that the lawyers, including of course myself, were in danger
of intermingling the concepts. Regrettably, it has taken me some time to fathom
this issue.
92.
In very general terms, the endeavour is to quantify the generation rate
of any chemical or particle of interest over any given period of time. It is
this metric, the emission rate properly so called, which is factored into the
plume model. The smoke plume contained a cocktail or soup of chemicals and
particles, and their individual emission factors varied. Beyond this general
explanation, it is possible to be more precise. Strictly speaking, an emission rate
is the product of the emission factor for any given chemical or
particle and what Dr Carruthers called the “burning rate” (i.e. Dr Mitcheson’s heat
of consumption, not the same as his heat release rate) for the remaining fire
load at the material time. Confusingly, Mrs Spanton’s preferred terminology is
not “burning rate” or “heat of consumption”, but “heat output”. In ordinary
parlance, a rate is, of course, time related, whereas a factor a
fraction. On this approach, an emission factor is measured in terms of
the mass of the chemical or particle of interest per equivalent mass of the
available combustible material (usually, g/kg); the burning rate (a.k.a.
heat of consumption or heat output) is measured in MJ/kg (see paragraph 79
above); and the resultant product, the emission rate, is measured in
g/s/MW.
93.
Confusion arises because the experts have tended to use their terms
interchangeably, confident in the knowledge that each fully understands the
other, but possibly oblivious to a lawyer’s very stale basic science. For the
avoidance of all doubt, it may be helpful if I were to set out my understanding
of the position. If the emission factor is 100 g/kg, and the burning rate or
heat of consumption is 10 MJ/kg (as Dr Mitcheson says it is), 100 g/kg becomes
10 g/MJ. As a joule is a watt per second, this becomes 10 g/s/MW. As Envirobods
have explained, there are other ways in which the same result may be attained,
entailing the application of a relatively simple formula. Thus, what looks like
a rate, because it is measured over time, is described as a factor.
94.
Now that the position is fully understood, no confusion arises. However,
it is necessary to be clear as to where this leads. Whatever the terminology,
the plume modellers have used two separate variables to arrive at the
generation rate over the course of the fire of the chemicals and particles of
interest. They appear to have used an emission rate expressed in mg/s/MW
(although they have called it a factor), and they have also used an appropriate
burning rate. This is the key concept Mr Redfern wanted me to understand. It
is obvious that as the quantity of combustible material falls, so must do the
generation of the relevant chemicals and particles. According to Dr Mitcheson’s
calculations, the heat release rate falls exponentially after midday on 13th
June, and on my understanding what the plume modellers call the burning rate or
heat output is logarithmic (assuming that my recollection of basic differential
calculus has not altogether deserted me). In truth, it matters not, because the
appropriate variable is factored into the ADMS model. However, it is important
to keep separate the concepts of emission factors and burning rates, since
otherwise there might be a tendency to conclude that because the fire is dying
down the emission factors must also be falling commensurately. The emission rate
will be falling, but not necessarily the emission factors – unless,
that is, other considerations come into play which independently impact on the
latter.
95.
Armed with the foregoing scientific logic, Mr Redfern submitted that the
emission factors for this fire must remain constant over stages 2 and 3. However,
that in my view is overly simplistic an approach. Putting to one side the
reduction in the burning rate, the parties’ experts are in fact agreed that the
emission factors vary as the fire progresses. This is a consequence of variables
changing independently of the burning rate, including the chemical environment
changing as well as the degree of ventilation and efficiency of combustion. The
experts are, however, far apart on matters of degree.
96.
The smoke plume contained hundreds if not thousands of chemicals and
particles of potential interest. The expert reports range over a vast array of
chemicals and toxins, but in the events which have occurred I may short-circuit
some of the debate. The present case is concerned with chemicals which possess
irritant qualities and with micro-particles. The possible relationship between
the two will be discussed in my section on toxicology. The chemicals with
irritant properties are primarily the aldehydes, but there were others too
within the fire plume that have not been quantified in any meaningful way,
whether in terms of their emission factors, the toxicology or the plume
modelling. The parties agree that the most important of the aldehydes for
present purposes is acrolein. Apart from the irritant chemicals, the parties
have been focussing on particulate matter which is less than 10 micro-metres in
diameter (the PM10) and the further sub-set of particulate matter which
is less than 2.5 micro-metres in diameter (the PM2.5).
97.
The parties are in agreement about the emission factors for acrolein in
particular and the aldehydes in general. For the former, Mr Shillito has
undertaken a literature review and arrived at what he describes as an emission
factor of 114 mg/s/MW. For the reasons he gives in his first report, and which
I accept, this is very generous to the Claimants. Adopting the same liberal approach
yields an emission factor of 600 mg/s/MW for all the aldehydes. The experts are
also in agreement that these emission factors may be deployed over the whole of
stages 2 and 3 of the fire. For reasons which are fully explored in paragraphs
114-118 below, I disagree with their approach, but I have no evidential basis
on which to advance different values, and (in the face of expert agreement on
the issue) it would not be right for me to do so. The Claimants do far better
out of this state of affairs than does the Defendant.
98.
Where the parties part company is in relation to the PM10s
and the PM2.5s. In this respect, the PM10 emission
factors are the most important, because the factors for the smaller
micro-particles are a derivative of the larger. Here, I need to take time to
explain the basis of the differences between Dr Carruthers and Mr Shillito.
99.
Dr Carruthers has examined three sources in the literature. First, the
publication entitled US EPA Emission Factors AP42 Compilation of Pollutant
Emission Factors addresses a number of potential analogues to the present
fire, and Dr Carruthers considers that the best comparable is the wood-burning
residential fireplace. According to this source, the emission factor for PM10s
in lbs/tons is 34.6, which translates to 17.3 g/kg. Two sections of the
narrative section of this publication are relevant:
“1.9.2 Fireplace emissions, caused mainly incomplete
combustion, include particulate matter, mainly PM10s … significant
quantities of unburnt combustibles are produced because fireplaces are
inefficient combustion devices, with high uncontrolled excess air rates and
without any sort of secondary combustion. The latter is especially important in
wood burning because of its high volatile matter content, typically 80% by dry
weight.
…
Fireplace emissions are highly variable and are a function of
many wood characteristics and operating practices. In general, conditions which
promote a fast burn rate and a higher flame intensity enhance secondary
combustion and thereby lower emissions. Conversely, higher emissions will
result from a slow burn rate and a lower flame intensity. Such generalisations
apply particularly to the earlier stages of the burning cycle, when significant
quantities of combustible volatile matter are being driven out of the wood.
Later in the burning cycle, when all volatile matter has been driven out of the
wood, the charcoal that remains burns with relatively few emissions.”
100.
In his final submissions Mr Kent drew attention to a further passage in
the US EPA document relating to “wood residue in boilers”. This indicates an
emission factor equating to 3.1 g/kg. However, none of the experts was invited
to comment on this.
101.
Secondly, Dr Carruthers referred to a paper by Stec et al published in
the Fire Safety Journal [44 (2009) 62-70], Comparison of Toxic Product
Yields from Bench Scale to ISO Room. I am far from convinced that much may
be derived from this paper. In Figure 6 of the paper, the authors are
considering amongst other things the product yields (i.e. emission factors) for
soot from the burning of MDF for a steady-state tube furnace, compared with an
ISO room, as a function of the carbon dioxide/monoxide ratio. Thus, the
emission factor for a different product, namely soot, is analysed in
comparative terms in a context distant from that of the instant case. As a
separate matter, Mr Kent relied on Figure 6 in support of his argument that
emission factors decrease significantly as the fuel load is consumed. I agree
that this Figure does show that the emission factor for soot decreases
exponentially as the carbon dioxide/monoxide ratio increases, but without a
much better understanding of this paper than anyone was able to give me, I
cannot accept that it necessarily supports the point Mr Kent was seeking to
make. On the other hand, I do accept that this paper lends further support for
the proposition, if such support were needed, that increasing the ventilation
reduces the emission factors.
102.
The centrepiece of the Claimants’ case on this issue was the document
co-authored by Larson and Koenig, A Summary of the Emissions
Characterisation and Non-cancer Respiratory Effects of Wood Smoke, a
version of which was also published in the Annual Review of Public Health in
1994. Table 1 of the Summary gives the PM10 emission factors for
“conventional wood stove” and “conventional fireplace” at, respectively, 7-30
and 15-32 g/kg of wood. The narrative section of this paper reads, insofar as
is material, as follows:
“The large variability in emission rates for a given
appliance is due to a number of factors including stove design, wood moisture
content and burn rate … In conventional stoves, increasing burn rate increases
combustion temperatures and efficiencies, but in catalytic and non-catalytic
devices the higher burn rates actually decrease combustion efficiency by
decreasing the times in the secondary combustion rate …
Compared to wood stoves, we know little about fireplace
emissions. Here we distinguish fireplaces from conventional fireplace inserts.
Inserts are a home-heating device with emissions similar to conventional wood
stoves. Standard open fireplaces can be a net home cooling device because of
the large amounts of air they draw from outside during maximum burn rates. In
general, conventional fireplaces emit comparable amounts of particulate matter
and less carbon monoxide per kg wood burned compared to conventional wood
stoves. However, fireplaces usually operate at higher wood burn rates and for
shorter time periods than most wood heating devices.”
103.
On the basis of the US EPA Emission Factors, Dr Carruthers has taken in
his March 2014 report an emission factor for PM10s of 17.3 g/kg.
Looking at the Larson and Koenig paper, this falls towards the middle of the
range. For PM2.5s Dr Carruthers has used a ratio of 0.82 derived on
my understanding from the Californian Fires paper, addressed more fully below.
No issue arises as to the ratio deployed, and the resultant emission factor for
PM2.5s is 14.2 g/kg.
104.
Dr Carruthers prepared a document for the Joint Experts’ meeting on 24th
October 2014 (privilege has since been waived) which reduces these figures by
20% to reflect the moisture content in the woodchips. Envirobods did not take
issue with that approach, although I note that Mr Shillito, who was advising
them, did not make a similar deduction from his much lower figure. The point
was not explored with any of the experts: either the parties assumed that it
was not in issue, or it was overlooked. Towards the end of the trial, I indicated
to the parties that I considered that the 20% deduction was incorrect in
principle. My understanding of the literature, including the US EPA document,
was that “dry” wood did not mean wood which was 100% devoid of moisture, but
wood that was at the drier end of the spectrum. I recognise that I was running
solo with a point which had not appealed to Mr Redfern. At that stage the
parties did not comment on my rationale or conclusion, but after the close of
the proceedings and following his interpretation of an apparent concession by
Mr Redfern in post-hearing email exchanges, Mr Kent returned to it and urged me
to reconsider. His submission was that Dr Carruthers accepted the 20%
deduction, and that it was supported by the US EPA’s reference to “dry” wood in
connection with the emission factors for the residential fireplace model.
105.
I appreciate that I am responsible for setting up an issue which would
not otherwise have arisen. However, Mr Kent had every opportunity to disabuse
me of it before the trial ended. Further, I remain of the view that the 20%
deduction is incorrect in principle, and the Claimants press me to adhere to
that position. At paragraph 4.14 of his September 2014 report Mr Shillito, when
addressing CERC’s emission factors for the micro-particles, did not contend
that they should in any event suffer a deduction for moisture. On its natural
and ordinarily meaning, “dry” does not mean wood which has been notionally
drained of all moisture. In any event, the US EPA document states that the moisture
content of wood ranges from 5-70%, and that “dry” wood includes wood with
anything up to 20% moisture. I do not read paragraph 1.9.2 of the US EPA
review, with its reference to dry wood, as indicating that all moisture is
squeezed out of the computation. Finally, I am not prepared to finesse this
issue by allowing a deduction lower than 20%. It follows that, although
moisture should obviously be taken into account in relation to the heat release
rates (as it has been), it should not be in relation to emission factors.
106.
Dr Carruthers advanced reasons of his own in justification of the US EPA
residential fireplace emission factors, but before considering these it is
convenient to set out Mr Shillito’s reliance on different literature sources.
107.
In Mr Shillito’s view, the closest analogue to stage 3 of this fire is
the wood-burning biomass boiler. His reasons in support of that thesis are
summarised below, but his source is a Report to the Scottish Government dated
September 2008, AEA Energy and Environment, Measurement and Modelling of
Fine Particulate Emissions from Wood-Burning Biomass Boilers. Mr Shillito
draws attention to Table 2.5 in that report, which summarises the findings of
the Nussbaumer et al study (2008) on “typical PM emission factors” for four different
boiler types including biomass boilers. Although the report refers to 80 g/GJ, this
is equivalent to an emission factor of 0.8 g/kg. It may immediately be seen how
far apart the experts are on this issue.
108.
According to paragraph 2.1.1.4 of the report:
“Smaller biomass boilers are generally not fitted with any
pollution abatement devises as these are generally not required to meet current
CAA requirements for emissions. However, most larger new automatic boilers are
fitted with some form of flue gas cleaning device to remove particle (dust)
from the flue gas before release to the atmosphere.”
109.
Mr Redfern quite rightly drew this passage to Mr Shillito’s attention,
and the latter agreed that larger biomass boilers operating in the UK
would possess a flue gas cleaning device which would serve to reduce emission
factors. On the other hand, it is clear from the report’s analysis of the
Nussbaumer at al study that the Austrian group which performed it were looking
at a wide range of boilers, and included within scope “worse case emissions”.
When an examination is made of Table 2.6 in the Scottish report (which was not
carried out during the trial), it is clear that the average PM10 emission
factors derived from local monitoring data were markedly lower than those noted
in Nussbaumer et al. It was perhaps for this reason that Mr Shillito felt able
to state in this report that Table 2.5, on which he was relying, probably
over-stated the position.
110.
In elaboration of his position, Dr Carruthers explained that the fireplace
analogue, albeit imperfect, represents the closest fit to the circumstances of
the fire with which we are concerned. The basic principle, which is universally
accepted, is that the better the ventilation the better the efficiency of the
burn and the lower the emission factors for any chemical or particle of
interest. There are other considerations which impact on emission factors, such
as the chemical constituents of the fire load as the fire progresses, but these
may be difficult to quantify. A residential fireplace is an open, uncontrolled
fire which is reasonably well ventilated. Thus, in stage 2 of the fire this
model would in Dr Carruthers’ view (as articulated at one stage in his oral evidence)
tend to underestimate the true emission factors for the micro-particles because
it is accepted by Dr Mitcheson that the fire was under-ventilated. The
fireplace model would be more apposite for stage 3. Given that Dr Carruthers
has chosen to use one emission factor for the small particles throughout stage
2 and 3 of the fire, the Claimants submit that he has in fact under-estimated
the position.
111.
On the other hand, I agree with Mr Kent that Dr Carruthers’ final
position was that he accepted that he had used an emission factor throughout
which was based on stage 2 when there was thick smoke with poor visibility. He
said, “I think we modelled the phase 2 fire. So we were looking at when the
fire was clearly very thick with smoke”. He also accepted that his
modelling was on a worst case basis.
112.
Dr Carruthers’ basic objection to the wood-burning biomass boiler is
that it is designed to achieve an automatic, controlled process, in other words
an efficient burn, where the emission factors would inevitably be low. The
presence of thick clouds of black smoke during stage 2 is completely
inconsistent with the controlled process within Mr Shillito’s presumed
contemplation. Furthermore, a biomass boiler would have to be compliant with
the Clean Air Act 1993, where stage 2 of the fire plainly was not. Dr
Carruthers also sought to draw inferences from certain photographs relating to
how far one could see through the smoke, but this evidence was too subjective
and impressionistic for my palate.
113.
In his oral evidence Mr Shillito elaborated on why he believed that the
biomass boiler was a better analogue than the residential fireplace. In his
evidence in chief he explained that (a) the fuel was very different, and he was
looking for “an effective fuel burnout”, and (b) given the dimensions of
our fire, it was appropriate to compare it to a model which was larger than a
residential fireplace. Like Dr Carruthers, Mr Shillito in his reports had
adopted a single emission factor for both stages of the fire, although had
queried the methodological soundness of this approach. On my reading of his
written evidence to the court, Mr Shillito was adopting an emission factor
which he considered was appropriate for stage 2, and then applied the same
value to the beginning of stage 3. In his oral evidence, however, Mr Shillito
said that his approach had always been to seek to ascertain the appropriate
emission factor for stage 3a of the fire (i.e. 12th June), as he
called it, and then apply the same value to stage 2. Mr Shillito struck me as
an entirely honest witness, but I do not read his reports in that way. I
consider that he was extrapolating from stage 2 to stage 3, not the other way
round.
114.
In his oral evidence, Mr Shillito conceded that his unitary emission
factor of 0.8 g/kg was too low for the first two hours of stage 2 by a multiple
of 3 or 4, but otherwise he adhered to his figure. Mr Redfern sought to exploit
this concession by putting to Mr Shillito in cross-examination that, given that
all aldehydes and other emissions are the result of incomplete combustion,
logic would surely suggest that all Mr Shillito’s emission factors
should bear the same increment. Mr Shillito was surprised by this question, and
did not really answer it satisfactorily, but the reality is that the premise on
which the question was posed was completely incorrect (I must confess that the
enthusiasm with which I harried Mr Shillito about this was misplaced). All
emissions are the product of incomplete combustion (i.e. complete combustion of
wood would produce carbon dioxide, water and nothing else): the issue is not
the fact of emissions, but their relative quantities. Further, the
parties have proceeded on the basis of agreed emission factors for all
aldehydes and acrolein in particular – these are safely derived from the
literature, and are not related to the emission factors for the
micro-particles. In any event, multiplying the emission factors for the
irritants by even a factor of four for the first two hours of stage 2 makes no
material difference to the outcome of this case.
115.
Mr Shillito recovered much of his poise during Mr Redfern’s extended and
able cross-examination of him on the issue of emission factors for the
micro-particles. Mr Shillito rejected the fireplace analogue because in his
view it predicates flaming combustion, which this fire was not. He stated that
the key point in the instant case is that by the beginning of stage 3 the fire
load was charred woodchips in respect of which the volatiles had already been
released (during stage 2). Mr Redfern put to Mr Shillito the concept of
“re-volatilisation”, but this was simply not understood: the volatiles in Mr
Shillito’s view would burn off once and for all when initially released. As for
the biomass boiler model, Mr Shillito accepted the point about statutory
compliance, but stated that the analogue remained apposite because wood-burning
boilers use a continuous source of woodchips (which, therefore, continue to
emit volatiles and aerosols), and a larger combustion bed tends to be more
efficient.
116.
It was put to Mr Shillito that during stage 3 the fire was inefficient.
He disagreed, and the transcript of the relevant section of his cross-examination
reads as follows:
“The fire was efficient in stage 3. It had plenty of oxygen
in stage 3. My emission factors were designed for stage 3.
Q. It was reverse smoulder. That's not efficient oxygen, is
it?
A. I think you will find it was quite efficient.
Q. You can't say that stage 3 was an efficient burn, can
you?
A. It's rather like a coke brazier.
Q. The fire is burning back on itself. That's reverse smouldering,
isn't it? It's inefficient.
A. The oxidation is happening at the surface. The heat is penetrating
downwards. As the top fuel burns away, the fuel below comes alight.
Q. It's only the top –
A. If you measure the carbon monoxide from a coke brazier, you
will find there is some, but the burning combustion efficiency is quite
effective. It's like the barbecue after the main thing is alight. It's a coke
brazier.”
117.
Notwithstanding that his own expert had been content to deploy it, Mr
Redfern ambitiously sought to persuade Mr Shillito that the residential
fireplace model was inapposite in the sense that its application would tend
grossly to under-estimate the emissions from the Sonae fire. Mr
Redfern’s point was that a fireplace has flame – which burns off emissions -
whereas our fire did not. Mr Shillito did not accept that this was so:
“The fire, I think, is -- if you start at the top of the page,
that fireplaces are primarily used for aesthetic effects and secondarily as
supplemental heating. The fire is designed to be pretty, to show a nice red
flame. The red flames in themselves produce carbon black. The redness of the
flame is in fact carbon black glowing in the flame. So the fire is designed to
produce soot which burns in the flame. The volatiles, which contain the
irritant substances, will burn preferentially in the flame to the carbon. So
as I see it, a nice red flame will produce black soot, but probably low
volatile contents, and that's one part of it. The volatile material escaping
from the fire will depend obviously on the way that the fire is arranged. But
to my mind, the black soot from the open fire is contributed by the loss of
heat to the outside environment, reducing the -- this is radiation loss from the
visible fire, and effectively quenching the red flames. This is the soot in
the basic wood fire chimney.”
118.
My approach to this important issue is as follows. Unlike the experts, I
am not prepared to adopt a unitary emission factor for the whole of stages 2
and 3. In my judgment, the emission factors changed significantly over the
course of the fire, and to take either a rough-and-ready or an average value
would not achieve justice. I will take one emission factor for stage 2 and
another for stage 3. Each will be at or near the top of the range in both
instances.
119.
With respect to Mr Shillito, who I felt was a very fair and helpful
witness, I cannot accept that the present case receives its best analogue from
the wood-burning biomass boiler. This is a controlled, automated device designed
to minimise emission factors, and the instant case is concerned with an
admittedly very large uncontrolled fire.
120.
In the absence of experimental or empirical data collected at the fire
scene, I consider that the residential fireplace model is the best that may be
achieved in these circumstances. As the authors of the US EPA report make
clear, a residential fireplace is an inefficient device and there will be
significant variances between different homes, configurations and wood piles.
The report also explains that emission factors will depend on - amongst other
matters - burn rate, the degree of ventilation and the degree of flame
intensity. Here, during stage 2 we have a fast burn rate, an under-ventilated
fire (exactly how under-ventilated is not readily quantifiable) and low flame
intensity. Two out of these three matters incline towards higher emission
factors.
121.
Dr Carruthers’ value is derived from the US EPA report and he does not
appear to have examined the Larson and Koenig report and paper which give
higher figures for residential fireplaces. I do not accept Mr Kent’s point that the Larson and Koenig data have in some way been superseded by the US
EPA. The issue arises as to whether it is open to me to taken on board these
data in all the circumstances of this case. Mr Kent objects to such a course,
essentially on two grounds. First, he submits that there is no evidential basis
for a higher value. Secondly, he submits that the Claimants should be bound by
the figure Dr Carruthers has advanced on their behalf, and that it would be
wrong and unjust to countenance a higher value at this late stage.
122.
As for the first objection, I consider that there is an evidential basis
for a higher value, namely the Larson and Koenig report. Mr Shillito was taken
to it, and I cannot accept his reasons for rejecting the simile (see paragraphs
115-117 above) – at least as regards stage 2 of the fire. I am entitled to draw
inferences from all the available evidence, including Mr Shillito’s answers. Although
common sense can be a dangerous guide in relation to scientific matters, I have
reached the clear conclusion that for stage 2 the instant case must fall
towards the upper end of the fireplace model, and of the spread of values
proffered by Larson and Koenig. Stage 2 of the fire was characterised by
voluminous quantities of dense black smoke engendered in a significantly
under-ventilated environment. During its early stages, the “letterbox” slots
were blocked. Moreover, Mr Shillito has not included the hydraulic oil, the foam
and the conveyor belting in his emission factors for the micro-particles, nor
has CERC modelled these (I understand that CERC has modelled the 0.8%
contamination, using the parallel of household waste). Although these have not
been quantified, the presence of these items (which on my findings were wholly
consumed within stage 2) gives me further confidence in moving towards the
upper end of the bracket.
123.
However, it would not be right to go beyond the figure of 32 g/kg as the
emission factor for the micro-particles, as at one stage Mr Redfern temptingly
submitted I should. That would be a leap in the dark, without an evidential
platform, and unfair to the Defendant. More precisely, whatever success he
achieved in cross-examining Mr Shillito does not underpin, or warrant, so
extravagant an approach.
124.
As for Mr Kent’s second submission that the Claimant should be bound by
Dr Carruthers’ value, I see the force of it but in the exceptional
circumstances of the present case I am prepared to allow the Claimants an element
of latitude. Given Mr Redfern’s forensic success with Mr Shillito, it would not
be in the interests of justice or the overriding objective to hold the
Claimants to the figure Dr Carruthers has put forward, no doubt in good faith
but absent consideration of all available evidence. The Defendant is not
prejudiced by this course. Furthermore, Mr Shillito was aware of Larson and
Koenig because he genuflected towards them in his reports (although whether he
was aware of the report, as opposed to the published paper, is less clear).
125.
Taking all this evidence on board, I am required to alight on the
correct value for the micro-particles during stage 2 of the fire. Doing the
best I can on all the available evidence, my emission factor for the PM10 fraction
is 27.5 g/kg. I reduce that by 0.82 for the PM2.5s, i.e. to 22.6
g/kg. In reaching these figures, I should make clear that I have erred on the
side of a liberal approach: in other words, these are generous to the
Claimants, and are tethered to the start of stage 2, not the end.
126.
The transition from stage 2 to stage 3 was not instantaneous, but in my
judgment by a fairly early juncture within the longitudinal course of stage 3
the emission factors for the micro-particles had fallen significantly. As the
authors of the US EPA study explain, later on in the burning cycle the
volatiles burn out, charcoal remains, and the emission factors decline. This
tends to chime with aspects of Mr Shillito’s evidence. On the other hand, Dr
Mitcheson proceeds on the basis that at the commencement of stage 3 there were
still approximately 850 Te of woodchips left to burn. Although many of the
surfaces of the individual woodchips were charred and most were “cooked”, I do no
accept that there was charring tout court. Accordingly, further
volatilisation was a probable phenomenon. Yet, it is indisputable that the
predominant characteristic of stage 3 was smoke which was between whitish and
light grey in colour. Furthermore, I accept Mr Shillito’s evidence that the
fire during stage 3 had become more efficient in consequence of the enhanced
ventilation - both through the slots and from above.
127.
In my judgment, the emission factors for the micro-particles fell
significantly during the course of stage 3. By how much is unclear. I do not propose
to reflect this consideration in my figure, either by selecting more than one
set of emission factors over the 27 days of stage 3, or by taking an average.
Like Mr Shillito, I believe that the proper focus is on Sunday 12th
June, when the wind was from the east. In reality, the graph of emission
factors plotted against time would show a marked decline from mid-afternoon on
Saturday 11th June (I take that point in time because the hydraulic
oil had burnt out by then) and about midday on 13th June. Thereafter,
the decline continued, but was very much slower. Fortunately for the
calculations, Saturday 11th June is far less important for virtually
everyone than the Sunday, because the wind was blowing from the west. Focusing
therefore as I am on Sunday 12th June, my conclusion is that the
emission factor for the PM10 fraction is 12.5 g/kg. Again, I reduce
that by 0.82 for the PM2.5s, i.e. to 10.25 g/kg. These factors apply
to the whole of stage 3. As before, this represents a liberal approach, even
though it is slightly below the Larson and Koenig bracket for the fireplace
model. In this regard I have taken account of Mr Shillito’s evidence regarding
the efficiency of the stage 3 fire.
Ash and Dust
Deposition
128.
In his report dated 25th March 2015, Dr Mitcheson addressed
the issue of ash and dust generation. In his opinion:
“If ash and dust were produced and transported from the
fireground, the most likely time would have been during the intense combustion
that occurred during stage 2.”
In other words, Dr Mitcheson
rejects out of hand the possibility that ash and dust might have been generated
during stage 3, and I understand his reasons for doing so.
129.
As for stage 2, Dr Mitcheson has performed some straightforward
calculations on the basis of a fairly limited literature base, and has
concluded:
“The larger volume of fly ash estimated above released during
stage 2 of the fire would therefore have formed an average covering over this
area of less than about 0.35 microns, i.e. about one third of one thousandth of
one millimetre.”
130.
Dr Mitcheson was not cross-examined on this report. The plume modellers
have not modelled dust and ash on the basis of any reliable data regarding the
sequence and history of the fire (CERC’s previous modelling has been
superseded), and in scientific terms the issue may be taken no further.
131.
However, there is a mass of evidence from the Test Claimants on this
issue which needs to be considered. Given that I am not considering claims in
nuisance which are not personal injury claims, this evidence is not directly
germane to my fact-finding exercise. However, it does bear on the issue of
credibility, and I will be returning to it later.
TOXICOLOGY
132.
Even as regards relatively low exposures of short duration, the general
principle of toxicology applies: “the dose determines the poison”. However, at
these low exposures in particular, considerable allowance must be made for
human susceptibility and variability.
133.
In this domain the forensic tournament was between Professor Alastair
Hay for the Claimants and Mr David Shillito for the Defendant. It is
immediately apparent that in one sense this was an unequal fight: Professor
Hay’s enormous lance pitted against Mr Shillito’s smaller weapon. Professor Hay
is Professor of Environmental Toxicology at the University of Leeds,
and an international authority in his subject. He is extremely experienced and
has sat on numerous governmental committees over the years. Mr Shillito is not
a toxicologist at all; he is a chemical engineer. However, his experience in
environmental issues, and his sense of fairness, cannot be doubted.
134.
Despite this obvious mismatch, I had the feeling that Professor Hay was
somewhat hampered by the instructions he had been given. His three reports are
similar to one another and speak at quite a high level of generality and
theory. They are not particularly quantitative. It is almost as if he was being
discouraged from pinning his precise colours to the mast until as late as
possible. Furthermore, I cannot place any weight on the following assertion in
one passage in his March 2014 report, based as it is on a misapprehension as to
the extent of this fire, and on modelling evidence which has been superseded:
“On the basis of what is known about the Sonae fire, the
photographic evidence of smoke from the fire, modelling of the fallout of
pollutants generated by the fire and the topography of the area, it is more
probable than not that many thousands of people would have been affected by the
pollutant emissions.”
135.
Fortunately, Professor Hay has been much more forthcoming in the witness
box and in the second Joint Statement of these experts. I found him to be an
extremely commanding expert witness. On a few occasions, he became slightly
argumentative, donning the mantle of the advocate, but I understood his passion
for this subject and the strength of his opinions.
136.
The areas of controversy as between these experts have been
significantly whittled down in the later stages of the forensic process.
137.
Aside from the micro-particles which I will address below, and where
there remains a dispute, the experts are in agreement that the focus must be on
the irritant chemicals rather than on the asphyxiates. The latter will not have
left the fireground in significant quantities. As regards the irritants, the
focus has primarily been on acrolein, but consideration has been given also to
the total aldehydes within the metaphorical soup of the fire plume. During the
course of Professor Hay’s evidence in chief, Mr Redfern invited his witness to
perform from the witness box a calculation designed to estimate the additive
effect of the agglomeration all the probable irritant chemicals in this mix, in
other words to look further than the limited number of compounds previously
considered. This calculation had not been attempted before, and I did not give
the Claimants permission to adduce evidence of this nature in this unheralded
fashion. I gave a short judgment at the time, and a transcript (for the
parties’ benefit only) appears on Livenote.
138.
Professor Hay’s evidence was that irritancy is an immediate, not a
delayed, effect. Once the chemical of interest reaches a certain dose, the body
will respond adversely and defensively. Professor Hay added that the effect is
usually transient, depending of course on dose and duration of exposure. The
position is clearly explained in Dr J.C. Wakefield’s paper for the Health
Protection Agency entitled A Toxicological Review of Products and Combustion
(2010). At paragraph 3.2:
“The injury following exposure to an irritant gas depends
upon the chemical involved, its concentration, the exposure duration and its
solubility. However, the initial effect of exposure to these irritant gases is
likely to be sensory irritation. Irritation of the eyes will cause pain and
stinging of the eyes, initiation of a blinking reflex and lacrimation … An
additional characteristic sign of exposure to irritant gases is a burning
sensation of the mucous membranes of the upper respiratory tract, including the
nose, mouth and throat. Pulmonary irritation will commonly occur following
sensory irritation, due to inhalation of the irritant gas into the lungs. The
irritation of the lungs gives rise to bronchoconstriction, coughing and
breathing difficulties.”
139.
Professor Hay stated in cross-examination that there is nothing in the
literature linking dermatological problems to smoke exposure.
140.
As for the level at which a human being may react adversely to an
irritant, it seems to me that I should be primarily focusing not on workplace
or AEGLs, but on short-term levels of a different nature. Here, the HPA review
paper is of assistance. It recognises that acrolein is the most potent of the
irritants, and various thresholds are given at page 15 of the document. In this
regard it is necessary for our purposes to “translate” parts per million into
micro-grams per cubic metre, and doing the best I can with the arithmetic one
arrives at the following:
(i)
eye irritation resulting from exposure to acrolein has been observed at
concentrations as low as c.146 μg/m³ (my emphasis), nasal
irritation at c.356 μg/m³, and respiratory symptoms at c.572 μg/m³ (I
note that Mr Kent’s arithmetic is slightly different). Like Mr Kent,
I assume that these values must be for healthy subjects. There is no evidence
as to what they might be for vulnerable individuals, and I cannot accept Mr Kent’s thesis that healthy people will be more sensitive to an irritant.
(ii)
concentrations of acrolein in the region of 1,100 μg/m³ to 11,000
μg/m³ have been shown to cause the onset of lacrimation and eye irritation
in human beings within a 10-minute exposure period.
(iii)
acrolein at 2,640 μg/m³ has been reported to cause lacrimation in
human beings within 5 seconds of exposure.
141.
On my understanding, these data are agreed between the experts, but they
need to be interpreted. Item (i) above is addressing the absolute minimum levels
at which human beings might begin to experience symptoms. Most healthy persons
will not experience symptoms at such levels or anything like them (assuming
these values are correct), but the higher the dose the more individuals will
begin to suffer. Further, the paper does not throw any light on duration of
exposure (and note item (iii)), although the experts appear to have interpreted
it as a trigger value regardless of length of exposure. Taking a threshold of
146 μg/m³ for acrolein in the context of its potential to cause eye
symptoms is extremely favourable to the Claimants. The plume modellers have
used this value, at my request, for the purposes of illustration. I should emphasise,
if further emphasis were required, that exceeding it does not mean that personal
injury was caused or even likely caused.
142.
For completeness, I should add that from page 16 of the HPA document it
may be gathered that the 8-hour threshold value for acrolein is 237.5
μg/m³, being a weighted average over that period, and the 15-minute value
is 712 μg/m³. I have already said that these are not my primary focus, but
no Test Claimant comes anywhere close to these modelled levels of exposure.
143.
In his plume modelling Dr Carruthers has used an odour threshold for
acrolein of 0.38 μg/m³. Mr Shillito’s explanation for this figure is that
it represents the threshold at which 50% of the population will recognise the smell
(but would not be able to name it as acrolein). On my understanding of his
evidence, Professor Hay felt that this was far too low - he suggested something
in the region of 460 μg/m³ - but this may have been a complaint threshold
rather than an odour recognition threshold. For present purposes I consider
that it is helpful to proceed on the basis of the 0.38 μg/m³ value, not in
any way as a health threshold (pace Dr Carruthers’ view that it is a “good
surrogate as a sort of envelope of the fire impact”), but as indicative of
being the sort of level at which many people would have been able to smell the
smoke plume.
144.
Aside from acrolein, Mr Shillito has also advised the court as to an
appropriate health threshold or trigger value for “total aldehydes”, and has
alighted on a value of 500 μg/m³. As I have already said, Professor Hay
did not perform a similar exercise for the purposes of his reports, but when I
asked him at the very end of his evidence about Mr Shillito’s figure, he told
me that his recent calculations were not “far off”. Much later, I had a
colloquy with Mr Kent about the significance of this value. I had found it
difficult to understand why the threshold for “all aldehydes” was higher than
that for acrolein. The supposition must be that there is some sort of dilution
effect, which I can understand in an experimental setting where relative
concentrations may be in play; but in the context of a given smoke plume with a
number of chemicals of the aldehyde family, one would have thought that the act
of placing more of these under the microscope would serve to increase, rather
than reduce, the irritancy potential. Mr Kent did not really advance a
persuasive rebuttal of this, but overall it matters not. There is no evidential
basis, or evidence-based methodology, which might enable me to reduce the
acrolein threshold below 146, 356 or 572 μg/m³ to reflect the
aggregation of aldehydes.
145.
The HPA report also contains helpful narrative exposition under the
rubric “smoke behaviour” (page 35):
“The exposure to individuals to the fire effluent in the zone
outside the immediate fire zone (zone 2) would be expected to be of most
concern to public health … The major immediate hazard to public health in zone
2 is therefore, expected to be exposure to irritants and particulates generated
in the effluent. Low concentrations of the irritant gases may cause significant
irritation of the eyes and respiratory tract, which may affect a large number
of people who are not directly exposed to the fire plume. The adverse effects
resulting from exposure to these irritants are likely to be completely resolved
following removal from the exposure, with no long term sequelae. However, the
generation of more complex products such as PAHs, dioxins, dibenzofurans and
particulate matter are of concern, but are likely to present a significantly
greater hazard from long term or repeated exposure than following a large
single acute exposure.”
146.
Where these experts disagree is in relation to the micro-particles.
Hereabouts, the disagreement resides on at least two levels.
147.
The first issue concerns the nature and mechanism of any irritant effect
of the micro-particles. On my understanding of his evidence, Mr Shillito does
not consider that the PM10s and the PM2.5s have any
independent or free-standing irritant effect. Professor Hay, on the other hand,
believes that the role of these micro-particles is primarily, albeit not
solely, as “porters” for irritant chemicals which become adsorbed onto them.
Put in these terms, the divergence of view between the experts is minor. In any
event, in the circumstances of the present case I do not consider that this
slight parting of the ways really matters, save perhaps in one respect. Whether
or not the PM10s and the PM2.5s could in theory have any
independent irritant effect, it must be obvious that virtually all of them
operating in this smoke plume were vigorous and prolific carriers of no doubt
numerous chemicals which were dispersed into the environs. I am prepared to
accept that particularly the smaller fraction could have had a free-standing
irritant effect, but it does not matter. The only point one should not lose
sight of is that the quantities of acrolein, for example, have been separately
modelled. This modelling includes all the acrolein, whether travelling on its
own, or aided by a micro-particle. The possibility of double counting must be
resisted.
148.
Mr Kent advanced the more robust submission that I should be ignoring
the micro-particles altogether. Given that they have little or no independent
irritant effect, and given also that the acrolein and aldehydes have been
separately modelled, there is no need for them as a surrogate; we have the real
thing. Mr Kent relied on logic and on Dr Hind (his respiratory expert) in
support of this submission.
149.
I cannot accept Mr Kent’s point. Scrutinising the micro-particles is
merely a different way of trying to examine this vexed issue. It “puts a
handle” on it, as both Mr Shillito and Professor Hay have agreed in their
joint report. Mr Shillito also agreed that micro-particles could be used as a
surrogate provided that due caution was accorded. For me, the issue is not
relevance, but weight. The fact that there is direct modelling evidence of the
aldehydes does not mean that it is wrong in principle to consider evidence of
an indirect nature, particularly given that (a) the micro-particles will be
porters for more than just the aldehydes, (b) the modelling evidence is not
especially robust, and the more of it the better, and (c) there is a mass of
academic literature which chooses to examine the micro-particles. Professor Hay
suggested in addition that scrutinising the micro-particles betokens a
conservative approach in any event because there must be numerous irritant
chemicals travelling independently of them in the plume, and so modelling the
micro-particles may underestimate rather that overestimate the global value of
the irritants. However, in my judgment this is somewhat speculative, given that
(a) many micro-particles may be free of irritant chemicals, and (b) no
scientific paper has on my understanding sought to ascertain the likely ratio
of micro-particles to chemicals of toxicological interest (pace the
answer Dr Hind gave to my question). Without this data, one cannot really say
how good or accurate a surrogate the micro-particles truly are.
150.
Professor Hay’s advice to me was to consider both the PM10s
and the PM2.5s. Although CERC’s recent plume modelling has not made
much of the PM10s, and the histograms have ignored them, I see no
reason for excluding them from account. The Defendant is not remotely prejudiced
because Mr Shillito has contributed fully to this discourse.
151.
As with the irritant chemicals, the issue arises as to the appropriate
threshold levels to take. The experts are agreed that the most authoritative
domestic source is the report by the Committee on the Medical Effects of Air
Pollutants (“COMEAP”), Review of the UK Air Quality Index. Although this
report is concerned not with the effects of smoke but with ambient air quality
in general, it provides considerable assistance with the issues I have to
resolve. The authors observe that at low concentrations of particles the
thresholds have an element of arbitrariness about them, and that it remains
uncertain whether any “safe” level exists. This is a matter which Mr Redfern
explored with Professor Hay in evidence. However, the authors also state:
“While we recognise the possibility that there is no
threshold of the health effects of pollutants, nonetheless we consider that AQI
can be developed that provides useful information on the possible effects on
health at different pollutant levels in the short-term, and identifies
individuals likely to be most susceptible.
…
The health response to increases in outdoor air pollution
varies between individuals and sub-groups of the population … Individual susceptibility
may affect the level at which health effects are noticed and the rate of
increase in symptoms as air concentrations increase.”
152.
In any event, (a) the burden of proof is on the Claimants, not on the
Defendant, and the best that Mr Redfern can do is persuade me to alight on appropriate
threshold levels in view of all the expert and other evidence in this case; and
(b) I cannot agree that any exposure is intrinsically unsafe. In answer
to my question, Professor Hay accepted that “you could come up with a value
… that the majority of people would not be affected at low levels”. Overall,
Mr Redfern’s submission amounts (in loose adaptation of Chaucer) to an impermissible
attempt to make a virtue out of uncertainty.
153.
The COMEAP report sets out two different sorts of threshold level. More
valuable for present purposes are the trigger thresholds based on two
consecutive hourly mean concentrations, subject to the second hourly mean
concentration being greater than the first. Although these are principally
warning levels, Professor Hay’s advice to me, which I accept, is that they
represent the sort of levels at which irritant effects might begin to be
experienced, adopting I have to say a highly precautionary approach. I do not,
however, accept Professor Hay’s point that only one hour’s exposure might be
sufficient. I do not consider that COMEAP may properly be rewritten in this
way, and it is also noteworthy that Professor Hay’s point was specifically
based on the premise that “the particulates are only one small fraction of
the material that will be arriving at somebody’s respiratory tract”. On the
basis that the aldehydes represent the majority of this material, they have of
course been separately modelled. At Table 3-2 of the COMEAP report (page 17 on
the internal numbering), various suggested thresholds are advanced for the
micro-particles, related to three bands, “moderate”, “high or above” and “very
high or above”. Professor Hay did not say which of these bands I should select
for present purposes, although he did in relation to the 24-hour mean
thresholds. Doing the best I can on the available evidence, I take the “high”
value for both PM10s and PM2.5s, namely 107 μg/m³
and 74 μg/m³ (as it happens, CERC’s recent modelling adopts these values).
These thresholds do not appear to discriminate between non-vulnerable and
vulnerable individuals, but the precautionary principle would suggest that they
are designed for the vulnerable.
154.
The second series of threshold levels are the 24-hour mean levels for
both micro-particles of interest, again set out in various bands. The experts
were not agreed as to which bands were appropriate, but I unhesitatingly prefer
Professor Hay’s evidence to Mr Shillito’s. Professor Hay advised me to select
the following thresholds from page 33 of the COMEAP report:
·
PM10s: 51 μg/m³ for vulnerable persons, 76
μg/m³ for the non-vulnerable.
·
PM2.5s: 36 μg/m³ for vulnerable persons, 55
μg/m³ for the non-vulnerable.
As before, this betokens a liberal
approach, namely one favourable to the Claimants.
155.
The COMEAP review also contains the following illuminating expository
passages:
“Short-term effects of air pollution on health
Air pollution has a range of effects on health. However, air
pollution in the UK does not rise to levels at which people need to make major
changes to their habits to avoid exposure; nobody need fear going outdoors.
Adults and children with lung or heart conditions. It
is well known that, when levels of air pollutants rise, adults suffering from heart
conditions, and adults and children with lung conditions, are at increased risk
of becoming ill and needing treatment. Only a minority of those who suffer from
these conditions are likely to be affected and it is not possible to predict in
advance who will be affected …
Older people are more likely to suffer from
heart and lung conditions than young people and so it makes good sense for them
to be aware of current air pollution concerns.
General Population At very high levels of air
pollution, some people may experience a sore or dry throat, sore eyes or, in
some cases, a tickly cough – even healthy individuals … [page 90]
…
There has been very little work conducted on timescales of
less than 24 hours and most knowledge of the acute effects upon health is based
on day-to-day changes in air pollutant concentrations.
The acute effects of particle exposure include increases in
hospital admissions and premature death of the old and sick due to diseases of
the respiratory and cardiovascular systems. The evidence is that both PM2.5s
and PM10s cause additional hospital admissions and deaths on high
pollution days. There are also less severe effects of short-term particle
exposure during pollution episodes, such as worsening of asthma symptoms and
even a general feeling of being unwell leading to a lower level of activity … [page
114]”
156.
The final point which arises in the context of the COMEAP review is the
salience of ambient background levels to the health threshold levels I have
specified. This is a point which meshes with the plume modelling evidence, and
may be expressed in these terms. If, for example, the ambient background level
(i.e. the level untrammelled by the smoke plume) is X μg/m³ of PM10s
for any given period and location, and the modelled concentration of PM10s
is Y μg/m³ (ignoring the background level) for the same period and
location, which value should be calibrated against the relevant health
threshold level for these micro-particles? In my judgment, the answer is X + Y,
applying the straightforward tortious principle of material contribution to the
damage. There are average hourly background data from the Briery Hey monitoring
station, some 1,250 m away from the Sonae plant. I assume for present purposes
that the background levels do not vary much over the whole area under
consideration, although they may be higher nearer the M57. Accordingly, these
data will be used in conjunction with the 24-hourly mean concentrations of PM10s
(see paragraph 152 above) as evaluated for a limited number of Test Claimants
(see paragraph 171 below).
157.
Professor Hay drew my attention to an important paper authored by Kunzli
et al, published in the American Journal of Critical Care Medicine in 2006, Health
Effects of the 2003 California Wildfires on Children. The focus of this
study was a vast, catastrophic series of forest fires in the State of California, visible from space. Local air quality monitors recorded hourly particulate
matter concentrations approaching 1,000 μg/m³, being 10-20 times the
typically observed ambient levels. The researchers collected data from
questionnaires sent out by email within about one month and eight months of the
fire (i.e. far sooner after the fire than the questionnaires in the present
case, and unrelated to any medico-legal context). The children suffered a range
of symptoms not at all dissimilar from those allegedly sustained in the instant
case. What is of great interest, though, is the recorded 5-day mean PM10 exposures
for children in the various locations identified in Table 2 of the paper. From
this table it may be seen that for children with exposures in the range of
30-52 μg/m³, there were precious few complaints of symptoms. However, as
will become apparent at a later stage in this judgment, the Californian cohort
suffered far higher mean levels of exposure to PM10s over a 5 day
period than did their analogues, including adults, in the present fire. Symptoms
were only experienced in significant numbers when the 5-day mean PM10 exposure
level was in the 100+ μg/m³ range. To my mind, this paper significantly avails
the Defendant and not the Claimants.
158.
The final point which falls to be addressed on Professor Hay’s evidence
is the approach to be taken to what Mr Redfern described as “sub-threshold”
levels of exposure. Perhaps anticipating that very few of his clients could
demonstrate on the science that they suffered an “above-threshold” exposure, Mr
Redfern was astute to draw out of Professor Hay evidence which might prove the
Claimants’ case on the balance of probabilities. Whereas it is quite true that
many of the Claimants were exposed on the plume modelling evidence to the odour
of acrolein, that is far from demonstrating that any of them suffered
actionable personal injury. Indeed, if anything it is a point which tells
against the Claimants owing to the impact of human suggestibility. If Claimant
X smelt absolutely nothing, then s/he would probably have to be dishonest to
bring a claim. No one is suggesting that the smoke plume contained odourless or
occult properties akin to carbon monoxide. If the Claimants smelt something,
they might believe that they were exposed to a chemical which might have
injured them in some way. I will be reverting to this point subsequently.
159.
A “sub-threshold” exposure leads a Claimant nowhere unless either the
science is wrong in some way, or the adverse health effects are additive or
cumulative. I did not permit Professor Hay to perform the additions he
obviously wished to, but I doubt whether my ruling truly impeded the Claimants
(and, if it did, I am not reversing it). As I have pointed out, Professor Hay
and Mr Shillito do not appear to be far apart in relation to the total
aldehydes. I asked Mr Shillito whether he would be prepared to add a figure or
percentage to his 500 μg/m³ threshold, in order to reflect the potential
impact of other irritant chemicals in the mix. He suggested a figure of 5%. In
the context of this case, that figure is de minimis and I ignore it. It
falls within the general margin for error in the toxicological and plume
modelling evidence. I have no other evidence before me on which to select any
different figure. As for the possible cumulative effects, these are already
addressed within the 24-hour mean thresholds. There is no proper basis on the
available evidence for aggregating a series of below-threshold 24-hour means in
order somehow to attain an above-threshold value.
160.
Professor Hay was not asked to comment on a paper authored by Larrieu et
al, Are the Short-Term Effects of Air Pollution Restricted to
Cardiorespiratory Diseases?, published in the American Journal of
Epidemiology in 2009. There, the authors examined over a six year period the
possible effects of 10 μg/m³ increases in the ambient PM10 levels
in relation to complaints of upper and lower respiratory tract diseases,
headache and asthenia, skin rashes and conjunctivitis. Strictly speaking,
therefore this study was not about the effects of smoke, but one might have
thought that these would be a fortiori. The study found that there were
relatively modest increases in complaints to GPs, ranging from 1.5% (for the
respiratory tract) to 3.5% (for skin rashes, including dermatitis). However, it
should be noted that the association for skin rashes was said to be “close to
statistical significance” and not above it. Interestingly, Dr Larrieu’s group
pointed out that asthma was not associated with any of the indicators
considered.
161.
In my judgment, it would not be right to put much weight on this single
study. The authors rightly observe that it is a unicentre study with a
population which might have changed during the study period. I accept the evidence
of Dr Iain Foulds that the results, even if valid, show only a slightly
enhanced attendance rate at GP practices, that we have no evidence as to the
severity, as opposed to the mere fact of the complaints, no indication of the
extent to which those complaints were objectively validated, and no replication
of these findings elsewhere.
162.
In his closing submissions Mr Redfern, armed with this study and the
separate WHO Guidelines, urged me to instruct further plume modelling based on
a 10 μg/m³ increase in PM10 levels. I have declined this
request. The WHO Guidelines, based on PM10 levels as low as 3-5 μg/m³,
are concerned only with long-term health effects. In my judgment, evidence
that increases as low as 10 μg/m³ might have significantly affected even
some of the Claimants is extremely tenuous and speculative, and I prefer to
proceed on the basis of the COMEAP data, setting out indicative health
thresholds which are already favourable to them.
THE
METEOROLOGICAL EVIDENCE
163.
Fortunately, the meteorological evidence in this case is now agreed, and
it is unnecessary for me to do more than quote from paragraph 18 of the Joint
Statement of Mr Norman Lynagh and Dr Richard Wild:
“On the basis of the ‘best estimate’ winds the following are
dates and approximate times on which the wind would have been blowing from the
Sonae factory towards at least part of the residential area or very close to
it:
9th June: 22:45 – midnight
10th June: 00:00 – 08:30
12th June: 04:00 – midnight
13th June: 03:00 – 05:00
14th June: 06:45 – 09:15 and 14:30 – 20:30
15th June: 01:00 – 13:30
16th June: 02:00 – 05:15
17th June: most of the day
18th June: 00:00 – 01:15
20th June: 05:45 – 07:30
21st June: 00:00 – 01:45
22nd June: 00:00 – 06:00
24th June: 19:30 – midnight
25th June: 00:00 – 05:30
26th June: 01:00 – midnight
27th June: 00:00 – 11:00
These are similar to the findings in our reports.
…
There were 6 days on which winds did not blow from the Sonae
factory towards any residential area at any time. These were 11th,
19th, 23rd, 28th, 29th and 30th.
There was only one day, the 12th, during which
winds of any strength were blowing directly from the Sonae factory towards
residential areas for an extended period of time.”
164.
The meteorological experts do not refer to July data, but the plume modellers
have taken these into account. Plainly, the period of greatest interest is 10th
– 13th June, when the emissions were at their highest levels. For
stage 2 of the fire, the wind was blowing from the east, towards Kirkby, only
for four hours (up to 08:30). For the first part of stage 3, the wind was
blowing in that direction for 20 hours on 12th June and for 2 hours
on 13th June. Given the wind direction, 17th June is also
a date of some importance.
THE PLUME
MODELLING
165.
Nothing now separates the plume modelling experts in relation to the
area of expertise with which they are strictly concerned. What previously
divided them were the data or inputs apt to be fed into the same version of the
ADMS computer model that each was using. Given that I have taken control of
these variables, the computer programme must yield the same results whoever
operates the programme.
166.
I fully appreciate and understand that plume modelling is not an exact
science. There is an element of inherent uncertainty inasmuch as the programme
has its limitations; it cannot replicate the fabulous complexity of the real
world. However, the degree of imprecision must not be over-stated, and I do not
accept Mr Redfern’s reference to “an educated approximation”. Nor must it be
assumed that the plume modelling underestimates indicative exposures. It is
just as likely that it overestimates them.
167.
I have already discussed aspects of the evidence of Dr David Carruthers
in relation to emission factors and the overall methodology of plume modelling.
In my view, he was a compelling and beguiling expert who had the knack of
explaining quite complex concepts clearly, elegantly and with appropriate
enthusiasm. I was not so appreciative of Mrs Angela Spanton, who gave the
impression of lacking a degree of confidence and authority. I fully recognise
and understand that it was always the Defendant’s intention to call Dr Hall to
speak to the reports of Envirobods, but unfortunately he died in February 2015.
However, I do not accept the point that Mr Redfern made in cross-examination
that Mrs Spanton must be incorrect in her assertion, based on extant modelling,
that only 30% or thereabouts of all 16,000 plus Claimants were meaningfully exposed
to the smoke plume at all. Looking at the location of the majority of the Claimants
in relation to the A580 East Lancs road and the M57, it does appear that about
70% of the total cohort, some of whom were represented within the constituency
of Test Claimants, were exposed only to minimal levels. Surpassing the acrolein
odour recognition threshold for short periods comes nowhere close to being able
to prove an adverse health impact. Dr Carruthers accepted in cross-examination
that his modelling showed the same general picture.
168.
Despite his compelling qualities as an expert, and above all his
presentational abilities, Dr Carruthers was in my judgment significantly
hampered, if not misled, by the information he was given by the Claimants’
solicitors. Notwithstanding what is said in his first report, this was by no
stretch of the imagination a fire which blazed for 16 days. Like Professor Hay,
he was “drip-fed” information over the course of his litigation, much of it
being inaccurate, unreliable or unsubstantiated. I should make clear that in no
respect does the fault lie with Dr Carruthers. The internal assumption may have
been that this case would settle, but there are obvious risks in not briefing
experts properly.
169.
As regards the Claimants’ plume modelling evidence, the foregoing point
may be illustrated in this way. CERC’s first attempt at modelling was on the
basis of nine separate factual scenarios, most of which were unsustainable (I
accept that it was at least arguable that there were more than 1,550 Te of
woodchips in the bunkers). That attempt was also predicated on a fire
history/timeline which was unsupported by any expert evidence, and
unsustainable in the face of the photographs. Once the Defendant’s expert
evidence was disclosed, what the Claimants needed to do was to regroup and
instruct CERC to remodel indicative exposures on the basis of Dr Mitcheson’s
report and/or a total mass of 3,000 Te in the six bunkers (if the latter course
were adopted, permission would have been needed to rely out of time on the
evidence of a fire engineer to combat Dr Mitcheson). Moreover, the remodelling
should have been done both generically and in relation to each Test Claimant.
Although CERC carried out this exercise on an informal basis (based as it
happens on Dr Mitcheson’s data), and various data and histograms were disclosed
during the course of without prejudice meetings with the Defendant’s experts, these
were not placed before the court on any proper basis until after the trial
started. Fortunately for the Claimants, Mr Kent had the good grace and judgment
not to object. That said, even if he had done I would have allowed this
evidence in, notwithstanding its tardiness.
170.
What is now available from the Claimants’ side is the following:
·
tables (showing the original 40 Test Claimants) examining the
emission rates for PM2.5s and PM10s using the residential
fireplace model for emission factors and the COMEAP trigger values of 74 and
107 μg/m³. Unhelpfully, the tables contain two sets of meteorological data,
but helpfully they depict the number of hours of exceedances.
·
tables (as before) examining the “total aldehydes” on the basis
of the two emission rates (described by him as factors) originally proposed by
Mr Shillito (although he is now content to proceed on the basis of the higher
rates of 600 mg/s/MW) and a health threshold of 500 μg/m³.
·
a similar table for acrolein based on Mr Shillito’s emission rate
of 114 mg/s/MW and the odour recognition threshold of 0.38 μg/m³.
·
three separate tables focusing on the three highest exposed
Claimants: these examine predicted hourly concentrations of PM10s on
alternative emission factors, and include the Briery Hey background values.
·
standardised histograms for each of the 20 Test Claimants
comparing their exposures hour by hour against five separate thresholds (the PM10
threshold has not been included).
·
various contour plots examining different chemical/particles and
emission factors.
171.
The landscape has of course changed in the light of my findings. Shortly
after the close of the trial, I invited CERC to undertake further modelling of
the smoke plume limited to the 20 Test Claimants now under scrutiny, using
agreed data where appropriate and the specific bases set out below, presented
and/or tabulated as follows:
·
a contour map showing the number of hours exceeding the acrolein
odour recognition threshold of 0.38 μg/m³.
·
a contour map showing the number of hours exceeding the lowest
recorded health threshold for acrolein of 146 μg/m³.
·
a contour map showing the number of hours exceeding the health
threshold for “total aldehydes” of 500 μg/m³.
·
a contour map showing the number of hours exceeding the PM10
trigger value of 107 μg/m³ (based on an emission factor of 27.5 g/kg
for stage 2 and an emission factor of 12.5 g/kg for stage 3). I appreciate that
when interpreting this contour map I will need to take into account the point
that COMEAP requires two consecutive hours.
·
a similar contour map for the PM2.5 particles based on
a trigger value of 74 μg/m³, and emission factors of 22.6 g/kg for stage 2
and 10.25 g/kg for stage 3.
·
a table (showing only the 20 Test Claimants and the agreed
meteorological data) examining exposures to PM10s using my emission
factors for stages 2 and 3 (viz. 27.5 g/kg and 12.5 g/kg) and the COMEAP
trigger value of 107 μg/m³. As before, the table will show the numbers of
hours of exceedances above this trigger value.
·
a table (showing only the 20 Test Claimants and the agreed
meteorological data) examining exposures to PM2.5s using my emission
factors for stages 2 and 3 (viz. 22.6 g/kg and 10.25 g/kg) and the COMEAP
trigger value of 74 μg/m³. As before, the table will show the numbers of
hours of exceedances above this trigger value.
·
a table examining the “total aldehydes” on the basis of an
emission rate of 600 mg/s/MW and a health threshold of 500 μg/m³. As
before, the table will show the numbers of hours of exceedances above this
trigger value.
·
a similar table for acrolein based on Mr Shillito’s emission rate
of 114 mg/s/MW and a lowest recorded health threshold for acrolein of 146
μg/m³.
·
a similar table for acrolein based on Mr Shillito’s emission
factor of 114 mg/s/MW and the odour recognition threshold of 0.38 μg/m³.
·
separate tables for Test Claimants numbered 24 (10th
and 12th June), 30 (10th, 11th and 27th
June), 33 (work) (11th, 15th and 20th June),
37 (10th, 12th and 17th June) and 39 (10th,
12th and 17th June), using my emission factors and rates,
and the agreed meteorological data, setting out the hourly concentrations of PM10s
and the Briery Hey background data for those dates.
·
one set of standardised histograms for each of the 20 Test
Claimants comparing their exposures hour by hour against the following separate
threshold values: the odour recognition value for acrolein; the lowest recorded
health value for acrolein, and total aldehydes (all based on the previously
stated emission factors and threshold values).
·
one set of standardised histograms for each of the 20 Test
Claimants comparing their exposures hour by hour to the PM2.5s and PM10s,
using the previously stated emission factors and rates, against the trigger
threshold values of 74 and 107 μg/m³ respectively.
172.
For the avoidance of doubt, I was not inviting CERC to deduct 20% in
relation to the PM2.5s and PM10s to reflect moisture
content. I was not asking CERC to model the hydraulic oil, the foam and the
conveyor belts (the emission factors for these are not available, and they are
being accounted for in a different way). As regards the 0.8% contamination,
CERC was required to model this in the same way as it had done previously, in
other words (on my understanding) taking emission factors for household waste.
Finally, CERC’s remodelling was carried out on the basis of my earlier findings
in relation to total initial tonnage in the bunkers, heat release rates etc.
173.
I appreciate that I had not specifically requested tabulation of CERC’s
remodelling against the 24-hour mean values for the PM10s (51
μg/m³ for vulnerable persons, 76 μg/m³ for the non-vulnerable) and
the PM2.5s (36 μg/m³ for vulnerable persons, 55 μg/m³ for
the non-vulnerable). However, when I gave my instructions to CERC I was
confident that I would be able to ascertain the position as regards these values
from the considerable array of data which I had requested, in particular the
five most heavily exposed Test Claimants. In the event, CERC has kindly provided
the 24-hour mean values for this sub-group.
174.
The fruits of CERC’s remodelling have been appended to this judgment (see
Appendix 2) and are analysed further below.
175.
Before leaving this section, I have to observe that there are features
of the plume modelling which are not wholly satisfactory. One specific matter
which concerns me is the ability of the model to provide a “handle” on subtle
changes in wind direction and of temperature, and the possible ability of smoke
to linger and seep. The model cannot account for the peripatetic nature of
human behaviour, and in many cases it is difficult to know the exact position
of any Test Claimant during daylight hours. On the other hand, the plume model
fixes on external exposures, and people remaining indoors will have been exposed
to less. Further, it is unlikely that most individuals’ natural daily movements
would have brought them closer to the Sonae plant; common sense would suggest
that they would have moved in the opposite direction. Mrs Spanton referred to
the “margin for error” within the model, but its nature and extent was not
explored. Many of the sociological points set out above were made during the
course of the trial, but the inherent lack of precision of the plume model was
not quantified. These concerns aside, the plume modelling is the best evidence
the present state of human ingenuity can presently provide.
176.
In my view, this is the now appropriate stage for me to set out the
legal principles which govern these claims.
GOVERNING LAW
177.
Most of the legal principles governing a claim of this nature are so
axiomatic that explicit recognition in this judgment is not required. However,
it is appropriate to address four specific areas.
178.
First, it is common ground that the Claimants cannot recover damages for
personal injuries unless they establish on the balance of probabilities that
they sustained what the law regards as “actionable injury”. It is insufficient
for them to prove, without more, inconvenience and distress. I examined the
relevant jurisprudence on this issue in my recent decision in Greenway and
others v Johnson Matthey Plc [2014] EWHC 3957 (QB). Although, at the time
of writing, I am aware that my decision is en route to the Court of Appeal, I
am confident that my coverage of the general principles (as opposed to their
application to the cases then under consideration) is uncontroversial. The
leading authorities are Cartledge v Jopling [1963] AC 758 (HL) and Rothwell
v Chemical and Insulating Co Limited (2008) 1 AC 281 (HL). At paragraph 26
of my judgment in Greenway, I said this:
“On my understanding of its reasoning, the House of Lords in Rothwell
did not seek to reinterpret its earlier decision in Cartledge, although
– as has been pointed out in the parties’ written submissions – their
Lordships’ individual formulations of the legal test varied slightly. For Lord
Hoffmann the test (in tort claims generally) involved the “abstract concept
of being worse off, physically or economically, so that compensation is an
appropriate remedy” (at 289D). For Lord Hope, the test was whether there
was “real damage, as distinct from damage which is purely minimal” (at
297E). For Lord Rodger, the test was “material damage” (at 311F). It
might be argued that some of the formulations tend to circularity. What may be
more valuable is to consider how the test was applied to the facts of both Cartledge
and Rothwell itself.”
179.
The facts of both Cartledge and Rothwell are far removed
from the present scenario, and in the passage I have set out above I have
alluded to the potential circularity which arises. Ultimately, in my judgment,
this must be a question of fact and degree. A transient, trifling,
self-limiting, reversible reaction to an irritant is not “actionable injury”
for the purposes of the law of tort. These could fairly be described as “normal
physiological responses”. However, the ubiquity of this concept cannot be
recognised because it could be used to characterise the reaction of human
tissue to hydrochloric acid. The normality of the burn does not rob the injury
from its characteristic of being actionable. In my judgment, if the degree of
irritation is severe enough, whether or not it becomes a pathological response
expressed in terms of inflammation, it may be possible to hold that the line
has been crossed. This is more likely to be so if there are several severe
irritant responses occurring simultaneously: i.e. to the eyes, the nose, the
respiratory tract, and they last long enough. Usually, one would expect
to see evidence of a resulting inflammation in such cases.
180.
The question does arise of whether a series of minor, sub-threshold
irritations is capable of overleaping the bar set by the concept of actionable
injury. Could 1,000 sneezes amount to a claim whereas 1, or even 10, sneezes
plainly could not? I accept that difficulties might arise at the margins
(imagine 1,000 consecutive sneezes), but ultimately this point collapses into
what is in common parlance called the “zero sum game” rather more elegantly
expressed by Lord Hope in Rothwell (see paragraph 42 of his opinion).
181.
Having regard to all the available evidence, I intend to adopt a broad,
common-sense approach to this issue. The clinicians differentiate between
irritation and inflammation (“... -itis”), but my approach will not be strictly
tethered to the strict medical or pathological concepts, although will
recognise that these have some general utility. However, there is still a
hurdle which each Test Claimant has to surmount.
182.
Secondly, the Claimants seek to argue that it is sufficient for their
purposes that they are able to prove that the Defendant’s breach of duty
materially contributed to the risk of injury. I was taken to the pre- and post-Fairchild
jurisprudence, as well as to a number of decisions of the highest authority
dealing with industrial disease. On this issue I am able to be quite brief,
because in my judgment Mr Redfern is seeking to lead me into frank error.
183.
In the present case we have one tortfeasor and, putting to one side for
the time being questions of pre-existing vulnerability and background air pollution,
one package of potentially causative agents. The issue is whether that package
of chemicals and particles caused or materially contributed to the Claimants’
alleged personal injuries. The Claimants do not have to prove sole cause, but
they do have to prove material cause. It is conceptually and legally incoherent
in a case such as the present to speak in terms of the smoke plume making it
more probable that the Claimants might have suffered personal injuries, or (to
put the same point in another way) that their risk of suffering personal
injuries was increased. The issue is a binary one: either, on the balance of
probabilities, they sustained an injury in consequence of tortious exposure, or
they did not.
184.
The Fairchild doctrine of “material contribution to the risk” is
designed to cover two situations. The first is where there are two or more
tortfeasors, and medical science cannot say which caused the injury. In order
to achieve justice for the Claimants, the law relaxes the “but for” test of
causation. However, in that situation it is beyond dispute that (a) the
Claimant suffered personal injury, and (b) that injury was caused by a tortious
agent (whose agent being the issue). The second situation is where there is one
tortfeasor and two potential causative agents (one “guilty” and the other
“innocent”), but it cannot be proven which actually caused the Claimant’s
injury. Again, in all these situations it is beyond dispute that (a) the
Claimant suffered personal injury, and (b) the industrial agent was capable of
causing that injury.
185.
I reviewed most of the relevant jurisprudence in Heneghan v
Manchester Dry Docks Ltd and others [2014] 4190 (QB), another case en route
to the Court of Appeal, but where my same general observation applies (see
paragraph 178 above). The locus classicus remains McGhee v NCB
[1973] 1 WLR 1. In “innocent” and “guilty” dust cases, the law does not require
strict probabilistic proof applying the “but for” test. Mr Redfern drew my
attention to the earlier decision of the House of Lords in Gardiner v
Motherwell Machinery and Scrap Co Ltd [1961] 1 WLR 1424, another case where
the first opinion was given by Lord Reid. Mr Gardiner claimed damages at common
law for exposing him to conditions liable to cause dermatitis, and in failing
to provide proper washing facilities. Lord Reid explained the basis for the
plaintiff’s recovery of damages for breach of duty in this way:
“I can now sum up my view in this way. The appellant never
suffered dermatitis before he was exposed during his employment by the
respondents to conditions liable to cause that disease. His original symptom –
an outbreak on the back of his hand – is admittedly typical of industrial
dermatitis …
In my opinion, when a man who has not previously suffered
from a disease contracts that disease after being subjected to conditions
likely to cause it, and when he shows that it starts in a way typical of
disease caused in such conditions, he establishes a prima facie presumption
that his disease was caused by those conditions. That presumption could be
displaced …”
Other members of the Appellate
Committee analysed the case on the basis that the appellant had proved his case
on all the available medical evidence. Thus, Lord Reid’s approach, albeit
immensely authoritative, should be regarded as evidencing a minority view. This
is the same minority view that Lord Wilberforce espoused in McGhee (see
7E), and in my judgment should be regarded as apart from the mainstream.
186.
The fundamental reason why the “material contribution to the risk”
principle, in any of its manifestations, cannot avail the Claimants is that it
is incumbent on them to prove on the balance of probabilities that they were
within the relevant envelope of material risk as that concept is properly
understood. It is insufficient for them say – whatever the strength of
their personal conviction may be – that they were at risk in the sense that
they had some exposure. On that argument they should succeed even if the
exposure were minuscule, measurable only in parts per trillion. In my judgment,
any Claimant was only at risk if s/he can prove exposure at a level which was
capable of causing personal injury. This the relevant risk for these purposes.
For many people, exposure at these levels would not in fact cause personal injury,
but the threshold defines the level at which they are at least “at risk”. The
sub-threshold terrain may not be “safe”, in the sense that it cannot
scientifically be proven to be 100% safe, but as I pointed out to Mr Redfern
when he was examining Professor Hay on this topic, the null hypothesis
works the same way in science and in law; all that varies is the standard of
proof.
187.
I should not be understood as being necessarily wedded to threshold
levels which are derived from experimentation and scientific inquiry. The
levels I have selected as indicative are, in fact, favourable to the Claimants,
but there remains room for an argument that they should be relaxed yet further
to reflect the scientific uncertainties which abound, and the difference between
the level of proof the law as opposed to science requires. The extent to which
I will succumb to that argument depends on balancing the strength of the
scientific evidence against that of the lay evidence. In the final analysis,
however, I will have to arrive at appropriate thresholds, even if they are
lower than those a purely scientific approach would mandate. To do otherwise
would not be to exercise the “complete autonomy” which Mr Redfern suggests I
possess, but to indulge in unprincipled decision-making. Whatever the final
position on the thresholds, the position remains the same: below them no
Claimant is within the envelope of risk.
188.
The third legal issue which arises avails the Claimants, and there is no
dispute about it. Given that a Claimant does not have to prove more than that
the smoke plume materially contributed to his or her personal injury, success
is achieved either if it is shown that exposure exacerbated a pre-existing
condition (even if a person without that condition would not have sustained any
injury), or if exposure, added to background levels of pollutant, took that
Claimant above a relevant threshold (even if the background level was
sub-threshold).
189.
The fourth legal issue which arises is the difference between the legal
and scientific standard of proof. The Court of Appeal has stated on a number of
occasions that there is a difference between these two standards (see, for
example, the judgment of Smith LJ in MoD v Wood [2011] EWCA Civ 792),
but what is more difficult is to specify exactly what it is. Without attempting
an academic or jurisprudential analysis in a case already bristling with
difficult issues, it seems to me that the relevant points may be made in this
way. First, a scientist would tend to discount retrospective accounts given
some considerable time after the events in question. A lawyer might treat such
accounts with condign appreciation, depending on their overall reliability,
credibility and consistency, because the approach of the common law has always
been more inclusively flexible than a purely scientific approach. So, the fact
that the lay evidence in the present case would not get past the front door of
any reputable scientific journal is not quite the point. Secondly, the evidence
supporting the various health threshold levels in the toxicological literature
may have been filtered through more robust and stringent filters than those
which would be required by a lawyer applying probabilistic standards (on the
other hand, I repeat the point that many of the COMEAP levels are
precautionary). Thirdly, there are respects in which the science is inherently
uncertain, notwithstanding its claim to precision. I have in mind the plume
modelling evidence. A scientist would say that if the modelling fails to prove
the case, that must be the end of the matter. A common lawyer would say that
there remains room for flexibility and reasonable latitude, and that the whole
picture must be held in mind. How much room, though, needs very carefully to be
considered.
190.
Mr Redfern drew attention to the decision of the Court of Appeal in Armstrong
v First York Ltd [2005] 1 WLR 2751. In that case, the claimants alleged
that they suffered soft-tissue injuries to their spines in consequence of a
relatively low-impact road traffic accident. The parties relied on accident
reconstruction evidence based on second-hand information about the damage the
vehicles had sustained. This evidence directly contradicted the claimants’
evidence and stated that they could not have sustained injuries as they alleged.
The trial judge found the expert evidence to be convincing and the claimants to
be blameless and honest witnesses. The judge preferred their account. The issue
which arose on appeal was whether the trial judge could have rejected the
expert evidence without finding any flaw in it. The Court of Appeal held that
he could: he had weighed up all the evidence in the case, and was entitled to
conclude that the claimants were not lying and that there had to be some
inaccuracy in the expert’s evidence.
191.
At paragraphs 26 and 29 of his judgment, Brooke LJ said this:
“In my judgment, in this very difficult case the judge
directed himself correctly as a matter of law. He was entitled to consider the
evidence he had been given by the Claimant extremely carefully, directing
himself about the dangers of witnesses who may seem to be plausible but in fact
are telling a pack of lies, and directing himself to consider very carefully
the evidence given on behalf of the defendant. He formed the view that he could
not be satisfied that these witnesses were telling a pack of lies. He was very
impressed by their evidence, and he concluded, when he had to balance the
evidence of each side, that there must be - although he accepted fully that he
could not say what it was – something that was not accurate in Mr Child’s
evidence in that particular case.
…
In my judgment, if we dismiss this appeal in this case we are
not opening the door to a whole lot of dishonest claimants to recover just
because there may be cases in which the honesty and force of a claimant’s
evidence impresses a trial judge in the way the evidence of these claimants did
on this particular occasion. In very many cases the evidence of a witness like
Mr Childs may well be sufficient to tip the balance strongly in the defendant’s
favour.”
192.
Brooke LJ also referred to the decision of the Court of Appeal in Coopers
Payen Ltd v Southampton Container Terminal Ltd [2004] 1 Ll Rep 331, where
Lightman J said this:
“There is no rule of law or practice in such a situation
requiring the judge to favour or accept the evidence of the expert or the
evidence of a witness of fact. The judge must consider whether he can reconcile
the evidence of the expert witness with that of the witness of fact. If he
cannot do so, he must consider whether there may be an explanation for the
conflict of evidence or for a possible error by either witness, and in the
light of all the circumstances make a considered choice which evidence to
accept. The circumstances may be such as to require the judge to reach only one
conclusion.”
193.
The context of Armstrong differs from the present case in a
number of respects. There, the choice was stark and binary for the trial judge:
the claimants were either truthful or they were liars. No witness may be heard
to contradict Newton’s Laws; but the science – in Armstrong, the
engineering evidence – unlike Newton, might have been flawed.
194.
In the present case the situation is far more complex. There is a mass
of science, of variable inherent weight across the board, and a mass of lay
evidence. Earlier sections of my judgment have addressed the science, but I am
about to move onto the evidence of the clinicians and the Test Claimants. My
approach will be to assess that evidence on a traditional, common law basis,
and finally in the concluding section of my judgment I will attempt the
syncretism that Lightman J recommends. If that reconciliation cannot be
achieved, each corpus of evidence will continue to be judged in its own right,
but at the end of the day something may have to yield.
THE EVIDENCE
FROM THE CLINICIANS
195.
Although this body of evidence was called after I heard from the Test
Claimants, I consider that it is appropriate to examine the generic aspects of
the evidence from the clinicians at this stage.
196.
I heard evidence in four disciplines: lower respiratory tract; upper
respiratory tract; skin; and eyes. All the medical experts underlined the
importance of taking a detailed and accurate history from a Claimant.
197.
Dr Christopher Hardy FRCP, consultant general and respiratory physician working
primarily at the Manchester Royal Infirmiary, was called by the Claimants. Dr
Charles Hind FRCP, consultant physician working primarily at the Liverpool
Heart and Chest Hospital, was called by the Defendant. Temperamentally very
different though they clearly were, their expertise and experience is immense
and I was extremely grateful for their evidence.
198.
The respiratory physicians examined the then 40 Test Claimants jointly
in November 2014 and provided separate reports for the Court. They also
provided a Joint Statement following a without prejudice meeting in the usual
way. Although the dates of examination varied slightly, the pattern was the
same in relation to the other disciplines.
199.
In a powerful and sustained piece of oral evidence, Dr Hardy explained
why he considered that the Test Claimants he saw were likely to have been
victims of exposure to the smoke plume, causing symptoms to the lower
respiratory tract. In his view, the cases tended to follow a clear pattern.
Many of the people were aware of the fire, owing to its terrible smell and
taste, which were new. Some of them described a very large black cloud crossing
their homes and gardens. At least one person showed the doctors a photograph on
his phone of the cloud in relation to his garden. All decided to batten-down
their houses, but the smell and taste persisted. Generally, within a day or
two, the Test Claimants developed symptoms. The first thing they tended to
describe was itchy eyes, of varying degrees of severity. Nasal symptoms were
described by virtually everyone: their noses were either very blocked or very
runny. Sore throats were very prominent. Virtually all of them would say that
their throats were very dry at night, and that they needed a glass of water by
their beds to keep their throats moist. Claimants also complained of a severe
cough with tenacious sputum, sometimes with breathlessness and wheeziness, and
some had skin symptoms.
200.
According to Dr Hardy, the differences in terms of the histories taken
related principally to the duration of symptoms. In relation to those who had
pre-existing problems or issues (e.g. asthma; COPD; smokers), the onset of
symptoms was different as well as their offset. It was difficult to time this
precisely, but as regards those who had no co-morbidity the symptoms tended to
last 3-6 weeks; in relation to those who did have other problems, the duration
of symptoms could be measured in months. Accordingly, in Dr Hardy’s view, these
were severe symptoms, albeit temporary.
201.
Dr Hardy addressed the possibility that some, many or all of the Test
Claimants might have suffered from a coincidental viral infection. He agreed
that there was a significant overlap between the presenting signs and symptoms
of viral illnesses, and the Claimants’ complaints of smoke exposure. Dr Hardy
drew to my attention the inherent implausibility of so many people suffering
from a viral illness (one might add, in the early summer), and he also referred
to the very similar time period of onset and what he called the constellation
of symptoms.
202.
Dr Hardy explained that when exposure finishes, it will take time for
the patient to recover. Smoke irritated and inflamed the mucosa, the lining of
the respiratory tract, and ultimately the airways with the development of
bronchitis. When the exposure ceases, the glands producing sputum will not turn
off like a tap, as he put it.
203.
Dr Hardy therefore felt that on the balance of probabilities, if a
Claimant had been exposed to the smoke plume, and developed exactly the same
symptoms as the others, then those symptoms were due to the Sonae fire.
204.
Dr Hardy’s understanding of the fire was that it was burning well for a
week, and then smouldering thereafter.
205.
Under cross-examination, Dr Hardy agreed that no definitive test existed
to prove that these symptoms, if they were truly experienced, were due to the
fire. He said that irritant chemicals can create an inflammation if the dose is
sufficiently severe. He did not agree that people would fall ill at once; it
might take up to 24-36 hours. In relation to the toxicological thresholds, he
made the point that people may respond very differently to the same dose.
206.
Later in his evidence, Dr Hardy said that people with underlying lung
disease who suffer an inhalation injury would be more likely to develop an
infection, because their immunological response will have been compromised.
207.
Dr Charles Hind said that there was considerable common ground between
him and Dr Hardy. The reaction of the lungs to an insult will depend on its
severity. The irritant effects occur within seconds, or at the most minutes, of
exposure. The noci-ceptors in the upper respiratory tract detect the presence
of irritants and operate like “smoke detectors”. The mucosal linings will
become moist, and in due course the goblet cells will secrete mucous, producing
mild physiological effects such as coughing, phlegm and tightness of the chest.
Dr Hind stated that more severe and prolonged exposure may result in acute
inflammation of the lining of the respiratory tract, which could cause symptoms
such as a persistent cough, difficulties in breathing and bronchospasm. Even in
these cases the recovery period is likely to be short.
208.
In Dr Hind’s view, the difference between the irritant and the
inflammatory response is likely to be a question of degree. He said that the
health thresholds suggested by the toxicological evidence (e.g. 146 μg/m³
for acrolein) might be the level at which some people would begin to experience
an irritant response. Dr Hind could not say at what level an individual might
begin to be at risk of an inflammatory response.
209.
Dr Hind also suggested that in June/early July the pollen count would
have been moderate to very high (the nearest monitoring station is at Rotherham). He agreed that asthma sufferers could well respond at lower exposure levels.
210.
In cross-examination, Dr Hind agreed that there were many vulnerable
groups who might require a lower dose before experiencing symptoms. In general
terms, he agreed that there was considerable individual variation, and that such
variation was also seen between asthmatics (Dr Hardy had told me that
asthmatics can vary in reactions to particular irritants by a factor of 40). He
did not agree that smokers formed such a group. He said that if the evidence
did not show significant or above threshold exposures to the smoke plume, one
would need to examine alternative explanations for these complaints.
211.
Dr Hind agreed with Dr Hardy that smoke exposure had the potential to
lead to an infection because the microphages might be overwhelmed. However, I
interpreted his evidence as suggesting that this might arise only if the body
has already shown an inflammatory response to the irritant chemical. This
chimed with Dr Hardy’s evidence that there would need to be “a lot” of
inflammation. It is very difficult to see how milder responses might induce
infections.
212.
I have set out the evidence of Dr Hardy and Dr Hind in some detail
because (a) there is little between them, and (b) the generic points they make
were mirrored in the evidence given by other clinicians. To my mind, four
points of general application need to be emphasised. First, the difference
between irritation and inflammation is likely to be one of degree, particularly
at the margins. Secondly, human variability occupies a significant range.
Thirdly, the strength of Dr Hardy’s mini-foray into epidemiology must depend at
the very least on the quality of the evidence, including the histories,
elicited from all the Test Claimants. Fourthly, and perhaps most importantly,
much of these experts’ clinical opinion depended on their chosen point of
departure. If the starting-point is exposure to smoke at levels which may have
been sufficient to yield symptoms, then Dr Hardy’s patterns and constellations
become a compelling explanation for the phenomenon under scrutiny; and,
moreover, evidential weaknesses in an individual Test Claimant’s case became
less important, because they may benefit from the similarities within the herd.
If, on the other hand, the starting-point is exposure to smoke at levels
insufficient to yield symptoms, then certainly the medical scientist would say
that the quest for alternative explanations is necessitated. At the very least,
a close examination of the individual circumstances of the Test Claimants
becomes more important.
213.
Moving on now to the upper respiratory tract, the forensic contest here
was between Mr Andrew Swift FRCS, consultant ENT surgeon and rhinologist,
primarily working at the Aintree University Hospital (for the Claimants) and Mr
Andrew Parker FRCS, consultant ENT surgeon, primarily based at the Royal
Hallamshire Hospital, Sheffield (for the Defendant). As with their lower
respiratory tract colleagues, I was greatly appreciative of their evidence.
214.
Mr Swift had seen the DVD of the fire, and told me that he would have
expected consequences from it, namely some degree of inflammation in the upper
respiratory tract. The main insult would be to the nose, but the throat and
larynx might also be entailed. Mr Swift’s explanation of the nature of the
irritant, and then the inflammatory responses, was very similar to his
colleagues’ in the related field, and need not be repeated.
215.
My interpretation of his evidence was that Mr Swift did not accept that
those who had suffered irritant responses would be more likely to experience
head colds. He believed that this would not be so, otherwise hay fever suffers
would succumb more readily to these. I did not understand Mr Swift to accept
that the position was necessarily the same as regards those who suffered
extensive inflammatory responses.
216.
Mr Swift saw 14 Test Claimants, and believed that there was a
commonality of complaints. The likely explanation for them would be irritation
from an external source. In the majority of those he saw, he diagnosed rhinitis
and pharyngitis.
217.
Under cross-examination, Mr Swift agreed that his diagnosis of
inflammation was based solely on the history he was given as to clinical
symptoms, and on his clinical opinion, not on biopsy. He also agreed that any
inflammatory response would be presaged by sensory irritation, in particular by
sneezing. Mr Swift said that if an individual has an inflammatory response, and
then is removed from the external source, it would take days, or more likely a
couple of weeks, for there to be full recovery.
218.
Mr Swift was a diligent, careful witness who was rightly concerned not
to over-state the Claimants’ case. Mr Andrew Parker was an engaging witness
with a flair for succinct, apposite explanations. Thus, in relation to one of
the leitmotifs in this case, being the difference between the irritant
and the inflammatory responses, he said this:
“Well, it depends upon how much irritant there is. If there
is a significant irritant, then there will be an [immediate] irritant
response. If there is more irritant, then it will turn into an inflammatory
response, which is a pathological step change. Essentially, your Lordship, an
inflammatory response is a final common pathway that the body has in relation
to potentially injurious incidents, one of which is an irritant up the nose.”
219.
In Mr Parker’s view, the nose is designed to filter out material which
could be injurious further down. An irritant response will settle down very
quickly after the irritant has gone, or has been deactivated by the nose.
Particulates will be washed away by mucous, or can be swallowed. Later in his
evidence in chief, Mr Parker said this:
“Q. So given the understanding, perhaps with the benefit of
Mr Redfern's description of the fire, of what the claimants you examined
experienced, would you have expected any of them, once the irritant was
removed, to have spent as much as a week or two weeks or three weeks symptomatically?
A. I would say on the balance of probability, not. If the alleged
exposure was for a period of a few days -- a period of a few weeks, then it's
conceivable that there has been inflammatory change in the nose during that
time because the exposure has been continuing.
Q. So are you contemplating a consistent level of concentration
of the irritant?
A. The injurious agent would have to be present in the air in
sufficient and significant dose for me to endorse that concept.”
220.
Under cross-examination, Mr Parker conceded that Claimants might have
sustained an inflammatory reaction if sufficient exposure to the smoke went on
long enough. In that sense, he was conceding very little: this is a truism. He
did not accept that constant sub-threshold exposures could have had an additive
component, but he fairly said that “there might be a range of opinion on
that”. I will bear this in mind in due course, but in terms of the science
of toxicology I have already said that I consider that possible additive and
cumulative effects are addressed within COMEAP, and that unless the science is
ignored, qualified or rewritten for the purposes of this judgment, one really
should not go any further. Mr Parker’s final view on this aspect emerged after
questioning by me:
“MR JUSTICE JAY: But I think what is being put is each time you
go in there will be a sub-threshold exposure, but it will happen often enough and
in sufficient temporal proximity. In other words it's ongoing, but ebbing and flowing
always below sub-threshold. There will come a point at which, bang, you start
to get symptoms, not because you're sensitised, but because there's a sort of build-up.
I just want to know what your reaction is to that.
A. My reaction is, on the balance of probability, I wouldn't
expect that. There would have to be sufficient exposure to maintain a
continued inflammatory reaction.”
221.
Mr Parker accepted in cross-examination that the absence of permanent
damage does not preclude the possibility of a prior inflammatory response. He
also accepted that it might take time for symptoms to resolve as the
concentration of the alleged irritant falls. Finally:
“If the claimant has not been exposed as alleged then any
symptoms that they report cannot be arising as a result of the alleged index
incident. On this basis they will be unrelated to it and arising as a result of
other mechanisms.”
222.
The dermatological expert evidence was given by Dr Paul August FRCP,
consultant dermatologist, primarily working at the Leighton Hospital, Crewe
(for the Claimants) and Dr Iain Foulds FRCP, honorary consultant dermatologist,
based at the University of Birmingham (for the Defendant). Extremely helpfully,
these experts were able to encapsulate areas of consensus and disagreement in a
Joint Statement dated 3rd June 2015.
223.
These experts made the same general points as did colleagues elsewhere.
They were in agreement that there is no literature bearing on the question of
possible contact dermatitis through smoke irritation. I have examined the
Larrieu paper at paragraph 160 above. Dr August pointed out that the difficulty
and cost of obtaining such evidence heavily militate against it, although he
was compelled to accept that skin symptoms were not mentioned in the
Californian Wildfires paper.
224.
Dr August told me that the present focus is on a number of similar
conditions, varying to some extent in nature and degree, namely puritus
(itching), purigo (lesions), urticaria (an irritable condition of the skin
caused by release of histamine) and dermatitis (an inflammatory condition which
can be caused by contact with an irritant). A number of the Test Claimants also
complained of acne excoriae and rosacea, which on my understanding are
predominantly constitutional conditions which could be aggravated by exposure
to irritants.
225.
Despite the absence of evidence in the literature, Dr August said that
he believed that about 1,000 out of the total cohort of 16,000+ Claimants were
complaining of skin symptoms. That corresponds with the known proportion of the
population which is vulnerable. However, in my view that piece of evidence
taken in isolation cannot avail the Claimants in any way – the issue surely is,
vulnerable to what? In any event, we know next to nothing about the non-Test
Claimants.
226.
Under cross-examination, Dr August accepted that timing of onset of
symptoms, and levels of the modelled dose, were extremely important
considerations. He, as did others giving evidence for the Claimants, accepted
the possibility of cumulative exposures. He did not accept that onset would
have to be immediate, but he did envisage that the probable time period for
onset was likely to be in the region of hours to days. He agreed that the eyes
were more sensitive than the skin, and he said that if the airways were safe,
he would have thought that the skin would also be safe. Dr August accepted, as
he was bound to, that the conditions of this litigation were removed from those
of a scientific study, owing to the confounding factor of individuals claiming
compensation serving to magnify recall bias.
227.
Dr Foulds’s evidence was of a piece with those in other disciplines
testifying for the Defendant. In a powerful passage in his evidence in chief,
he said this:
“Well, we talked about irritant contact dermatitis, and irritants
you can divide into absolute irritants and relative irritants. Absolute
irritants will cause damage to the skin with one or two exposures. So, for
example, hydrofluoric acid, if you pour that on your skin, is going to drill a
hole in your skin. That's an absolute irritant, whereas relative irritants
work by damaging the lipid cell surface membranes within the skin, causing
damage to the integrity of the barrier function of the skin cumulatively over a
period of time. So irritants are anything which dries the skin, degreases the
skin, chemically attacks the skin over a period of time. So in practice
exposure to irritants usually requires months or years of repeated exposure to damage
the barrier level of the skin to cause problems, to break through the threshold
of the actual barrier function of the skin to actually cause dermatitis. Now,
most dermatitis will occur from cumulative damage unless that individual has
had repeated exposure over a period of time just beneath the threshold and then
the final insult will take them through the threshold. But in practice you need
months or years of repeated exposure to develop irritant dermatitis, and that irritant
dermatitis has to occur on areas which are susceptible. So hands from a wear
and tear point of view, or if you're talking about an airborne irritant, the
first place to get affected will be the eyelids, around the eyes and on the
face. Yet none of the people that we examined had problems on their eyelids. So
from irritation, I think it pretty well rules that out as a possibility. If
it's an airborne thing, it's got to affect the areas exposed to the skin. Airborne
irritants, airborne allergens where people become allergic to chemicals, affect
the skin that is exposed to the air and not on covered sites. Yet a lot of the
individuals we examined had problems on covered sites as well.”
228.
In his closing arguments, Mr Kent relied heavily on Dr Foulds’ evidence
about what the latter called the “me too” syndrome, which is particularly
prevalent in industrial or potential product liability cases. For example, close
investigation of an alleged problem (e.g. contact dermatitis caused by a “new
system” wash-powder) demonstrated that very few individuals, if any, had problems
genuinely attributable to the agent under scrutiny. Their causes were shown to
have been unrelated.
229.
Under cross-examination, Dr Foulds was asked whether he derived comfort
from the Envirobods and Shillito evidence appearing to show that the Claimants
were not sufficiently exposed. He said not, and contended that the stronger
point here was the absence of a common factor or a common clinical picture. Dr
Foulds said that there was a contradiction between the symptoms as they
described them and the histories that were elicited. Most said that their
symptoms cleared up within a short space of time. Dr Foulds denied that those
with pre-existing conditions were more vulnerable.
230.
The only generic issue on the dermatological evidence which I need
resolve at this stage is whether exposure to smoke is capable of causing
contact dermatitis. Professor Hay has advised me that there is no evidence that
it can, and I have already discussed the Larrieu et al paper. In my judgment,
the evidence base in support of the proposition that exposure to smoke at
relatively low levels (i.e, at the sort of levels suggested by the plume
modelling evidence) can cause dermatological problems must be regarded as
extremely sparse, based on little more than clinical impression alone.
231.
Finally, I heard evidence from two distinguished consultant
ophthalmologists, namely Mr Louis Clearkin FRCS, working primarily at the Arrowe
Park Hospital in the Wirral (for the Claimants), and Mr Ian Marsh FRCS,
primarily working at the University Hospital, Aintree (for the Defendant). Mr
Clearkin described himself as a “jobbing ophthalmologist”, perhaps with
a modicum of self-deprecating irony. I appreciated his charm and sense of
humour.
232.
All the Test Claimants the ophthalmologists examined had symptoms of
tear film instability due to underlying meibomian gland dysfunction. These
glands reside in the lid of the eye and are involved in the production of tears
and mucin. Tear film instability may result when the external environment of
the eye becomes abnormal in some way, causing tears to evaporate or become
otherwise dysfunctional and the tear film to break down. In Mr Clearkin’s view,
exposure to the smoke has brought forward symptoms of tear film instability by
3-5 years. He put the point rather compellingly in this way:
“I work on the Wirral. It's a very different area. Very refreshing
to meet the good folk of Kirkby. You know, solid people, gave a proper account
of themselves, pleasure to meet some of them, pleasure to meet all of them to a
degree. As I say, I've never been to Rodney Street before. It was a life
changing experience in many ways, but certainly it was a good gig in terms of dealing
with patients. This was a very straightforward experience.
Q. I wasn't asking about your pleasure.
A. I do apologise.
Q. I was asking how you found the group as far as the presentation
of their conditions.
A. It made me wish I worked in Kirkby and had much more straightforward
people to deal with than on the Wirral. But I hope nobody has written that
down. But they're very straightforward people. They struck me as no side to
them, gave an account that I found, with one exception, one minor exception, entirely
straightforward. They told me a story that fitted in with their clinical
signs. I hear this story half a dozen times at clinic in terms of symptomatic tear
film instability.
Q. Due to exposure to smoke?
A. No, due to a variety -- it's a common final pathway disease.
Many things can precipitate symptomatology.
Q. Smoke is one of them?
A. Smoke is one of them. Sunburn, for example. A
particularly dry day. A particularly cold day. It doesn't take much. It's a
complex mechanism. It's very, very robust. When it goes, it goes.”
233.
Under cross-examination, Mr Clearkin agreed that he was making an implied
assumption about the levels of smoke exposure being sufficient. He said that an
irritant chemical, for example the sulphur compounds produced by an onion,
might provoke tears, which might wash away the tear film components, which
might then precipitate chronic symptomatology. Ultimately, however, Mr
Clearkin’s evidence was that the posited environmental trigger is the final
insult in the causative chain, the metaphorical straw which breaks the camel’s
back.
234.
Mr Ian Marsh did not disagree with the general principle of tear film
instability; his dispute with Mr Clearkin was as regards its causes, and as to
the reliability of the Test Claimants’ accounts. Unlike Mr Clearkin, he
deferred to me on this last aspect. Mr Marsh emphasised that we have no
antecedent examination of these individuals before the alleged exposure; all we
have is what may now be observed four years after the relevant events. Mr Marsh
did not accept the possibility of cumulative effects: if those were a real
phenomenon, one would have expected a predominance of patients coming to
ophthalmic clinics with the signs and symptoms of this dysfunction, having
sustained only small doses of an irritant. Mr Marsh did not disagree with the
general principle of one final insult pushing a patient over the edge as
regards meibomian gland dysfunction, but could not endorse the proposition that
the acceleration might have been by as much as 3-5 years. Nor did he accept
that it was other than speculation that smoke should have accelerated a chronic
condition.
235.
Under cross-examination, Mr Marsh told me that there were some
similarities, and also some differences, as to the various Test Claimants’
symptoms and their onset. He agreed that by and large they presented with the
symptoms that one would expect from exposure to large quantities of smoke.
236.
I found Mr Marsh to be a somewhat dour witness who appeared to have been
discomfited by the forensic process and Mr Clearkin’s no doubt well-intentioned
jibes about his consulting rooms. I cannot accept his contention that because
the Test Claimants’ evidence is “subjective” it cannot carry any weight.
Rather, it is a factor to be weighed in the overall evidential mix. Even so, I
have no hesitation in preferring his evidence over Mr Clearkin’s at least as
regards the sole generic issue that I am choosing to resolve at this juncture.
I cannot accept the assertion that exposure to smoke could have accelerated
symptoms by anything like 3-5 years. The notion that smoke might advance symptoms
is theoretically possible in extreme cases, but is not really supported by
other than somewhat speculative, assertive evidence. These Claimants are all
likely to have had pre-existing tear film instability which ebbed and flowed in
the ordinary course of the condition. I accept the possibility that a few
developed this dysfunction after the fire, but it is no more than guesswork to
postulate that exposure to the smoke might have accelerated the process. Although
Mr Clearkin did not advance the argument in this manner, I accept that it is
possible that smoke exacerbated eye symptoms in previously vulnerable
individuals, including those suffering from meibomian gland dysfunction, during
the course of exposure to it and a recovery period thereafter. Whether the
exposure to this smoke plume caused such an exacerbation is entirely
case-specific and must be resolved on all the available evidence.
237.
To my mind, the following matters of general application arising out of
the clinical evidence from the eight experts I heard may be made at this stage.
First, in all four disciplines the experts spoke of a gradation between mild
irritation on the one end of the spectrum and severe inflammation at the other.
Issues plainly arise in the grey area in the middle, but generally speaking I
consider that it is valid to think in terms of irritation being transient,
self-limiting and a normal physiological response, and inflammation being
pathological and, albeit in all these cases non-permanent, probably over the
line and into the realm of personal injury and actionable damage. This
interlaces with my analysis of actionable damage in my section on the “Governing
Law” (see paragraphs 178-181 above). Secondly, I accept Dr Hind’s evidence,
read in conjunction with my interpretation of Professor Hay’s, that the lowest
health thresholds for a chemical such as acrolein are probably designed to
indicate the sort of concentrations where certain individuals may be expected
to experience an irritant, rather than an inflammatory response. Thirdly, and
as a heavy caveat on the previous point, it should continue to be recognised
that there is considerable variability, vulnerability and range of tolerance
thresholds over any given population. Fourthly, it is common ground between the
experts that timing of onset of symptoms matters. In my judgment, the irritant
response will be immediate, and in relation to an incident of this nature most
people will be likely to know within a short space of time what is causing that
response. It is the Claimants’ case, after all, that the smoke had a nasty,
pungent smell. On the other hand, I agree with Mr Redfern that one might expect
considerable variability as regards the timing of onset and offset of any
inflammatory response. Finally, and to reiterate a previous conclusion of mine,
I do not accept Mr Redfern’s submission that the medical evidence, viewed as a
whole, supports the possibility of an additive, in the sense of a cumulative,
response to sub-threshold exposures. The Claimants can do no better than rely
on the trigger values (based on two, consecutive hourly means) and 24-hour
means set out in the COMEAP report.
238.
There are other generic points too, but I will address these in the
final section of this judgment. Perhaps the most important, and controversial,
of these is the argument advanced by the Claimants’ experts and not the
Defendant’s that it is appropriate to draw inferences as to causation from the
patterns they believed they discerned as to a common, time-associated
constellation of symptoms.
THE TEST
CLAIMANTS
239.
Pursuant to CPR Part 19.13(b) and my order of 5th May 2015
(varying the previous order of 17th June 2014), I am trying 20 Test
claims within the overall framework of the GLO issues. The parties originally
selected 40 Test Claimants (20 a piece) with the objective of examining the
broad range of geographical and personal circumstances across the whole group.
I doubt whether the parties’ selections were wholly dispassionate and
objective, because it must be obvious that the Claimants will have alighted on
what they hoped were their best cases, and vice versa. Whittling down
this sub-cohort from 40 to 20 (with the parties now choosing 10 a piece), in
line with proportionate case management and the overriding objective, has
enabled me to examine what must be a broadly representative cross-section of
the group as a whole. However, I do not make the error of supposing that this
sample of 20 would be regarded as statistically significant by any
epidemiologist. It is another example of the pragmatism of the common law in
operation.
240.
My evaluation of the Test Claimants must be both inductive and
deductive. Inductive in the sense that their individual features must be
scrutinised with care before seeking to draw any more general inferences from
them; deductive in the sense that the generic evidence I have already examined
may be capable of throwing light on their individual cases. In a case of this
sort, the court must move rapidly from the particular to the general, to the
general to the particular, and then back again.
241.
Appendix 1 to this judgment comprises a list of the 20 Test Claimants
(with information as their post-codes and straight line distance from the
plant) and a map marking their locations with reference to the numbers the
parties have allocated them.
242.
Evidence bearing on the individual Test Claimants is derived from a
number of sources. First, they were asked to complete questionnaires as part of
the litigation process. Most of these were completed in the first half of 2013,
already well over a year after the incident. Secondly, each Claimant has
provided a witness statement, and in some instances a supplementary witness
statement, in line with court orders. The vast majority of these statements
were signed in September 2014. Thirdly, there is the evidence of what each
Claimant told the examining clinicians as recorded by them. Finally, but only
in some cases, there are relevant contemporaneous GP records. All this evidence
needs to be compared and evaluated in this case, assessed as appropriate
against the oral evidence given from the witness box.
243.
I will examine the Test Claimants in the order in which they gave
evidence before me. I need to explain my approach. At this stage I will be
doing so without express reference to the plume modelling evidence. This is to
avoid the potentially mechanistic thinking which underlay the Defendant’s
clinical experts’ approach, namely that because any given Test Claimant was
insufficiently exposed it must follow that s/he could not have suffered any
symptoms from exposure. I believe that I have already made clear that a more
fluid, less rigidly “scientific”, approach is required (at least at this stage
in my decision-making), although I certainly should not be understood as saying
that the plume modelling evidence can be ignored or circumvented. I will be
returning to it at a later stage of my analysis. In assessing the Test
Claimants, the focus will be primarily on the individual features of their
cases, but I will be keeping an eye on a possible “bigger picture” and
identification of patterns and constellations. However, this “bigger picture”
cannot drive my inquiry, since that would be to commit the logical fallacy of
assuming what needs to be proved. I have already said that I will be taking on
board all the available evidence, but an issue does arise as to the weight to
be given to expert clinical opinion on the Claimants’ side that, generally
speaking, the Test Claimants were honest individuals who gave reliable
accounts. Dr Swift and Dr August spoke in different terms but to the same
effect of intuitive judgments forged from lengthy experience in history-taking
and clinical examinations. The Defendant’s experts, on the other hand, deferred
to me on these matters.
244.
I have thought very carefully about this last point, but I cannot agree
with Mr Redfern that I should be affording “significant weight” to these
expressions of opinion. It is striking in this case that by the stage any Test
Claimant was seen by the experts in this case, there were no relevant signs to
witness, and no enduring symptomatology. Accordingly, there was no possibility
of correlating claimed symptoms with any meaningful clinical examination. It
follows that the clinical experts were really in no better position than I was
to assess matters of individual credibility and reliability, especially in a
medico-legal (as distinct from a purely clinical) context. With respect to
them, it might well be said that I was in a somewhat better position inasmuch
as the Test Claimants’ accounts were thoroughly tested in the crucible of the
forensic process. I do not propose to ignore the Claimants’ experts’ generally
favourable impressions; the weight to be accorded to them should, however, be
moderate.
245.
Another generic point which falls to be addressed at this stage is the absence,
in all bar one case, of any contemporaneous medical note either recording a
complaint about the fire or linking symptoms to the fire. I do not accept that
there is any solid evidence supporting the proposition that some GP surgeries
had signs discouraging appointments and encouraging over the counter remedies.
Dr Hardy told me about this, but his sources are unclear and I did not hear it
directly from any Test Claimant. I do accept Dr August’s point that it is
understandable that some Claimants might not mention symptoms to their GPs at
appointments for other complaints, but I cannot accept that this should be
treated as a universal panacea. Nor can it explain a failure to mention the
fire in instances where Claimants were attending their GPs complaining
of what they now say are fire-related symptoms. On the other hand, I do accept
and understand the bewildering variability across human nature: some patients
are not interested in possible causes and explanations; all they seek is a remedy.
246.
As a related matter, a number of the Test Claimants told me that their
GP records are either inaccurate or incomplete. I accept this possibility
inasmuch as GPs are extremely busy professionals who may not always write down
everything that is said, and may occasionally err. I am more inclined to accept
the possibility of a record being incomplete than erroneous. If a trained
history-taker records “symptoms 1/52”, that will almost invariably be his or
her best interpretation of the account being given.
247.
The final generic point to be made at this stage concerns the approach I
should be taking to the obvious delays in this case. Owing to these, and to the
fallibility of human recollection, it is inevitable that witnesses may be
unreliable historians and unable to give me more than a general sense of what
happened. Some allowances need to be made for this, but not to the point of
excess. The burden of proof remains on the Claimants, and they need to satisfy
me that they suffered the symptoms they claimed. In very many cases, apart from
recourse to the wider picture of apparently similar complaints, the Claimants
have nothing else to go on apart from their own evidence.
Mr Gary
Mangan
248.
Mr Mangan was born on 5th April 1985 and at the material time
lived 0.53km from the Sonae plant. In 2011 he was working as a retail
supervisor, but he is now employed in a very responsible role as a submarine
engineer in the Royal Navy. Mr Mangan does not smoke but he had a history of
upper respiratory tract infections, including one incident of shortness of
breath in 2008. At about 16:00 on Friday 10th June he went home and
could see black or dark grey smoke from the factory. There was an unpleasant
burning smell and a lot of smoke. Mr Mangan went running on the Friday evening,
and again on the Saturday, modifying his route on account of the smoke plume.
He felt a bit chesty when running, and his chest was “quite tight” that
Saturday evening (he denied any symptoms on the Friday). He did not go running
on the Sunday, but remained at home all day. On Monday he went to his GP,
without a prior appointment, where he was diagnosed with an upper respiratory
tract infection for which antibiotics were prescribed. He had symptoms of a
tight chest, a cough, and phlegm. These symptoms, including those of low energy
and disturbed sleep, lasted for about 10 weeks, and he remembered returning to
his doctor some weeks later.
249.
Under cross-examination, Mr Mangan said that he had no difficulty
obtaining an off-the-street consultation with his GP. Paragraph 9 of his
witness statement, which stated that he “decided to make an appointment to
see his GP”, was incorrect. In my judgment, it is difficult to understand
why so elementary a mistake was made, if it was indeed made. The GP noted the
presence of ulcers on the right side of the palate by the right tonsil. Mr
Mangan explained that he did not mention the smoke to his GP on this occasion
because he just attended “for my health”, and obviously everyone was
aware in the area what was going on. He had made the connection between his
symptoms and the fire.
250.
The GP records show that he returned to the practice on 16th
August 2011 for a night cough. He made no mention of the fire. His explanation
for this omission was that “I go to the doctors for my health”. I
understood that to mean that Mr Mangan is not concerned with the underlying
reasons for any ill-health, but just practical solutions.
251.
Dr Hind felt that Mr Mangan is likely to have suffered a coincidental
upper respiratory tract infection. Dr Hardy, taking into account the absence of
a temperature, the ineffectiveness of the antibiotics, and the fact that an
ulcerated palate is not commonly associated with infection, originally
concluded on the balance of probabilities that this Claimant did suffer from
the effects of smoke inhalation. However, in cross-examination it was pointed
out to Dr Hardy that Mr Mangan claimed to develop symptoms before 12th
June (i.e. before the date of any significant exposure to the smoke), and Mr
Kent pressed him on the GP record. Dr Hardy then said, “possibly he had an
infection; it is likely at that stage he had an infection”. He agreed that
in his report he could equally have said that Mr Mangan’s account was
consistent with smoke exposure.
252.
In my judgment, Mr Mangan was no better than a reasonable witness who,
like many others, could not remember much of the fine detail of what happened. In
such circumstances, I cannot conclude that his account was particularly
reliable. Not without some hesitation, I do not find that on Friday 10th
June he had already booked an appointment to see his GP on the following Monday
(had I made such a finding, it would ineluctably have followed that he was
suffering from an upper respiratory tract infection before he was aware of any
of the effects of smoke inhalation). Even so, on the balance of probabilities I
conclude that Mr Mangan was probably suffering from a coincidental throat
infection. His symptoms started before there was any significant exposure to
the smoke plume, and Dr Hardy agreed in cross-examination that it was likely
that this Claimant had an infection.
253.
In any event, I am not satisfied that Mr Mangan’s symptoms lasted for
anything like as long as 10 weeks. If, as a fit young man he was concerned to
see his GP for what he believed to be a mere throaty cold, suggesting a low
complaint threshold, and had it not gone away after the usual week or so, I
regard it as inconceivable that he would not have arranged to see his GP whilst
still apparently suffering symptoms. Furthermore, when he did see his GP on 16th
August, there was no mention of the fire.
254.
I will set out my final conclusions in relation to Mr Mangan’s case only
after considering all the plume modelling evidence in conjunction with the
evidence of the other Test Claimants.
Mrs Tracey
Beatham
255.
Mrs Beatham was born on 21st August 1972 and lives 1.96km
from the Sonae plant. She works as a domestic at hospital, in proximity to
cancer patients, and the nature of her employment means that she has to be
particularly cautious in not bringing ordinary colds and infections into her
work environment.
256.
Mrs Beatham is a moderate smoker and in February 2010 was suffering from
a persistent cough.
257.
According to paragraph 5 of her witness statement:
“I was not aware of the fire until the following morning when
I got up to get ready for work. I noticed a terrible smell of burning. When I
looked out of the window, I could see that the whole area was covered with
smoke. In particular, I noticed that my garden was covered in dust and ash. The
smoke was extremely thick and dark and was blowing towards my house and into my
estate. I cannot recall the plume being particularly high at the time of seeing
it.”
This was at
about 06:15, when the wind was blowing eastwards from the plant. Mrs Beatham
also noticed considerable quantities of ash and dust which lasted for weeks, as
did the pungent smell. She could not hang her washing outside. Many other
Claimants gave evidence to similar effect.
258.
Mrs Beatham complained of symptoms including a severe cough and chest
tightness which lasted for approximately 8 weeks in all. She saw her GP on 24th
June, and the following medical record has been retained:
“Upper Respiratory Tract Infection NOS 1/52 tired, sore
throat, cough, running nose. o/e throat red nil pus chest clear advice given.
Delayed script”
259.
Mrs Beatham has given inconsistent accounts of when her symptoms
started. The natural interpretation of the GP note is that her symptoms
commenced at around 17th June. According to her questionnaire, they
developed within two weeks. Her history as given to Dr Hardy was “2 days
after the onset she developed cough and phlegm so much that she vomited after
coughing the phlegm”. According to her witness statement, they started
within the first week of the fire. In the witness box, Mrs Beatham said that
her cough started on the third day, and that after about a week she took time
off work. She had to wait 3-4 days for the doctor’s appointment.
260.
In her oral evidence, Mrs Beatham said that she linked her chest
symptoms to the fire straight away, as soon as she had her cough (i.e. at
around the 2 day point). She said in evidence that she asked her GP if her
cough could be related to the fire, but he did not answer. Her witness
statement had said that she could not recall mentioning the fire to her GP at
the time. This is consistent with what she told Dr Hind, namely that she
assumed that she had picked something up. She could not explain this
discrepancy.
261.
Under cross-examination, Mrs Beatham said that she also had eye symptoms
which she mentioned to her GP. Her questionnaire and witness statement had made
no such claim. She could not explain this inconsistency. When asked about the
GP note, Mrs Beatham denied that her chest was clear. When it was put to her
that she told Dr Hind that “she was not aware of dust inside the house”,
she denied that she was exaggerating the position.
262.
Dr Hardy accepted in evidence that if the symptoms did not begin until
one week after the fire, as the GP note recorded and other evidence suggested,
then it is less likely that her symptoms were caused by the smoke: the more
probable explanation is viral infection.
263.
In my judgment, Mrs Beatham was an unreliable witness whose oral
evidence could not be accommodated within the far more reliable documentary record.
Her account, particularly in relation to the extent of the accumulation of dust
and the duration of any symptoms, contains elements of subconscious
exaggeration. I express the matter in those terms because I do not believe that
Mrs Beatham was intent on deliberately misleading the court, and that in any
event has (wisely) not been suggested. Mrs Beatham is, however, a good example
of a suggestible witness who could not remember what actually happened, and
therefore tended to say what she assumed could be right because that fitted
into her mindset of what this fire must have caused.
264.
In my judgment, Mrs Beatham’s case cannot succeed on the basis of her
own testimony. I accept that the unsatisfactory nature of her evidence does not
exclude the possibility that she may have suffered from relatively minor
symptoms hovering at the threshold of legal actionability, but (at least as
regards her own evidence viewed in isolation) she has failed to discharge the
burden of proof which remains on her. Unless the plume modelling evidence is
supportive and/or she is able to rely on a powerful intra-cohort “constellation
of symptoms” effect, her claim should fail.
Ms Jessica
Alexander
265.
Ms Alexander was born on 17th October 1993 and was only 17 at
the time of the fire. She was studying at a sixth form college which was 1.42km
away from the Sonae plant. Her home is 1.56km away from it.
266.
Ms Alexander is a non-smoker who had pre-existing eczema, including a
flare-up over her elbows and knees in January 2011. According to her witness
statement, but not her questionnaire, she had previously suffered from styes in
or near her eyelids which could cause swelling and streaming.
267.
According to Ms Alexander’s questionnaire completed on 22nd
February 2013, she suffered a range of symptoms, all of immediate onset and
floridly described. Her eyes were sore and dry, she was constantly rubbing
them, and although her symptoms resolved within two weeks, she believes that
her myopia was brought on by this experience. She developed red and itchy
patches across her torso and face, which made her self-conscious at school and
caused problems with sleep. After two months, her GP diagnosed contact
dermatitis, and after treatment it took a further two months for symptoms to
resolve. She developed migrainous headaches which interfered with her exams,
and rendered her unable to attend her maths A level exam (this must be a
typographical error: according to her witness statement, this was a GCSE maths
re-sit). These acute symptoms lasted for around 2 weeks. She also experienced
dizzy spells, an increased temperature, and a sore throat.
268.
In her witness statement, Ms Alexander stated that there was a lot of
dust and ash in the area at the time of the fire. It was sufficiently tenacious
to seep into the house, and it was a “constant job” to keep on top of
it.
269.
Ms Alexander was neither a confident nor a reliable witness. In my
judgment, she was self-conscious about her appearance before the fire, as many
young women are, and it is difficult to link cause with effect. Her myopia
could not have had anything to do with the fire, and it became clear from
contemporaneous, pre-fire documents that Ms Alexander was experiencing eye
problems which were either due to a fly entering her left eye, causing
swelling, and/or pre-existing lid margin problems – a feature of meibomian
gland dysfunction. Mr Clearkin agreed in cross-examination that it could have
been either, but appeared to favour the manifestation of symptoms from the
pre-existing condition.
270.
Although Ms Alexander was a regular attendee at her GP, she did not make
an appointment to see him after the fire. Indeed, when she saw him on 14th
June she made no mention of the fire, explaining to me that she was
self-medicating and that “everyone knew about the fire”. Reading through
her substantial, pre-fire medical history, I cannot accept that explanation –
it would only make sense if she had not associated her symptoms with the fire
at all, which was not her case. She saw her GP again on 8th July and
he gave her a sickness certificate covering the period 4th – 11th
July, presumably to excuse her from attendance at college. However, by then the
exam season had concluded. On 16th August her GP diagnosed “contact
dermatitis”, and it is surprising that on this occasion Ms Alexander did not
mention the fire if she believed, as she told me, that it had caused it. Dr
August agreed with the proposition that the itchy patches across the torso
described by Ms Alexander are difficult to explain because more naturally
exposed parts of the body would receive greater toxicological insult.
271.
There is no medical evidence supporting Ms Alexander’s other claimed
symptoms. Given her unreliability as a witness, I do not accept that she has
proved her case in these respects. Her elevated temperature, for example, is
highly unlikely to have had a toxicological origin. Her eye and skin problems
were pre-existing, and in her case there is nothing to cause me to wish to
depart from the advice of Professor Hay regarding the absence of evidence
linking dermatological symptoms to smoke. I cannot exclude the possibility that
smoke exposure exacerbated Ms Alexander’s pre-existing eye condition, but the
resolution of that issue depends mainly on the plume modelling evidence.
Otherwise, Ms Alexander’s case is in the same category as Mrs Beatham’s.
Ms Kelly
Colebourne
272.
Ms Colebourne was born on 29th October 1979 and lived 2.16km
from the Sonae plant. She continues to work as a fitness instructor. She
remains a non-smoker, and save for one issue relating to possible pre-existing
asthma, she enjoyed very good health.
273.
Ms Colebourne told me that she awoke at about 05:40 on Friday 10th
June to see a thick black cloud of smoke crossing the clear blue sky. By 14:45,
when she returned from work, it was “just smoggy, foggy, cloudy – like smog”.
The smokiness and dustiness continued that weekend, and Ms Colebourne described
a “char-grilled smell, acid-y at the back of the throat”. She said that
her breathing felt a bit funny. After about one week of the fire, according to
her questionnaire, Ms Colebourne experienced severe respiratory symptoms, and a
deep and chesty cough, which was very uncomfortable. She also suffered sore,
itchy and runny eyes, which became red and bloodshot. Her eye symptoms lasted
for about 4 weeks. These symptoms also caused low energy and a general feeling
of being increasingly worn down.
274.
On 5th July 2011 Ms Colebourne suffered a severe asthma
attack which resulted in her being hospitalised.
275.
Ms Colebourne was cross-examined closely in relation to the timing of
the onset of her asthma symptoms. According to her questionnaire:
“I was absolutely fine before the fire, and only started to
suffer these horrible symptoms after it started. As I mentioned above, I had no
history of asthma at all before this, and I was not exposed to any other
irritants that could have induced it, so it seems obvious that the fire was to
blame. ”
276.
In fact, an examination of Ms Colebourne’s medical record reveals that
she was complaining of general tiredness symptoms in July 2010, of acute tracheitis
in November 2010, and that asthma was diagnosed in February 2011 – in the
context of complaints of wheeziness and general malaise. Ms Colebourne informed
me that this diagnosis was incorrect, notwithstanding that she was given an
inhaler.
277.
On 15th June 2011 Ms Colebourne saw her GP, was diagnosed
with hay fever, and was advised to take her inhaler. It did not enter her head,
she said, to mention the fire to her GP, notwithstanding (a) the terms of her
witness statement, to the effect that it seems obvious that the fire was to
blame, and (b) the apparent need to contradict the GP’s diagnosis if there
appeared to be some more plausible explanation for her symptoms.
278.
On 5th July the history as recorded by the OOH service was as
follows:
“… since yesterday has had problems with chest since
November, not formerly diagnosed with asthma but given a ventolin inhaler. Non
smoker. Since yesterday has been coughing phlegm and struggling to clear chest.
Feels SOB and has used ventolin 4 + times today. On the phone able to speak in
long full sentences but sounds congested …”
279.
I read the “since yesterday” as a reference to the more serious
symptoms Ms Colebourne was obviously experiencing. However, it rather excludes
the sort of serious respiratory problems, dating back to one fire after the
fire, mentioned in her questionnaire. I also mention the hospital record dated
6th July which states that “over the past several months has been
suffering from increased shortness of breath”.
280.
I was not impressed by Dr Hardy’s evidence in relation to this Claimant.
He attributed her symptoms to the fire because of the temporal association, and
because she had a life-threatening attack after the fire. However, even a
cursory examination of the contemporaneous medical records does not bear this
out. I much prefer Dr Hind’s evidence on this issue. Nor can I remotely accept
Dr Hardy’s attempt to attribute six months’ of symptoms to smoke inhalation.
281.
In my judgment, Ms Colebourne was not a dishonest witness but she has
persuaded herself into believing, some considerable time after the relevant
events, that the fire caused her asthma attack. Ms Colebourne told me that
Camps (or their agents) knocked on her door to recruit her to this litigation,
and it is also noteworthy that her questionnaire contains serious errors
relating to her “very physical life” which, to be fair to her, she
disowned.
282.
It is possible that Ms Colebourne experienced respiratory problems
between 10th June and 5th July which were due, at least
in part, to the fire, but the only way that she can prove that she did is with
regard to the plume modelling evidence and/or the possible constellation of
symptoms effect.
Ms Dawn
Bunting
283.
Ms Bunting was born on 13th January 1974 and lives 0.44km
from the Sonae plant. As the crow flies, she is the closest of all the
Claimants to the original source of the smoke plume. However, that does not
mean that her exposures were likely to have been the greatest.
284.
Ms Bunting is a moderate smoker and in the past suffered from rosacea at
times of stress.
285.
Her case is complicated, if not bedevilled, by the fact that she has
completed two questionnaires containing different information. In her first
questionnaire, she stated that she first developed a sore throat, sore eyes and
a headache within two days of the fire, and that these symptoms resolved within
three to four months. She denied that she smoked or had any pre-existing skin
condition. In her oral evidence, Ms Bunting agreed that the questionnaire was “highly
inaccurate”, but a genuine mistake on her part. In her second
questionnaire, completed about two months later, she stated that she developed
symptoms within 24 hours of the fire, and that her respiratory symptoms lasted
two months, her eye symptoms one week, and her skin problems three weeks. Her
witness statement times the onset of symptoms at “within 48 hours”.
286.
There were thick layers of dust or ash inside and around the house. This
was really bad within the first week, and took about one month to settle down.
287.
There were numerous inconsistencies in Ms Bunting’s evidence, which in
my view were not satisfactorily explained. According to her first
questionnaire, “I did only think it was a passing flu at first”.
However, in her oral evidence she said that she associated her symptoms with
the fire straight away, and her sons had the same symptoms. When her attention
was then drawn to the questionnaire, she said that it was a long time ago, and “maybe
I did think it was a passing flu at the time”. In my judgment, this is the
more likely explanation, particularly when it is noted that Ms Bunting attended
her GP on 20th June 2011. She went to see him for a long-term
problem, but sought to persuade me that she did tell her GP about her cough and
sore eyes. She could not explain why this was not recorded. She did accept that
she could not recall if she attributed these problems to the fire. I cannot
accept that there was any complaint to the GP on 20th June. Ms
Bunting’s witness statement makes no mention of it.
288.
Ms Bunting was recruited to this group when she was out shopping and saw
a sign “were you affected by the fire?” In my view, she was another
Claimant who has permitted herself to embrace a narrative which gained full
currency long after the event. I am not to be understood as finding that her solicitors
have created a false account; I am making the more parsimonious point that
certain individuals are vulnerable, compliant and suggestible.
289.
Dr August was asked about the opinions expressed in his report:
“Past History Rosacea. This has been present for the
last 5-6 years beginning in 2008-2009 when it was severe for 3 months. This
became worse after the fire, particularly on the cheeks and around the eyes
where the skin became lumpy and cracked. This seemed to be bad for about 2
months and then settled back to its pre-fire severity.
…
Opinion She seems to have had redding [sic] of the
face which was worse than before. The rash was certainly confined to the face
only. The overall impression is that of rosacea exacerbated by the fire for a
period of 3 weeks, possibly longer.”
290.
Dr August agreed that the evidence in Ms Bunting’s case was “complicated”
because she has not given a consistent account. On any view, her skin problems
were not mentioned to her GP on 20th June. There is sparse evidence
linking dermatological conditions to smoke exposure, but in any event I am not
satisfied on her oral evidence that the case is made out.
291.
Hers is another case which is not necessarily doomed to fail on account
of her unreliable testimony, but requires a solid basis on the plume modelling and/or
a constellation of symptoms effect to stand any realistic chance of succeeding.
Mr Terence
Dunn
292.
Mr
was born on 12th January 1948 and lives
2.31km from the Sonae plant. He is retired, and in June 2011 went out for
substantial morning runs.
293.
Mr Dunn had no pre-existing health history of note. He gave up his
modest smoking habit in 2006 or thereabouts.
294.
According to his questionnaire, Mr Dunn suffered from the immediate
onset of respiratory, eye, nose and throat symptoms, together with headaches,
dizziness and stomach pain. More specifically, he had a nasty chesty cough,
producing shortness of breath, mainly on exertion. This prevented him from
going running. His eyes were sore and stinging, and he suffered from what he
told me was “extreme discomfort”. His nose was very blocked and he had
an “incredibly sore” throat.
295.
On the first morning of the fire, Mr Dunn told me that he was on his
usual 6½ mile run but could only do about half. He could not breathe; there was
coughing, spluttering and his eyes were watering. Mr Dunn described a “real
putrid, horrible smell”. First of all, he thought it was akin to a pig farm
(he might have been smelling the ammonia in the wood); it left an acid-y biting
taste in the mouth.
296.
The quantities of dust and ash were such that Mrs Dunn insisted that
their vertical blinds be replaced. He paid cash - £200-300. The manner in which
Mr Dunn’s evidence was given was convincing and credible.
297.
Overall, Mr Dunn appeared to give his evidence in a moderate and
understated manner. He said that his nose symptoms resolved within one week,
and the remaining symptoms within a further two weeks. He self-medicated for
these.
298.
Provisionally impressed as I was by Mr Dunn’s reliability as a witness,
I asked him to describe the colour of the smoke plume to me in more detail. He said
this:
“From the first time I saw, it was black, very black.
MR JUSTICE JAY: Very black, yes.
A. And then over a period, it would go blackish grey, if you
was looking over that way, but we didn't tend to a lot, and then it would
sometimes go a bit white. That was the colours I seen when I looked.
MR JUSTICE JAY: After about a week or so, was it still going
black?
A. No.
MR JUSTICE JAY: Was it –
A. It had changed colour, my Lord, after a week. It wasn't black
anymore.
MR JUSTICE JAY: In terms of the quantities of smoke, can you
give me an idea of that?
A. First few days, my Lord, was really bad. Really bad, and
then it just started to settle down. Just keep -- you know, there was smoke
coming from it all the time, rising, but never as serious as the first few
days, in my opinion.
MR JUSTICE JAY: Yes. I know it's difficult to describe, but
after the first few days, just give me a picture of the quantities of smoke.
A. It's very difficult to, you know -- because, as you say, it
had changed colour. So it was not as though you could look over and see
something black all the time. You know, you'd notice all the time, wouldn't
you? But there were a change in colour. Sometimes it would go very easy and
then sometimes it would flare up again and you'd see a white plume or a grey
plume. But that's only if you was out looking over all the time.”
299.
Entirely credible as a witness though Mr Dunn was, this seam of evidence
demonstrates how witnesses can be unreliable when it comes to the detail of
describing events that happened years before. The memory can pick out the worst
features of the event (in some people, the memory can blot these out
completely), and in Mr Dunn’s case he has unwittingly prolonged the period of
the black smoke well beyond its proper confines of the afternoon of Friday 10th
June – as vouched by all the expert and photographic evidence.
300.
The same unwitting process of prolongation and exaggeration may have
impacted on Mr Dunn’s evidence regarding his physical symptoms, and the ash and
dust. That evidence needs to be balanced against the plume modelling evidence
in his case. I will be examining this with care before expressing any further
conclusions about him.
Ms Julie Carney
301.
Ms Carney was born on 9th March 1977 and lives with her five
children (all of whom are also Claimants) 1.94km from the Sonae plant.
302.
She is a light smoker who had pre-existing dermatitis, on and off, from
the early 2000s, and asthma-like breathing problems for which she had been
receiving no treatment.
303.
According to Ms Carney’s questionnaire, she suffered from a range of
respiratory, skin and nose problems “soon after the fire started”. These
problems are ongoing. She did not link her symptoms to the fire until early
2013.
304.
Ms Carney’s primary complaint related to her dry, scaly skin – according
to her questionnaire, “most noticeable on backs, arms and torso”.
Plainly, these were the covered areas of the body where one would least expect
to see evidence of contact-related skin problems, setting aside the causation
difficulties that she in any event faced as regards the dermatology.
305.
Ms Carney was taken in cross-examination to her GP records which showed
that she was complaining of similar skin problems before the fire. These may
have been partly stress-related. She tried to persuade me that the spots on her
skin had completely cleared by the time the fire started, but I simply cannot
accept her evidence in this regard. Paragraph 24 of her witness statement said “I
have not suffered with my skin since 2009 prior to the fire”.
306.
The following passage taken from Ms Carney’s expert, patient
cross-examination by Mr Michael Jones serves to demonstrate the overall poor
quality of her evidence:
“Can you explain why these very serious symptoms are described
in this witness statement, when it seems that's not your recollection of the
symptoms that you have?
A. It's human error, isn't it? It's a misprint on that -- that
bit. I'd said -- when I've described my symptoms to the lady who was writing
it down, I said my nose was congested and my chest felt heavy and I found it difficult
to breathe.
Q. When you were answering questions from my learned friend Mr
Redfern, he asked you whether you went to your GP and you said you didn't, and
the reason you wouldn't go to your GP was because you had a little cough. You wouldn't
trouble a GP with a little cough.
A. I don't trouble the GP with anything.
Q. I haven't asked you the question yet. What you're
describing in this witness statement could not fairly be described as a little
cough, could it?
A. I just got on with it. I've got five kids. I'm on my
own looking after them. So I haven't got time to sit in the doctor's to be
told: it's stress and I can't give you antibiotics.”
307.
Ms Carney went to see her GP on 13th September 2011. She was
advised that her rash and cough were down to stress. Ms Carney now feels that
they are down to both. However, she agreed in cross-examination she had not
made the link with the fire. Given the smell that she described (akin to a
hamster cage – not implausible in itself), and the quantities of “billowing”
smoke that she witnessed, it is very difficult to accept that she did not make
the connection – on the premise, that is, that her descriptions are correct.
308.
Unfortunately for Ms Carney and for others, her cross-examination
concluded on an extremely damaging series of notes:
“Q. What I suggest, Ms Carney, is that you have no idea if any
symptoms you have had since June 2011 are related to this fire, do you?
A. I'm not a specialist, am I?
Q. No. So you've no idea?
A. No, because the doctor hasn't turned round to me and said:
this is all down to the Sonae factory fire. He said it's down to stress. But
in the area people have got the exact same symptoms and had the same problems.
Q. So you think because other people might have symptoms that
they say are caused, you say yours might be caused?
A. There's got to be a link somewhere, hasn't there?
Q. In fact, in 2013, when you went to that shopping centre in
Kirkby, you jumped on a passing bandwagon, didn't you?
A. No, I was asked a question and I answered.
Q. What was the question?
A. If I'd suffered anything -- any of these conditions. It was
chest, any chest symptoms from the fire, and I said yes, I had. And then they
said, would you like to come along and talk to us, and I said yes, because I
don't want something like that in the area where my kids are. My kids have got
to live here, haven't they? It's not jumping on a bandwagon. It's looking
after your family, isn't it?”
Ms Karen
Court
309.
Ms Court was born on 23rd July 1964 and lives 2.27km from the
Sonae plant. She now works in a responsible position as a volunteer care
co-ordinator. At the time of the fire she was a training manager.
310.
Ms Court completed, and apparently signed, two separate questionnaires.
I deploy that adverb because her two signatures look rather different, but she
assured me that they were both hers. I have to accept her evidence in this
respect.
311.
In her first questionnaire (Tandem Law), Ms Court stated that she had
not had the opportunity to review her medical records, but to the best of her
recollection and knowledge she first developed serious symptoms “some two
weeks after the fire started”. These symptoms included chest pain, a sore
throat, reflux, itchy eyes, itchy skin and a cough. She only became aware of
the causal link when she realised that other people in the area were
experiencing similar symptoms. According to this questionnaire, she received
medical attention at her GP surgery.
312.
In her second questionnaire (Walter Barr) she first suffered symptoms on
9th/10th June and these comprised a chesty cough (“coughing
a lot”), itchy eyes and itchy skin, and it took three weeks for the eyes
and two or three months for the remaining symptoms to recover. Ms
Court gave a different smoking history in this questionnaire. She claimed
that the Tandem Law questionnaire was rushed, and that she was happier with the
Walter Barr one, but it looks the other way round to me.
313.
In her oral evidence, Ms Court described a big white cloud of smoke
coming towards her house. The smell was “a little bit like rubber”. There
were “loads and loads” of debris. Like many other witnesses, Ms
Court was unable to hang out her washing. Her oral evidence was to the effect
that her itchy eyes lasted for four months, and her cough for approximately
four months. In my judgment, it was clear that she was exaggerating the length
of any symptoms, which calls into question her characterisations of the extent of
any ash and dust.
314.
As with the previous Test Claimant, Ms Carney, Ms Court unwittingly let
slip some very revealing answers during her cross-examination by Mr Jones:
“No, you asked me, when did you first become aware of something;
right? And I remember seeing that and thinking -- first thing I thought, I'll
be honest, is we were at risk. That fire means that we were at risk. I'd
forgotten about it because no one come to the house and said you need to be
screened, you could have been at risk, you might have got respiratory whatever.
Q. You had forgotten about the fire?
A. When I seen that I thought, oh, there's been fault with Sonae.
There's a claim. Where there's claim, there's blame. And I thought: hang on a
minute, my itchy skin and everything, what have I been exposed to?
Q. So that was the first time you'd made a connection between
your itchy skin?
A. Yes.
Q. I think you said that was two years later?
A. Yes.
….
Q. Let me ask you a narrower question. You'd forgotten
about the fire; yes? That's your evidence?
A. Yes.
Q. You're walking through Kirkby centre. You see the unit and
it says that Sonae is at fault, I think, is the phrase you used a moment ago. Had
you not seen that sort of material saying Sonae is at fault, one, you probably
would have forgotten about the fire still.
A. I didn't forget about the fire. I'd forgotten about Sonae
itself, if you know what I mean.”
315.
Ms Court was convinced that she first saw thick smoke after 20:00 on the
evening of 9th June. She must be mistaken about that.
Notwithstanding her first questionnaire, she claimed that she first experienced
symptoms immediately, in other words, that night. Her feeling at the time was
that her symptoms would be a temporary inconvenience, but her prolonged
dermatitis suggested otherwise.
316.
Ms Court saw her GP on 10th and 13th June in
relation to other matters. She said that although there was no mention of any
symptoms from the fire, she was sure that she did discuss it. The GP’s advice
was to take Betnovate for the dermatitis. She was convinced that this advice
was given on the second occasion. Paragraph 19 of her witness statement claimed
that she could recall one occasion on which her cough was so bad that she
thought that she would die. According to her oral evidence, this was the
immediate impact of the fire, which must have been before 13th June.
If that is right, one would have expected the GP to have noted a complaint; and
even if Ms Court is wrong and this occasion was after 13th June, it
is very surprising that symptoms of this severity did not attract a specific
visit for medical advice. I note too that Ms Court disowned paragraph 32 of her
witness statement, which claimed that a week after the fire she took her son to
the GP because he was unwell, and the GP recommended lotion for her skin.
317.
Finally, I should state that Ms Court agreed that her claim in the sum
of £500 for additional paint and cleaning material was probably overestimated.
318.
In my judgment, Ms Court was an unsatisfactory witness the reliability
of whose evidence I cannot accept. Her claim only has a prospect of success if
it supported by the plume modelling evidence and/or a constellation of symptoms
effect.
Mrs Annette
Farrell
319.
Mrs Farrell was born on 18th April 1952 and lives 1.81km from
the fire. She was an administrative officer at a sports college, and retired in
September 2011.
320.
She is a light smoker and had pre-existing problems with bronchitis and
shingles.
321.
According to her questionnaire, Mrs Farrell suffered a range of
respiratory, eye and ENT problems following the Sonae fire. These all developed
within 48 hours. Her respiratory problems are ongoing; her eye symptoms
resolved within one month, her ENT problems within three months.
322.
In her oral evidence Mrs Farrell described the colour and quality of the
smoke, in particular its horrible, chemical smell – “a bit like glue”.
She said that it burnt the back of her throat, went inside her nose and made
her eyes water. The gritty atmosphere, which was similar to the morning after
bonfire night, lasted for two to three days.
323.
Mrs Farrell was diagnosed with asthma in September 2011, and in November
2011 went onto the asthma register.
324.
In cross-examination, Mrs Farrell said that she had not suffered from
breathing problems before the fire. However, a letter from the Aintree Chest
Centre to her GP dated 10th November 2010 indicates clearly that she
had a wheezy cough and was quite breathless on exertion. The physician wondered
if she had bronchial hyper-reactivity.
325.
On various occasions in 2010 and 2011, Mrs Farrell was prescribed
Salbutamol. On 23rd March 2011 she was prescribed steroids for her
chest. According to his report, she told Dr Hind that she used an inhaler
approximately once a day during the year before the fire. She could not
remember telling him this, nor could she really explain why her questionnaire
had denied any asthma symptoms.
326.
Mrs Farrell told me that she was sure that she working at the time of
the fire. She was taken to a series of medical records showing that she was
given sick certificates for shingles between April and August 2011. She said
that some of these were backdated, and that she was back at work on 6th
June. At the time she was giving evidence, her occupational health records were
not available, but now that they have been obtained they clearly show that the
sickness certificates were not backdated and that Mrs Farrell was off work with
shingles over the whole of this period. I accept that Mrs Farrell was not
seeking deliberately to mislead me, and – as her recent witness statement says
- that she may have become confused about the exact dates. However, the
revelation of these records significantly undermines the reliability of her
evidence.
327.
Mrs Farrell attended her GP on 23rd June 2011 but there is no
record of her mentioning any eye and nose complaints to him. She told me that
this was an omission in the GP notes, and that she did; but that answer is
difficult to reconcile with the note of a complaint of a wheezy cough, which
was in very similar vein to previous complaints. If there had been something
new, it is highly likely that the GP would have recorded it. I have taken on
board Mr Swift’s point, made in the context of Mrs Farrell’s case, that when
people go to their GP they do not always mention all their symptoms; but her evidence
was that she did so on this occasion.
328.
Mr Swift also had this to say about Mrs Farrell’s case, which I
considered to be illuminating:
“There is also -- it's not necessarily the person that's
trying to tell mistruths. It may be their perception of things. So you find
that if someone suffers from, say, anxiety and depression, which are quite
common disorders, certainly in the rhinology field, their perception of having
a stuffy nose will be much greater than someone who is happy with life. I'll
quite often sit in clinic, trying to work out why they've come to see me,
because my nose is generally much worse than theirs, and that is an honest
opinion on that.”
329.
Overall, Mrs Farrell was not a reliable witness, and her case cannot in
my view succeed on the basis of her own testimony. As with other Test Claimants
falling within this category, she requires the plume modelling evidence and/or
a constellation of symptoms effect to support her.
Mr James
Reece
330.
Mr Reece was born on 21st January 1953 and lives 3.1km from
the Sonae plant. He works as a night janitor at Knowsley business park. He has
a history of chest symptoms and hay fever, and is a heavy smoker.
331.
According to his questionnaire, he developed symptoms on or about 12th
June 2011. He described these as “a bit of a cough and … cold flu like
symptoms”. He believes that he now has asthma as a result of being exposed.
Maybe it was for this reason that he described his symptoms as “ongoing”.
It was not until he saw an advert in a newspaper that other people had
apparently suffered similarly that he made the link between his symptoms and
the fire.
332.
In his oral evidence, Mr Reece explained that he felt that his symptoms
– of what he believed was hay fever – came on a bit stronger. He felt
miserable.
333.
Under cross-examination, Mr Reece said that he was sure that he saw the
fire before 04:00 on 10th June, when he went outside for a smoke
during the course of his employment. He must be mistaken about that. He made an
appointment to see his GP on 22nd June but did not attend. He told
me that he wasn’t thinking straight, although the appointment was probably
arranged for his symptoms. On 5th December 2011 he attended his GP
complaining off a cough which had lasted for two months. The GP records show
that asthma was not diagnosed until 19th October 2012.
334.
Dr Hardy’s report ascribes conjunctivitis and rhinitis to smoke
inhalation, and also a severe acute bronchitis which became chronic. Dr Hardy
is unclear about the aetiology of Mr Reece’s asthma. Dr Hind defers to my view
of Mr Reece’s credibility and the plume modelling. In my judgment, Mr Reece was
an entirely unconvincing witness, and I would be unwilling to attribute any
symptoms to smoke inhalation unless the plume modelling evidence and/or a
constellation of symptoms effect is available to support him.
Mr Edmund
Kenny
335.
Mr Kenny was born on 8th December 1951, and lived 1.8km from
the Sonae plant. He is retired and for some years cared for his mother, who
sadly passed away in February 2015.
336.
Unfortunately, Mr Kenny’s overall health is not good. He has a heart
condition and is diabetic. He was a heavy smoker for many years, suffers from
hay fever, and has experienced episodes of shortness of breath. Mr Kenny has
also been an asthmatic since 1990, but he told me that he manages to keep it
under control.
337.
Mr Kenny was at home at the time of the fire. He told me that he was
aware of it during the evening of 9th June. By the morning, the
smoke was a grey/white colour. At lunchtime, it went black. There was loads of
it; it was like the smoke coming off the top of a volcano. Mr Kenny also
described an awful, glue-like smell with chemical overtones.
338.
Unlike many other witnesses, Mr Kenny has given a consistent account
throughout the course of this litigation. In his oral evidence, he said that
his breathing “went terrible” within a couple of days. His eyes were
sore; he had a blocked nose and sore throat; he just felt rotten. Consequently,
Mr Kenny had to use his inhaler twice as normal, and he used Optrex 4-5 times a
day. His symptoms lasted for approximately three weeks in all.
339.
Mr Kenny also told me about “an awful lot” of dust and ash in the
smoke. It was grey, and got everywhere. It was completely different from “Sahara
sand dust”. He had to clean and wash more often, and try to keep the
windows closed. He placed masking tape on the gap over the double-glazing. A
sense of the duration of this phenomenon did not clearly emerge from Mr Kenny’s
evidence in chief, but he told Dr Hardy that he had to keep the windows and
doors closed for 2-3 days. Under cross-examination, he said that the dust etc
lasted for at least a week.
340.
On 20th June 2011, Mr Kenny saw his GP, Dr Mohammed Khan. The
computer records reads:
“H/O; asthma. Flare up after recent Sonic factory fire.
Speaking full sentences. Resp sys – b/l air entry equal. b/l scattered wheeze+.
RR-18/min. Was more worse over w/e, it seems. P]- Oral steroids. Continue
inhalers …”
341.
The Defendant accepts that Mr Kenny suffered an exacerbation of asthma
in mid-June 2011. The issue is what caused it. Mr Kenny said in
cross-examination that his hay fever tends to be worse in May/June, and then in
August/September. He agreed that the general pattern was of “good and bad
days”. There had been a deterioration in 2010 and Mr Kenny was on inhalers
throughout that and the following year. He was taking prednisolone before the
fire.
342.
Mr Kenny was asked about Dr Khan’s note, “was worse over weekend”,
which he agreed was accurate. He said that it was still musty and foggy over
the weekend on 18th/19th June. He was not sure whether
there was still smoke and dust. Mr Kenny made no mention to his GP of any nose
and eye symptoms. He agreed that his cough was getting better by then.
343.
Mr Kenny suffered from a serious bout of food poisoning at the end of
June 2011. When hospitalised on 2nd July it was noted that he had no
respiratory symptoms.
344.
In my judgment, Mr Kenny was an entirely honest witness. He is the sort
of person who I would also describe as being reliable, but an issue arises as
to the quality of his recollection, as it would in relation to anyone being
asked to recall events of this nature occurring some time ago. Thus, if he
tells me that the dust lasted for a week, I believe him; but he could simply be
mistaken about it.
345.
Mr Kenny is convinced that cause and effect has been established in
these circumstances, and I fully understand his reasons. A final decision
cannot be made in his case without considering the plume modelling evidence.
Mr Paul
McLoughlin
346.
Mr McLoughlin was born on 26th January 1962, and lives 1.61km
from the fire. He is a taxi driver who works school shifts and a number of night
shifts. He is a light smoker, and has no pre-existing health history of note.
347.
For obvious reasons, given the nature of Mr McLoughlin’s work, the plume
modelling in his case has been difficult to undertake. It has been tethered to
his home address; no other modelling exercise would have been possible. I have
to take a sensible view about this. Mr McLoughlin’s driving would have taken
him over a reasonably broad area; and, on occasion, closer to the Sonae plant
than his home. There is no satisfactory evidence as to the extent to which the
“boxed” environment of a motor vehicle provides any measure of protection.
348.
According to Mr McLoughlin’s questionnaire, he developed respiratory,
eye and skin symptoms within 48 hours of the onset of the fire, as well as
headaches. He complained of a persistent cough, sometimes painful and causing
difficulties in sleeping. His eyes felt dry, itchy and sore, and would water
when driving such that he had to pull over to the side of the road and apply
eye drops. His forearms turned red and itchy, and the skin flaked as he
scratched. He had to apply Sudacrem and an anti-bacterial soap. The headaches
caused a lot of pain in his forehead and elsewhere. All his symptoms resolved
within about two weeks.
349.
Mr McLoughlin told me that he was at home when the fire started. He saw
grey, dark soot-coloured smoke and experienced the “very unpleasant smell” of
burning wood and creosote. He also said that there were substantial quantities
of ash and dust, which meant that he and his family had to keep the windows and
doors closed.
350.
An issue arose in cross-examination as to whether Mr McLoughlin was
working on 12th/13th June. The computer record suggests
not, but he said that he worked because he had to, and would have used a different
computer code. I accept his evidence on this point.
351.
On 23rd June 2011 Mr McLoughlin saw his GP. He is not a
frequent attendee. The computer record reads as follows:
“C/O – cough had cough for a few weeks now, has been taking
OTC medication, chest seems clear. Advised to continue with meds and come back
in 2 weeks if no better.”
352.
Mr McLoughin said that he did not mention his other symptoms to his GP;
he was more concerned about the cough. He said that he thought that the fire
was mentioned to his doctor in passing. I do not find that it was, otherwise
the other symptoms would surely have been raised.
353.
Dr August was cross-examined about “the main symptoms of pruritus
unspecified” which “could be inferred as irritant dermatitis (but there
is no direct clinical evidence)” or “urticaria … or prurigo”. Dr
August agreed that, as a general proposition, one would expect such
condition(s) to be more widespread, and not confined to the forearms. However,
a lot is not known about the distribution of skin rashes. Further:
“MR KENT: It sounds as though this is quite difficult retrospectively
to diagnose.
DR AUGUST: Yes. It's inspired guesswork, really. It's a
hunch, what do you think is the best fit.”
354.
In my judgment, Mr McLoughlin’s skin symptoms require consideration
within the ambit of the overall frame of the toxicological evidence in this
case. As I have already made clear, that evidence is unsupportive. As for his
eye complaints, Mr Clearkin’s view is that these lasted just two weeks, but he
did not accept that this presentation was more consistent with infection than
tear film instability. I have difficulty with Mr Clearkin’s logic, and I take
Mr Marsh’s point that eye problems do not appear to have been mentioned at the
GP consultation on 23rd June.
355.
I have found Mr McLoughlin to be one of the most difficult witnesses to
assess. He came across as a reliable person, pleasant and understated. I have
little doubt that some key features of this experience have remained in his
mind: the smoke; the unpleasant smell; the quantities of ash; the cough; the
itchiness. However, as with other witnesses, I was left without a clear
impression of timing, duration and severity.
Mr Peter Shaw
356.
Mr Shaw was born on 31st May 1967. He works as a driver and
labourer. His depot is the premises of his employer, Kings Construction, which
is based on the Knowsley Industrial Estate 0.55km from the Sonae plant.
357.
Mr Shaw is a non-smoker who had no chest symptoms of any note for a
number of years.
358.
Mr Shaw falls into a different category from other witnesses. His
workplace is south-east of the Sonae plant. For him, therefore, Saturday 11th
June is a potentially important date.
359.
Mr Shaw normally works Monday-Fridays. His work pattern was and remains
such that he is at the depot for approximately 80-90 minutes a day; otherwise,
he is on the road. Mr Shaw arrived at work at approximately 06:50 on Friday 10th
June. He saw fire engines and a lot of black/grey smoke. He started to suffer
from a cough the day after the fire started and while he was at work. Over the
weekend, he began to suffer from itchy eyes. He found it difficult to breathe
and his work and sleep were affected.
360.
Mr Shaw told Dr Hardy that he was “probably” working on Saturday
11th June, and Mr Clearkin that he was working on that date. Since
then, his payslips have been obtained, and these contradict his account. His
explanation is that he “may have been mistaken”. It was put to Mr Shaw
that he well knew that his case would be enhanced if he could show that he was
exposed to the smoke plume on that date, and that in effect he has sought
deliberately to misrepresent the position. Not without some hesitation, I
acquit Mr Shaw of that aspersion. He was not a particularly impressive witness,
but I do not conclude that he would so brazenly have attempted to mislead.
361.
A clear issue arises as to the timing of the onset of Mr Shaw’s cough.
Under cross-examination he said that his sore throat developed over the Friday
afternoon, and the sore eyes, cough and phlegm over the weekend. On 13th
June he saw his GP who recorded “cough one week” and prescribed
amoxicillin. At that stage, Mr Shaw said that he had not made a link in his
mind between the smoke and his cough. However, he contested the accuracy of the
note. On 20th June he re-attended: he was still “bunged up”,
and the GP prescribed a short course of steroids. Mr Shaw told me that on that
occasion he did not mention the fire. It was only “maybe a week or two
after” that he began to make that connection.
362.
Mr Shaw also said that his cough largely cleared after one week, but he
was not totally better until 6-8 weeks later.
363.
In my judgment, Mr Shaw’s case faces problems whichever way the evidence
is interpreted. If the medical record is correct, which in my view it probably
is, then his cough was not due to the fire. The possibility that the fire
exacerbated his symptoms cannot be excluded, but cannot be substantiated on the
balance of probabilities on the basis of Mr Shaw’s account alone. If the cough
in fact developed on Saturday, when Mr Shaw as at home far away from the scope
of the smoke, Dr Hardy conceded that “it’s not due to the smoke, I guess”.
Mrs Teri
O’Brien
364.
Mrs O’Brien was born on 25th June 1981, and lives 2.63km from
the Sonae plant. Until recently, she worked as an emergency operator for
Merseyside Police, and is now a Probation Service officer.
365.
Mrs O’Brien is an ex-smoker. She suffers from hay fever, intermittent
chest symptoms from smoking-related bronchitis, and possibly late-onset asthma.
366.
According to her questionnaire, Mrs O’Brien suffered from a range of
eye, respiratory, throat and nasal symptoms, accompanied by headache and
fatigue, all starting about 48 hours after the onset of the fire. She had never
experienced similar symptoms before. These symptoms all resolved after three
weeks. She was working normally throughout this period – she could not take
time off, because the Police are sticklers for sickness absences.
367.
Mrs O’Brien was asked about the timing of the onset and offset of the
smoke and accompanying acrid, chemical smell. She said this:
“That day it was quite intense, for the first few days
leading off, and then obviously towards the end of that week it petered out a
bit.”
368.
In answer to my questions, Mrs O’Brien said that she saw black smoke at
around 13:30 on Friday 10th June, when it was close to her house,
although she could not say how far away. Given that the wind had been blowing
from the west for the past five hours, at the very least Mrs O’Brien’s timings
must be incorrect. On subsequent days, she said that the atmosphere was smoggy
and murky.
369.
She also said that she attempted to make an appointment at her GP. She
gave similar evidence to other witnesses about dust and not hanging out washing
outdoors.
370.
Under cross-examination, Mrs O’Brien was asked to be more precise about
the severity of her symptoms. Her evidence was that they were more intense
during the first week, but began to abate thereafter. Mrs O’Brien said that her
symptoms were “alarming”, but I agree with Mr Kent that if this were
really the case it is difficult to understand why she was unable to fit a
doctor’s appointment into her part-time work schedule. Her explanation was that
the appointments she was offered were inconvenient, and that she had other
things to do.
371.
In my judgment, Mrs O’Brien was a reasonable witness but, in common with
many others, imprecise on key issues such as timing and intensity of symptoms.
As I have already observed, the notion that her symptoms were “intense”
does not tally with her explanation for not seeing her GP. Another difficulty
from her perspective is her distance from the Sonae plant at all material times.
I will be returning to this issue in the context of the plume modelling
evidence.
Mr Francis Glascott
372.
Mr Glascott was born on 17th November 1945. He lives 2.1km
from the Sonae plant, and is retired. Owing to mental health difficulties, his
witness statement was admitted in evidence under the Civil Evidence Act 1968. I
also acceded to Mr Redfern’s application that a Litigation Friend be appointed.
373.
Mr Glascott has a history of chest pain and hypertension. COPD was
diagnosed after the fire. He claims that within two weeks of the commencement
of the fire, he developed respiratory symptoms which lasted for 10-12 weeks.
Inexplicably, Dr Hardy has attributed six months’ symptoms to the fire. In Dr
Hind’s view, the entirety of Mr Glascott’s symptoms are ascribable to smoking
and undiagnosed COPD.
374.
On 30th May 2013 Mr Patrick White of GT Law, Solicitors,
wrote a “Final Chaser” to Mr Glascott. He was told that the Statement of Truth
to be appended to his questionnaire had to be completed and signed by him
immediately, so that it could be returned to the Defendant. He was told that if
he failed to comply, there could be costs sanctions against him personally. Aggrieved
by the peremptory terms of this letter, Mr Glascott wrote to Clyde & Co (undated,
but stamped as received on 11th June 2013) and said this:
“1. Cold called on doorstep by young man regarding fire at Sonae
factory in Kirkby.
2. Was asked had it affected me and although I said no, I was
persuaded to give my details and answer some questions (including health
questions).
3. As I had breathing difficulties (and told him so) I
decided to go ahead and sign the, what I thought, the questionnaire.
3. Was subsequently phoned by GT Law about signing a
statement of truth.
4. Had been diagnosed that my breathing problem was mild
emphysema caused by my long-term smoking so I informed GT Law that I did not
wish to proceed and I did not believe that the Sonae fire had any bearing on my
current health problem.
5. Was told that I couldn’t withdraw my claim as the 7 day
cooling off period from the date of the cold caller visit had expired.
6. I told them I did not wish to proceed with what would then
be a fraudulent claim and was informed that if I withdrew I would have to pay
their costs.
7. Subsequently received enclosed letter reiterating their
claim for costs …”
375.
The Defendant has now pleaded that Mr Glascott’s is a fraudulent claim.
It should be noted that, notwithstanding the terms of his letter, he has signed
a witness statement and did submit to examination by the respiratory
physicians.
376.
Mr Patrick White agreed to give evidence in line with his witness
statement dated 21st May 2015. He denied that Mr Glascott had been
cold-called, and said that the latter would have attended GT Law’s Kirkby
office. He agreed that GT Law’s agents went round to Mr Glascott’s home in
order to ask him to sign the questionnaire. Mr White told me that when Mr
Glascott spoke to him on 14th May 2014, he did not wish to proceed.
Mr White accepted that he explained to Mr Glascott that he might suffer a costs
penalty if he withdrew. Under the terms of the CFA, it was open to GT Law to
claim costs from the client, but Mr White said that it is unlikely that they
would have done so. According to the terms of the attendance note of the call,
Mr Glascott was warned that if he backed out now, the Defendant “will seek
him for any charges”. This was notwithstanding the terms of Clyde &
Co’s letter dated 11th July 2012 under which the Defendant
irrevocably undertook not to seek payment of their legal costs. Mr White tried
to suggest that it would have been negligent of him not to mention possible
costs consequences, but in my judgment the letter could not have been clearer.
Mr White denied that he was treating Mr Glascott as a “cash cow”. He
said that Mr Glascott terminated the call by saying, “f – off”.
377.
Mr White was asked a close series of questions about Mr Glascott’s
questionnaire and the signature on the Statement of Truth. There are obvious
errors and inconsistencies in it. The signature looks nothing like Mr
Glascott’s signature elsewhere, including his signature on the letter to Clyde
& Co. Mr White maintained that it was Mr Glascott’s signature. I am not
satisfied that it is.
378.
Mr White sought to persuade me that he was acting at all material times
in Mr Glascott’s best interests. In my judgment, he was a poor, rather
self-important witness who was acting in what he thought were the interests of
his firm rather than those of his client.
379.
I am not satisfied that Mr Glascott is guilty of advancing a fraudulent
claim. He cannot be held responsible for the conduct of his solicitors. In
order to reach such a conclusion, I would need to know more about the
circumstances in which he agreed to sign a witness statement and to submit to
medical examination. However, he cannot persuade me by dint of his oral
evidence (or indeed Dr Hardy’s exorbitant attributions) of any causal
connection between the fire and symptoms. He is solely reliant on the plume
modelling evidence.
380.
This leaves the position of Mr Patrick White and GT Law. Mr White is not
a solicitor, but he was acting under the direction of his principals. I direct
that a copy of this judgment be sent to the Solicitors Regulation Authority for
investigation of the issues raised by Mr Glascott’s case.
381.
This nugget of evidence not merely leaves an unpleasant miasma of
concern and dubiety in relation to Mr Glascott’s case, it has the potential to
infect the integrity of GT Law’s processes overall, and other claims. Whether
that potential is achieved in all the circumstances of this GLO will need to be
addressed later.
Mr Leon Swift
382.
Mr Swift was born on 14th February 1989 and at the time of
the fire was a trainee accountant (he is now chartered). His place of work was
0.88km east north-east of the Sonae factory.
383.
Mr Swift arrived at work at about 08:45 on Friday 10th June.
Whilst driving to work along the East Lancs road he could see a large cloud of
pale-coloured smoke. Nearer the office, it was smoggy and foggy. From
closer-up, the smoke was in a vast quantity and a lightish/dark grey. The smell
was strange and different from normal. It did not appear to impact on his
breathing at that point.
384.
Later on, while Mr Swift was in his office, he began to suffer from
itchy eyes and sinuses. This caused him to sneeze. Everyone was talking about
the fire.
385.
On Monday 13th June the atmosphere was not as foggy as on the
Friday, but there was “definitely” still a large cloud above the
factory. Although there was less ash on his car, his symptoms had deteriorated.
He had a slight headache, and his eye and sinus problems continued. Mr Swift
told me that he tends not to visit his GP, and so he self-medicated. He bought
stronger anti-histamines than he ordinarily used, but these did not really
work. It took him 2-3 months to recover completely.
386.
Given other evidence in this case which I will be addressing below, the
Defendant has pleaded that this is a fraudulent claim. In these circumstances,
it is necessary to examine the evidence Mr Swift gave under cross-examination
with particular care.
387.
Mr Swift completed the standard questionnaire on 27th August
2013. He stated that his symptoms lasted “3-6 months” (cf. his oral
evidence), and that he made the connection with the fire only several weeks
after the incident, following talking to colleagues. Given that the symptoms
were apparently of immediate onset (cf. his oral evidence, which suggests a
short delay) I find that difficult to accept. Mr Swift also accepted in
cross-examination that the 3-6 month attribution was “excessive”.
388.
Mr Swift was taken to an undated and unsigned “Sonae Enquiry Form” which
appears to relate to him, and states that his symptoms of headaches and nausea lasted
for 4 months. He denied writing it. However, in his supplemental witness
statement dated 15th May 2015, Mr Swift said that he “completed
and returned” this form on 19th March. In the witness box he
said he may have chatted to someone over the phone. He tried to persuade me
that he did not know what the word “nausea” meant.
389.
On or about 22nd March 2013, Mr Swift completed a short
questionnaire. In it he stated that “days after the fire I began to be
affected with headaches as well as this I suffered breathing problems/ an
irritating cough developed”. Thus, here appears a somewhat different
account. Paragraph 3 of this questionnaire is also relevant:
“When did your symptoms reach a stage when you informed
your employer or GP?
Unfortunately I did not as I believed the headaches related
to working at a computer. It is only now that it has been brought to my
attention that I have linked the symptoms to the fire.”
390.
Mr Swift told Dr Hardy that he worked on Saturday 11th June. Dr
Hind’s note of Mr Swift’s history is somewhat internally inconsistent. Mr
Swift’s oral evidence was that he did not work on the Saturday. He believed
that his account must have been lost by Dr Hardy in the translation.
391.
Mr Swift agreed that in the first week after the fire he played 5-a-side
football and went to the gym as usual.
392.
In December 2008 and December 2009 Mr Swift was involved in road traffic
accidents, and brought claims for compensation which were successfully
resolved.
393.
On 22nd February 2013, Mr Swift was involved in the following
conversation on Twitter:
“Leon Swift either of you’s jumped on this sonae claim
bandwagon?
TC been all over the radio
MC residents living close going to solicitors due to
harmful emissions from the plant
MC looks like everyone’s doing it now because it’s
shut down
Leon Swift they’ve admitted liability so anyone living
or working in the area at the time of the fire can claim
MC get on it ken/tom
MC not for me #too honest
Leon Swift too honest ya, good one matt. I’m getting
involved I reckon, pays for the summer holiday if it goes thru
TC ha ha you’re a bad man Leon
MC he’s a fraud Tom
Leon Swift takes a fraud to know a fraud Matthew. Mr
‘I was in that car that crashed ye’ #showmethemoney
MC my neck was sore when Dave crashed #thetruth
Leon Swift Asking for trouble driving in flip flops
MC if you crash give us a shout #whiplashclaim
…
MC I’m sure you was fine that time Dave had a crash
Leon Swift least I was in the car though Matthew
MC so was I”
394.
Mr Swift tried to dig himself out of the massive hole created by these
exchanges. He said that the use of the term “bandwagon” was not the best
choice of words. He agreed that the Tweets could be construed as indicating
that any claim he made would be fraudulent. However, he told me that he was not
saying at the time that his claim was not genuine. He well understood, he said,
that an admission of liability did not mean that one could recover damages regardless
of injury.
395.
I watched Mr Swift very closely during the course of Mr Jones’
well-briefed and well-constructed cross-examination. One possible explanation
for his extreme discomfiture and obvious embarrassment was that his Tweets were
being taken out of context, and he was ashamed by the impression they may have
been making. Another explanation is that he well knew that the Tweets contained
accurate insights into his true state of mind. Making allowances as I do for
the degree of banter that may accompany much discourse over these social
networks, but having regard to all the available evidence, I regret that I have
to favour the second explanation.
396.
Mr Swift is a well-educated young man and ought to be ashamed of
himself. The Defendant’s pleaded case of fraud has been proved to the requisite
standard. His claim fails.
397.
Extremely damagingly not merely for him but potentially for others, is
the following exchange with counsel at the end of Mr Swift’s cross-examination:
“Q. If you were able positively to make a link, you would have
made that link when the fire was burning, not later?
A. Yes.
Q. You have just said "yes". Are you agreeing
with that proposition?
A. No. Like it is difficult to remember exactly when you do
make the association of the two. As I said previously, a lot of symptoms that
I did experience are very similar symptoms to what I experienced on a regular basis.
So it is difficult to differentiate between the two.
Q. Exactly. Mr Swift, what happened is this. You would have
great difficulty differentiating between symptoms you had anyway and symptoms
from the fire, which is why you didn't make any association in those two months
or so that you've said occurred before you made an association.
A. Yes, but that's not to say that there wasn't necessarily an
association between the two sets.
Q. That's a separate question. The question is whether you can
say there's an association. What I suggest is it was only a very significant period
later, whether months or in fact I suggest early 2013, that you saw advertising
literature, and you thought: well, I can say that those symptoms -- I'm not sure
how they were caused -- were caused by that fire and I can get some money; do
you accept that?
A. That may have been the trigger that made me think about it
again, but it wasn't the financial thing that I was thinking about in terms of
making a claim. It was just I realised that the nuisance it had caused at the
time, that I basically wanted to bring the claim.
Q. The nuisance it had caused? What do you mean by the nuisance
it had caused?
A. Basically, if you're sitting in an office and you've got itchy
eyes and tickly cough and sore nose, it's just -- it's inconvenience that you
could do without when you're trying to work, isn't it?
Q. But those are symptoms that are so similar to the symptoms
you had anyway at the time of the year each year that you couldn't positively
link those symptoms to the smoke, could you?
A. As I said, though, those symptoms were heightened considerably.
For example, I take Cetirizine, and that controls my hay fever. Things like
that. I don't need to take anything additional during the time of the fire, I
had to then go and purchase additional in order to try and appease the symptoms
that I was referring to.
Q. If that was true, Mr Swift, you would have made the link there
and then, wouldn't you? You would have thought: why is any normal medication
that always resolves my problems not resolving my problems?
A. You would think so, yes.”
398.
Finally, I note that in his report Dr Hardy fairly stated that Mr Swift
developed no chest symptoms whatsoever in consequence of smoke inhalation, but
then felt able to say that he probably suffered from conjunctivitis, rhinitis
and acute bronchitis (cough) for “up to six months”. My only observation
is that his sort of expression of opinion discloses the dangers of leading with
the chin.
Mr Shaun West
399.
Mr West was born on 29th December 1988 and lives with his
mother 0.58km from the Sonae plant. In 2011 he worked in Aintree as a sales’
advisor.
400.
Although a virtual non-smoker, Mr West has a history of skin rash (2001-2009),
asthma (since 1999), URTIs (1994-2010), rhinitis, sore throat, eczema and hay
fever.
401.
At paragraph 17 of his questionnaire, Mr West stated that he experienced
respiratory symptoms for a period of less than 2 months, eye symptoms for less
than 1 week, skin problems for less than 3 weeks, nasal symptoms for less than
2 months, and generalised dizziness, fatigue and aches and pains for less than
2 months. In the witness box he said that he felt that he had “short-changed”
some of his symptoms, in particular the eyes.
402.
In his oral evidence Mr West said that when he came home from work on
the evening of Thursday 9th June he was aware of the fire almost
immediately. He had a clear view from the hallway window of his home. Between
20:00 and 21:00 that evening, he could see flames and smoke; he was very
confident of that (his confidence was misplaced). The next day, in the morning,
the fire was really bad and the smoke was starting to billow. It was
relentless, and a very dark colour. He could smell and taste it - Mr West, in
common with others, described a “chemically” smell. By the time he returned
home at around 16:00 to 17:00, the smoke “still looked incredibly bad”.
Once he was in the house, he shut all the windows.
403.
Mr West said that it was very likely that he remained at home that
weekend. There was no real respite from the smoke. He figured that everyone was
in the same position, and that his GP would not be able to change his
environment.
404.
In terms of the evolution of the smoke plume, Mr West said this:
“But I'd say a couple of days in, after the immediate fire
getting very severe, there was one or two days when it would be a lot worse in
terms of maybe the smoke being lower. The house, I was always surrounded by
it, and to be honest, I constantly had the curtain shut.”
and
subsequently:
“Q. One final question. What was the atmosphere outside the
house like in the period of the fire and the period immediately following it?
The air quality, if you like.
A. Very poor. It felt like I was trapped in the house. Any
instance where I would have normally walked to the shop to get, you know, even
bread and milk, I would have drove to a garage in (inaudible) because I didn't
really want to go walking down the road.
Q. That's what you did as a result of it, but what was the air
quality like? Can you describe it?
A. I would cough immediately.
Q. That's a consequence.
A. A consequence.
Q. What was the air quality like?
A. Okay. Sorry, could you rephrase that?
Q. Yes. When you walked outside, was it a nice clear day or
what?
A. It obviously got worse on some days. So some days I
couldn't see across the fields because of the direction the smoke was going in
and I live very close to the fields. It was constantly smelling of the smoke
and the fire and whatever else. God knows what was in there. But it was
pretty horrid, to be honest.”
405.
In this sequence of evidence, Mr West was certainly not guilty of
short-changing himself or the Claimants generally. Being much closer to the
Sonae plant than almost every other Claimant, he was well-placed to describe
the direct and obvious consequences of the fire. However, his account bears no sensible
relation to all the objective evidence in the case, in particular the expert
evidence of Dr Mitcheson, the lay evidence of Dr Jowett and Mr Whitrow (in
particular), and the photographs which were separately provided to me by the
Defendant on a memory stick, including the photograph I mentioned at paragraph
76 above. Unwittingly or otherwise, Mr West’s account was heavily freighted
with hyperbole.
406.
Mr West was cross-examined closely about his claim that there were
considerable quantities of dust, ash and debris on the field between his
property and the plant. He said in his questionnaire that the field was covered
in dust and debris, and he was unable to take his usual walk. The photographs
do not bear him out at all. Under cross-examination Mr West made clear that he
did not examine the field in any detail, because it was not a good place to be.
He later said that there was bound to be dust and debris after a fire, but
could not support that assertion with his own evidence.
407.
On 24th August 2011 Mr West saw his GP, complaining of eye
symptoms. On examination, the GP noted the complaint of soreness, but recorded
that “there was not much to see”. Mr West claimed that he had a long
conversation with his GP about his other symptoms, about possible causes for
them, including the fire, and that he was self-medicating. If that was the
case, the GP would surely have made some note of it.
408.
In my judgment, Mr West was a poor witness who was neither credible nor
reliable. His evidence was replete with exaggeration and, at times, evasion.
The weaknesses in his oral evidence will need to be balanced against the plume
modelling evidence.
Mrs Kathleen
Tully
409.
Mrs Tully was born on 12th January 1970 and lives 1.53km from
the Sonae plant. She has a history of coughs, respiratory tract infections,
chest pain (but not for some years), conjunctivitis and sore throat.
410.
Mrs Tully said that she suffered from a number of symptoms following the
fire, including a sore throat, breathing problems, a chesty cough, sore eyes
and a congested nose.
411.
In her oral evidence, Mrs Tully described a very intense, acid-y smell
and smoggy, heavy conditions. It looked like the day after bonfire day, and
cars were white with dust.
412.
On 16th June 2011 Mrs Tully went to see her GP. His
computerised records reads as follows:
“Diagnosis Ganglion of wrist right-sided, noticed a
few weeks ago, some constant discomfort, able to use hand normally, no
pins/needles. O/E – ganglion, radial – N, sensation – N. Explained and
reassured.
Symptom Has a sore throat last 3 days, no fever, feels
achy all over, able to eat and drink a little, some diarrhoea, foul smelling,
no blood. O/E -well hydrated, systemically well, throat – tonsils inflamed,
pus bilate[ral] explained bacterial tonsillitis …”
413.
Under cross-examination, Mrs Tully said that she had made a connection
between her symptoms and the fire, and when she put this to her GP he said that
he was not sure. Mrs Tully said that she was sure it was then, but immediately
retracted this and said that it was possible that she mistaken about it. Given
that there is no mention of this account in her witness statement, I have
difficulty in accepting it.
414.
On 27th June Mrs Tully returned to her GP complaining of the
symptoms of acute conjunctivitis “for 5/7 now”. She had sore, itchy
eyes. As regards the timing, Mrs Tully said in evidence that she did not think
that her eye symptoms started on 22nd June, and that she must have
misremembered the position when she spoke to her GP. She did associate her eye
symptoms with the fire, but was unsure why she did not mention this to the
doctor on 16th June.
415.
In Dr Hardy and Dr Hind’s opinion, Mrs Tully suffered from severe bacterial
tonsillitis which was unrelated to the fire. Mr Swift’s contrary conclusion
that there was a causal relationship with smoke inhalation was based only on
clinical judgment and the temporal association. He said that the GP must have
failed to investigate the matter with sufficient care. Given the signs on
examination, the clear presentation of a severe bacterial infection, and his
own expert judgment that such infections are not the result of smoke
inhalation, in my view Mr Swift’s approach rather demonstrates the dangers of
relying on ex post facto clinical judgments in this sort of situation.
Nor can I accept Mr Clearkin’s diagnosis of tear-film instability. The clinical
findings, Mr Marsh’s sound opinion, and Occam’s Razor all point strongly in favour
of an unrelated bacterial conjunctivitis.
416.
Mrs Tully was a pleasant and entirely reasonable witness. I will be
examining the plume modelling evidence in her case, but all the reliable and
compelling evidence in her case points towards this being a coincidental
infection.
Master
Bradley Woods
417.
Bradley was born on 30th April 2005 and at the time of the
fire was aged only 6. He lives with his mother and sister 0.8km from the Sonae
plant.
418.
Bradley is reliant on the witness statement of his mother and Litigation
Friend, Mrs Kathleen Woods. According to his questionnaire, Bradley developed
respiratory, eye and skin problems within 24 hours of the fire. He had a
persistent cough and complained of a frequent wheeze. His eyes became very
itchy following the fire, and he developed a temperature. Bradley’s symptoms
had resolved within 2 weeks of the fire.
419.
Mrs Woods does not have other than a vague recollection of conditions in
the days following the fire, although she spoke of light grey smoke and “ashy”
conditions outdoors.
420.
On 14th June 2011 Bradley was taken to see his GP, who
recorded that he had been coughing and suffering from a temperature for two
days. This is inconsistent with the questionnaire. The GP diagnosed an upper
respiratory tract infection.
421.
Mrs Woods agreed that she did not mention her son’s eyes to the GP: her
explanation was that she was just bathing them.
422.
Bradley clearly did suffer from a coincidental viral infection which was
properly diagnosed on 14th June. It is of course possible that smoke
inhalation might have aggravated his symptoms from this, but I would only be
prepared to reach such a conclusion on the back of, at the very least, compelling
plume modelling evidence supporting an above threshold exposure.
Mr Steven
Woolvine
423.
Mr Woolvine was born on 2nd June 1984. He lives 2.59km from
the Sonae plant, and works as a customer service advisor at a location 1.65km
from the fire.
424.
Mr Woolvine has a history of hay fever, childhood eczema and dry skin
complaints. He is a moderate smoker.
425.
Mr Woolvine’s solicitors throughout have been Walter Barr. There are two
questionnaires relevant to his claim. Walter Barr told Mr Woolvine that this was
due to “administrative error”. The first questionnaire, dated 8th
August 2013, was completed and signed by Mr Woolvine. The second questionnaire,
dated 16th September 2013, was neither signed nor completed by him.
It contains several errors, and Mr Woolvine told me on oath that the signature
is not his. I accept his evidence. It follows that Walter Barr, or their agents,
have forged Mr Woolvine’s signature. This is a serious matter, and I direct
that a copy of his judgment be sent to the Solicitors Regulation Authority for
investigation of this issue.
426.
According to the first questionnaire, Mr Woolvine developed symptoms “right
away” and these comprised cold sores, a cough, chapped lips, a chest
infection and an eczematous rash. He claimed to have received medical treatment
at his GP surgery. This questionnaire is vague and unsatisfactory.
427.
Mr Woolvine’s witness statement does provide further detail. He said
that he developed a range of breathing, eye and skin problems in consequence of
the fire. They were particularly bad for the first couple of weeks, and took
approximately two months to resolve.
428.
Under cross-examination, Mr Woolvine accepted that he did not make the
connection between the fire and his symptoms until April 2013. He said that his
eye and chest symptoms resolved within two weeks, but it took two months for
the skin problems to recover.
429.
Mr Woolvine saw his GP on 8th July 2011 in relation to an
unrelated matter. He accepted that his questionnaire was incorrect in relation
to medical treatment, and explained that he had misunderstood it.
430.
Mr Woolvine was an unimpressive witness. Counsel began to fathom the bottom
of his case during this sequence of cross-examination:
“Q. Why didn't you go to the GP before 8 July, if you had
the symptoms you've talked about?
A. Because the symptoms that I had, I felt were manageable. I
don't want to go to the GP about every little thing, because I obviously go
quite a lot with regards to my depression and anxiety. I don't want to bombard
him with every little thing.
Q. No. So your cough never got so bad that you thought, well,
I really need to go and see a doctor?
A. No.
Q. Nor your shortness of breath?
A. No. Because at that time my shortness of breath, initially
I put it down to smoking, until it carried on for a couple of weeks, and then,
because of the other symptoms I got, I related it to the fire.
Q. It's just it was suggested at one point in the papers
[the account given by Mr Woolvine to Dr Hardy] that at one point you got so
breathless you had to sit down on a wall when you got to the church because you
were too breathless; is that right or not?
A. Yes. That's correct.
Q. If you really had that symptom at this time, you would have
gone to the GP, wouldn't you?
A. No, because, as I say, initially, I did put it down to smoking
and I did try and cut down at that stage, and after the two weeks it did ease
off.
Q. So when you cut down the cigarettes, the symptoms reduced?
A. Yes, but I've never had problems -- I've smoked for 10, 12
years, on and off, so I've never experienced problems like that before, and it
was just a bit coincidental that that happened at that period.
Q. The association you made between your symptoms and the fire
came very much later, didn't it? The association in your mind that the fire
may have caused problems came much later?
A. When I properly thought about it, yes.”
431.
In my judgment, Mr Woolvine grossly exaggerated his symptoms to Dr
Hardy, and he has also given an exaggerated account to me. I entirely accept
that this conclusion does not rule out the possibility of less severe symptoms
resulting from exposure to the smoke plume, which symptoms may have crossed the
threshold of actionable injury. However, as with other Test Claimants in his
position, Mr Woolvine’s difficulty is that he has to invoke something other
than his oral evidence to persuade me of that proposition.
432.
Having reviewed the evidence of the Test Claimants, and reached
provisional conclusions in relation to many of them, this is now the
appropriate moment at which to return to the plume modelling evidence.
THE
REMODELLING BY THE PLUME MODELLERS: RESULTS AND DISCUSSION
433.
On 7th July 2015 the results of CERC’s plume remodelling
exercise became available, and I invited further written submissions from the
parties to be provided within seven days.
434.
It is clear from Appendix 2 that CERC has followed my directions to the
letter. I have included, unedited, their explanations of their work, for ease
of comprehension. CERC’s results may be summarised as follows.
435.
Looking first of all at acrolein, it is clear that the majority of the
Test Claimants were exposed to levels greater than the odour recognition
threshold for many hours, the maximum being 44 hours (for Shaun West). The
minimum levels of hourly exceedances are for Jessica Alexander (6 hours), Kelly
Colebourne (2 hours), Karen Court (3 hours),
(4 hours), Teri
O’Brien (3 hours), James Reece (zero) and Steven Woolvine (2 hours). However,
as I have already said the odour recognition threshold is not a health
threshold; for that, and as an indicative starting-point, I have taken a value
of 146 μg/m³ for acrolein. The maximum theoretical hourly concentration
for any Test Claimant is 12.01μg/m³, i.e. more than 10 times below this
level. In fact, this Test Claimant is Peter Shaw who happened not to be at work
on that day, and so was not exposed to such a dose. The second highest
concentration is 9.48 μg/m³ (for Shaun West); for the vast majority of the
Test Claimants the exposures are below 3 μg/m³. I appreciate that the 146
μg/m³ threshold is a trigger value, and not an hourly mean, but given the
nature of this fire I doubt whether over relatively short periods of time this
makes a significant difference. It would only have done so if the wind had changed
over the course of any relevant hour.
436.
A consideration of the 8-hour and 15-minute threshold values for
acrolein of 237.5 μg/m³ and 712 μg/m³ respectively (see paragraph 142
above) demonstrates that all the Claimants come nowhere near these figures.
437.
The position is very similar as regards the total aldehydes. In this
instance, there are no examples of hourly exposures above the 500 μg/m³
threshold; indeed, the maxima are 41.0 (for Gary Mangan), 63.2 (for Peter Shaw
– not that he was there), and 49.9 (for Shaun West).
438.
As regards the PM10s, the position is less unfavourable from
the Claimants’ perspective, but still not propitious. Here, I have taken the
COMEAP trigger value of 107 μg/m³. In their remodelling, CERC has included
the Briery Hey background concentrations because this was in accordance with my
directions and ordinary tortious principles. For the vast majority of the Test
Claimants, their maximum exposures were on 17th June 2011, and their
highest recorded level was 100 μg/m³ (for a single hour – as to which, see
paragraph 443 below). The modelling for these Claimants does not show two
consecutive hours’ exceedances; indeed, in most instances the hourly exposures
were in the range of 10-50 μg/m³ (and typically within the band of 20-30
μg/m³) - in other words, at or scarcely above the background
concentrations recorded at Briery Hey. There are a limited number of Test Claimants
who fare somewhat better (in the forensic sense) with regard to the PM10s.
On 12th June, Gary Mangan incurred three consecutive hours’ exposures
of 103.6, 114.8 and 101.9 μg/m³ respectively. However, COMEAP would not
have placed him at risk inasmuch as he was not exposed to two consecutive hours
above 107 μg/m³. On 10th June, Peter Shaw (had he been at work)
would have been exposed to a maximum concentration of 140.1 μg/m³. He
would not been exposed to two consecutive hours over 107 μg/m³. On 12th
June, Shaun West was exposed to two sets of three consecutive hourly
concentrations which were very close to, or above, the 107 μg/m³ level. On
17th June he was exposed to one single hour’s concentration of 100.9
(although on that occasion the Briery Hey background level was high – 100.0).
439.
As regards the PM2.5s, the position is broadly similar.
Strictly speaking, Gary Mangan cannot demonstrate exposures to levels above the
COMEAP trigger value of 74 μg/m³ (for two consecutive hours), but he comes
extremely close. Shaun West was above the trigger value on two occasions on 12th
June. No one else threatens these levels.
440.
CERC has also calculated the 24-hour mean concentrations for the five
most heavily exposed Test Claimants. For Messrs Shaw and Swift, and Master
Bradley Woods, their exposures were well below the CERC guideline values for
the PM10s (of 51 μg/m³ for vulnerable persons and 76 μg/m³
for non-vulnerable) and for the PM2.5s (of 36 μg/m³ for
vulnerable persons and 55 μg/m³ for non-vulnerable). Moreover, their
exposures were not significantly above the Briery Hey background levels. However,
on 12th June Gary Mangan’s 24-hour mean concentrations were 54.3
μg/m³ for the PM10s and 35.8 μg/m³ for the PM2.5s.
Likewise, on the same day Shaun West’s mean concentrations were 65.6 μg/m³
and 45.0 μg/m³ respectively. Thus, it is open to them argue that there
were certainly in the vicinity or “ball-park” of the 24-hour thresholds,
depending on whether they should be regarded as vulnerable.
441.
It is no accident that Gary Mangan and Shaun West were the most heavily
exposed: they live relatively close to the Sonae plant. Interestingly, the
comparable data for Dawn Bunting - as the crow flies, being the closest of all
the Test Claimants to the source of the emissions - demonstrate a materially
different pattern. Save for 17th June, her exposures to the PM10s
were broadly similar to the bulk of the Test Claimants’, namely not
substantially above background concentrations. The fact that her home is
approximately 200m south of Messrs Mangan and West materially affects her
exposure levels. When one then examines the positions of Paul McLoughlin,
Bradley Woods and Kathleen Tully, being the sub-group of Test Claimants next
closest to the plant, their exposures to the PM10s and the PM2.5s
were scarcely distinguishable from those of the remainder, and much lower than
Messrs Mangan’s and West’s. This exercise shows that only a very small coterie
of Claimants living north-west of the plant were close to being within the
“scientific” envelope of risk, and then only for relatively brief periods on 12th
June (I exclude from account 17th June in relation to Shaun West,
owing to the high background levels).
442.
The contour maps within Appendix 2 illustrate the same point in a
different way. In relation to the micro-particles, these maps show that anyone
living further away from the plant than Gary Mangan received no exposures
higher than the COMEAP trigger values. On my reckoning, a maximum of 250
individuals could have been living within the outer contour line. Their cases
have not been individually examined, but it is possible that some of these
could demonstrate two consecutive hours’ exposure above the COMEAP trigger
values. That, without more, would not be sufficient to prove actionable injury,
but it would at least be a modest platform. Put slightly differently, such
individuals might have the makings of a claim, but success would depend
on their personal circumstances. I return to this issue at paragraph 465 below.
443.
In his closing arguments delivered upon the conclusion of the oral
evidence, Mr Kent submitted that the Briery Hey monitoring station did not show
a “spike” in PM10s in consequence of the fire. Mr Redfern did not
contradict that submission the following day, and it is borne out by the
remodelling data. For example, as regards those Test Claimants who live
nearest to Briery Hey, namely Jessica Alexander, James Glascott and Julie
Carney, there is no evidence of any “spike” once the known Briery Hey values
are removed from account. Further, I agree with Mr Kent that the 100 μg/m³
maximum value consistently referable by the remodelling to 17th June
must be attributed to background levels rather than to the fire, and that the
same analysis applies to the PM2.5s on 5th July, where
the remodelled value is about 66 μg/m³.
FINAL
ANALYSIS, SYNTHESIS AND CONCLUSIONS
444.
Viewed in isolation, the scientific evidence in this case does not begin
to support these claims, save possibly for those of Gary Mangan and Shaun West.
Indeed, viewed in those terms this evidence demonstrates that virtually all the
Test Claimants could not have suffered actionable injury.
445.
The key question which arises is whether I should be lowering the
exposure thresholds to reflect scientific uncertainty, the difference between
the scientific and the legal standards of proof, the quality of the Test
Claimants’ lay evidence and/or the views of Dr Hardy, Mr Swift and Mr Clearkin.
446.
The matters I have identified as being potentially to the Claimants’
advantage need to be addressed both individually and cumulatively.
447.
Plainly, we are not in the realm of what might be called hard-edged
science. An element of uncertainty has afflicted the exercise at every stage:
as to Dr Mitcheson’s heat release rates; the selection of the appropriate
emission factors; the toxicology (at these low-exposure levels); and the plume
modelling. However, three points need to be made. First, in relation to these
issues I have applied a liberal approach throughout this judgment: that is to
say, an approach which favours the Claimants where the evidence permits it.
Secondly, the vast majority of the Test Claimants have fallen a long way short
of demonstrating any significant exposures. Thirdly, there is no obvious reason
why the Claimants should be the greater victims of scientific uncertainty than
the Defendant. In my view, uncertainty is likely to be normally distributed.
448.
I have mentioned the scientific uncertainties in connection with the
ascertainment of the toxicological thresholds for low exposures. A related
question arises as to whether the thresholds should be lowered to reflect
pre-existing vulnerability. Many of the Test Claimants did not enjoy good
general health, despite some of their assertions to the contrary. Many may have
been prone to respiratory problems, and all those who were seen by the
ophthalmologists have current signs of meibomian gland dysfunction. A number of
Test Claimants, in particular Edmund Kenny, Kelly Colebourne and Annette
Farrell, had pre-existing asthma. However, putting that aside for one moment,
there is a lack of any solid, quantitative basis for making a discount for vulnerability.
Many Claimants might have been vulnerable, but there is no proper means of
assessing or quantifying this. Dr Hardy asserted that those without
pre-existing pathologies tended to recover within 3-6 weeks of exposure,
whereas those who were vulnerable required 3-6 months; but that assertion is
simply not borne out by a close examination of the circumstances of their
individual cases, or indeed a proper identification of how and why they were
“vulnerable”. In any event, the level of discount must be an exercise in
speculation, and for the vast majority of Test Claimants it would have to be
very considerable for them to get anywhere. I note too that the differences
between the COMEAP thresholds for vulnerable and non-vulnerable individuals are
not great, and certainly well short of the magnitudes which would be required
to avail any vulnerable Test Claimant.
449.
A related point is that the available evidence fails to demonstrate any
dose-related response. Listening as I did to all the Test Claimants give their
evidence, the accounts they gave of the smoke plume and of the nature and
severity of their symptoms bore no relationship with their modelled exposures.
The smell and duration of the smoke was described in more or less exactly the
same way irrespective of location. Indeed, I might be forgiven for thinking
that some of the Test Claimants who in fact lived the furthest away from the
plant were almost adjacent to it. Overall, the claimed symptoms appeared to be
independent of exposure and dose. It was as if the Test Claimants had
experienced a monolithic phenomenon. I appreciate that human beings differ, but
I would expected to have heard accounts which varied according to the now
ascertained doses.
450.
Secondly, I do not consider that the application of a lower standard of
proof requires me to approach the scientific evidence in any different way,
save to recognise the scale of the potential uncertainties. I have already
addressed that issue in paragraph 447 above. Where the law differs from the
science is the weight it chooses to accord to lay evidence. This brings me to
the third point.
451.
In my judgment, the lay evidence viewed as a whole was unimpressive. It
was vague, impressionistic, imprecise, sometimes inconsistent with the known
behaviour of the smoke plume, and often internally inconsistent. Only three of
the Test Claimants gave evidence which impressed me as being potentially
reliable. Given that no one appears to have kept a contemporaneous record of
his or her experiences, this generic failure to provide a coherent, consistent
account of what occurred is hardly surprising, but in my judgment cannot be a
factor in the Claimants’ favour.
452.
Had there being a critical mass of impressive, reliable lay evidence
from the Claimants, I might have been prepared to revisit the toxicological
thresholds and the plume modelling evidence. In the absence of these desiderata,
I have absolutely no proper basis for lowering the bar.
453.
The three Test Claimants who did impress me were Messrs Dunn, Kenny and
McLoughlin. They all live north-west of the Sonae plant, but some considerable
distance away. Mr Dunn, in many ways the most impressive witness, lives 2.3km
away. His exposures were modest. Mr McLoughin gave quite convincing evidence in
relation to his skin problems, but in the end I cannot accept that the science
could be so wrong that he could be right. Mr Redfern submitted that the absence
of any relationship between the good cases/witnesses and the modelled exposures
somehow avails the Claimants, but in my judgment the true position is exactly
the converse.
454.
This brings me to the “constellation of symptoms” effect, and Dr Hardy’s
eloquent foray into quasi-epidemiology (Mr Swift and Mr Clearkin were less
impassioned, but gave evidence to like effect). The difficulty with these
arguments is that they entail an overly generous and macroscopic view of the
Test Claimants’ evidence. Ultimately, they are founded on the apparent temporal
association. What I have to call this ersatz epidemiology falls away as soon as
the individual cases are scrutinised with the care they deserve in a forensic
setting. As soon as that process occurred, the inconsistencies and weaknesses
in most of the Test cases became evident. Furthermore, as soon as the plume
modelling evidence is factored into the equation – as it has never been by the
Claimants’ clinical team – the claims become weaker still. In my judgment,
these experts have sought to discern a constellation by gazing hopefully into
the sky, without taking time to look closely at the individual stars.
455.
The possibility arises that the science is just plain wrong, and that in
many years’ time a proper epidemiological study will prove that the residents
of Kirkby were right all along. I cannot exclude that possibility. However, I
have to use the best scientific evidence that is available, and then balance it
against the lay evidence. Performing that exercise, I am satisfied on the
balance of probabilities that the lay evidence I have heard cannot outweigh the
combined effect of the science. Indeed, I would put the matter higher than that
– in my view, the lay evidence creates no significant dent into the science,
the latter emerging unscathed.
456.
In my judgment, there are serious weaknesses in the Claimants’ overall
case which I need to make explicit. I have already alluded to some of them.
First, the case is severely damaged by the delay in bringing these claims and
the absence of any contemporaneous evidence. Had 16,000 people really suffered
symptoms of the severity claimed, one would surely have seen evidence of
complaints to newspapers and to the local council, increases in GP attendances,
and some contemporary record of a problem. None has been brought to my
attention. Secondly, recall bias is always an issue in scientific research
based on retrospective evidence, and this phenomenon is hugely magnified when
one brings into the equation the obvious corollaries of the medico-legal
component. Human beings are naturally susceptible and suggestible, particularly
if they are made to believe that they form part of a coherent group with shared
experiences, and if they risk none of their own resources in bringing a claim.
The standard-form questionnaires asked a series of leading questions. Many of
the questionnaires examined in the context of the Test Claimants were shown to
be inaccurate and exaggerated, calling into question the objectivity and
integrity of the whole process. Nor does the whole set up of pop-up shops and
cold-calling of potential Claimants inspire any degree of confidence.
457.
My concerns in this regard are heightened by the fact that two of the
questionnaires were shown to bear forged signatures, and that whole families
have been signed up, apparently willy-nilly, to the group. The Defendant has
drawn my attention, through the evidence of Ms Adele Wilson, to the sort of
behaviour that has been going on. According to paragraph 6 of her witness
statement:
“In approximately January 2012, I was at work when I received
a telephone call from my partner, Greg Taft. Greg told me that a lady had
visited our home in Tower Hill who had told him that she was acting on behalf
of GT Law solicitors who was dealing with claims against Sonae relating to
smoke inhalation from the fire in June 2011. She said that Sonae had accepted
liability and that compensation had already been paid out to claimants. The
lady was attempting to encourage Greg to sign up in order to put forward a
claim against Sonae for symptoms relating to smoke inhalation. Greg told her
that he was not interested in making a claim and asked her to leave.”
Ms Wilson was not cross-examined
about this evidence, which is admittedly hearsay. However, there is no reason
to doubt its accuracy. The information Mr Taft was given was inaccurate – there
had been no admission of liability, and no money had been paid. Misleading
information of this sort had the obvious tendency to encourage the bringing of
claims, on the basis that the Defendant was a soft target and this was easy
money. That this information was understood in exactly this way is revealed by
the terms of the Facebook posts referred to at paragraphs 9, 10 and 12 of Ms
Wilson’s witness statement, as well as by the evidence in Leon Swift’s case. I
strongly deprecate this sort of practice. Not merely does it sail close to the
wind in terms of its professional propriety, it is severely counter-productive
as and when the case comes to trial.
458.
I have considered the possibility of an alternative narrative pursuant
to which a number of Claimants might succeed. It runs like this. The GP records
are all incorrect/inaccurate; the Claimants have short-changed themselves in
terms of their timings and the exact sequence of events (they must not be
criticised for not remembering); when all the inconsistencies, exaggerations
and excrescences are stripped away, there lies a hard kernel of truth – a truth
which says that many of the Claimants did suffer actionable injury, albeit
maybe not for as long as they have claimed. In many cases, so this argument
might run, Claimants did sustain exacerbations of pre-existing conditions.
459.
Mr Redfern did not advance submissions along precisely these lines, for
obvious reasons – he could not be heard to do so. However, it is clearly right
that I should be considering this alternative viewpoint. Apart from the
scientific evidence, which strongly tells against such a narrative being
correct, there is this added difficulty. At its highest, the narrative I am
postulating might just be true, but there is no basis for holding that
it is probably true. Furthermore, there is no sensible or remotely
plausible basis for concluding that so much hard evidence, including the
contemporaneous GP record, is incorrect, and it simply would not be right to
make findings of fact based on a version of events that does not match the
evidence the Claimants chose to give.
460.
I return to the cases of the three Test Claimants whose evidence was, as
I have said, prima facie reliable. Given that the scientific evidence is
so heavily against them, there is in my judgment no proper, principled basis
for allowing their claims. That they were good witnesses is insufficient: that
does not preclude their being mistaken (in my judgment, they are
mistaken) and/or being sucked into the vortex of suggestibility created by the
claims environment which obtained in Kirkby in 2013.
461.
The strongest case out of the 20 is Mr Edmund Kenny’s. He was an
impressive witness and also immensely likeable. He did not exaggerate his
symptoms in any way. It is clear that he did suffer a flare-up in his asthma
symptoms in June 2011, and that he told his GP that he suspected a causal link.
He accepted in cross-examination that he did not know whether his suspicions
were correct. Ultimately, it is not his view which counts but the opinion of an
expert in respiratory diseases. Plainly, neither Dr Hardy nor Dr Hind made a
contemporaneous examination. Mr Kenny has the benefit of no contemporaneous
medical examination, and retrospective diagnosis is problematic. His exposures
were low: scarcely above the background levels for the micro-particles (I have
deduced that the majority of the “spike” on 17th June, and certainly
the single 100 μg/m³ reading, is unrelated to the fire), and a maximum
hourly concentration of 1.45 μg/m³ for acrolein. In my judgment, he fails
to satisfy me of a causal link.
462.
As for Gary Mangan and Shaun West, on account of their exposures they
stood the best chance of proving actionable injury in consequence of the Sonae
fire, but in my judgment their claims fail nonetheless. Mr Mangan is a fit
young man who could not convincingly be described as vulnerable. The plume
modelling measures out-of-door exposures, and Mr Mangan did not tell me that he
ventured outside at the relevant time. His case lies at the margins of the PM10
trigger levels, but is considerably lower than the threshold levels for the
irritants. In any event, the better view on the balance of probabilities is
that he suffered from a coincidental upper respiratory tract infection. Mr West
was not a good witness, and there were clear inconsistencies and exaggerations
in his account. He too could not be described as vulnerable. The generic
considerations set out at paragraph 465 below also apply.
463.
Where does the truth lie in all of this? It is not my function to say
what the truth is; my role is limited to deciding whether these claims succeed
or fail, applying standard legal methods. However, out of fairness to the
Claimants my conclusions about what happened in June 2011 are as follows. There
is no unified field theory or overarching explanation. The majority of
Claimants experienced an extremely nasty, unusual smell and some may have been
concerned about the possible consequences, albeit not so concerned to seek
medical advice. Many Claimants - it is not clear to me how many – suffered some
symptoms of shortness of breath, lacrimation and soreness of the throat. These
symptoms were short-lived, as were any significant quantities of smoke. For the
majority of the time, the smoke was blowing away from the plant. The better
view on all the available evidence is that these symptoms did not exceed the
hurdle the law sets for actionable personal injury, because they were symptoms
of irritation rather than of inflammation. It is difficult to say for how long
the smoke and these mild symptoms lasted, but I have in mind a maximum period
of about one week. Many months later – it is unclear exactly how and why - lawyers
arrived on the scene and sensed the opening of a business opportunity. It
proved not very difficult to recruit willing Claimants to the group, not least
because there was a lot of ill-feeling in the neighbourhood directed towards
Sonae, and many people genuinely believed that they must have been harmed in
some way. The legal process preyed on human susceptibility and vulnerability,
and the rest is history.
464.
I accept that for a period of time, probably 2-3 days, there were deposits
of ash and dust which proved recalcitrant and pervasive. It is regrettable that
Dr Mitcheson was not cross-examined about this, but I am not prepared to
disbelieve the entirety of the Claimants’ evidence on this point. However, I
should not be understood as excluding from account the probability of poetic
licence and exaggeration.
465.
Previously, I have referred to a maximum of 250 people living within the
outer contour line on the CERC contour maps marking exposures to the
micro-particles at above the COMEAP trigger values (albeit, I reiterate, not
for two consecutive hours). I do not know how many of these are Claimants. I
cannot exclude the possibility that some of these might have suffered personal
injury, but I have three observations. First, the Claimants have only asked me
to examine one individual within this sub-cohort, namely Gary Mangan.
Presumably, he was selected because he was representative of the others, and/or
because those advising the Claimants believed that he would be a good witness. My
observation would be that if there were stronger cases within this sub-group,
they should have been put forward as Test claims. Secondly, I suspect that only
those with pre-existing conditions might have had a realistic prospect of
proving actionable damage. I should not be interpreted as overlooking the fact
that all these individuals fell vastly below the relevant health threshold for
acrolein, and well below the PM10 levels at which significant
numbers of children complained of symptoms as demonstrated in the Californian
Wildfires study (see paragraph 157 above). Thirdly, after a multi-million pound
group action which has failed, in my judgment it would scarcely be proportionate
to start examining even a handful of these cases, in the pursuit of identifying
what would be, at best, modest claims. In my judgment, the Claimants’ chance
has come and gone.
466.
There are clear lessons to be learned from this litigation. The
Claimants’ legal team should have worked out the science at a much earlier
stage. Working on a reasonable best case scenario (as I have done), sound
toxicological evidence (which they had at their disposal) and plume modelling,
they should have investigated whether the case stacked up. Instead, at all
material times, the Claimants’ legal team appear to have wanted to make a virtue
out of uncertainty – perhaps because they clung to the notion that the
litigation would settle. Alternatively, they believed that the judge would not
be that interested in the science, and/or they placed undue faith on the likely
cogency of the lay evidence.
467.
On all counts, they have been proven wrong. Further, rather than give
the Claimants the opportunity to rely positively on uncertainty, I have taken
proactive steps to enable further modelling to be undertaken, thereby creating
as robust an evidential basis as human ingenuity may currently provide. The
Claimants have lost no money, but their expectations, always unsustainable in
my view, have not been fulfilled. I regret that their hopes were raised in the
first place.
468.
These claims must all be dismissed, and judgment must be entered for the
Defendant.
APPENDIX 1
.jpg)
|
CLAIMANT NUMBER
|
CLAIMANT NAME
|
POSTCODE
|
DISTANCE FROM SONAE (KM)
|
|
2
|
JESSICA ALEXANDER
|
L32 8TX
|
1.56
|
|
2
|
JESSICA ALEXANDER
COLLEGE
|
L33 8XF
|
1.42
|
|
3
|
TRACEY BEATHAM
|
L33 2DE
|
1.96
|
|
7
|
DAWN BUNTING
|
L33 6XB
|
0.44
|
|
10
|
JULIE CARNEY
|
L32 9PQ
|
1.94
|
|
13
|
KELLY COLEBOURN
|
L32 7PZ
|
2.16
|
|
14
|
KAREN COURT
|
L33 4DH
|
2.27
|
|
17
|
TERENCE DUNN
|
L33 4DP
|
2.31
|
|
18
|
ANNETTE FARRELL
|
L33 1UW
|
1.81
|
|
18
|
ANNETTE FARRELL WORK
|
L32 9PP
|
2.27
|
|
20
|
FRANCIS GLASCOTT
|
L32 9QD
|
2.1
|
|
23
|
EDMUND KENNY
|
L33 1YF
|
1.8
|
|
24
|
GARY MANGAN
|
L33 9XF
|
0.53
|
|
25
|
PAUL MCLOUGHLIN
|
L33 1WD
|
1.61
|
|
27
|
TERI O’BRIEN
|
L32 2AR
|
2.63
|
|
28
|
JAMES REECE
|
L32 4SP
|
3.01
|
|
28
|
JAMES REECE WORK
|
L32 9HN
|
2.87
|
|
30
|
PETER SHAW WORK
|
L33 7TJ
|
0.55
|
|
33
|
LEON SWIFT
|
L33 7UY
|
0.88
|
|
35
|
KATHLEEN TULLY
|
L33 1UG
|
1.53
|
|
37
|
SHAUN WEST
|
L33 9UJ
|
0.58
|
|
39
|
BRADLEY WOODS
|
L33 1RF
|
1.09
|
|
40
|
STEVEN WOOLVINE
|
L32 7RP
|
2.59
|
|
40
|
STEVEN WOOLVINE WORK
|
L33 7RX
|
1.65
|
APPENDIX 2
Sonae GLO: Further Modelling
Contents
Following
the instructions of Mr Justice Jay further modelling by CERC is presented in
the accompanying seven documents. As specified by Mr Justice Jay, the modelling
is based on:
- 1550 tonnes of material consumed in fire;
- The heat release and burning rates
specified by Dr Mitcheson, with 10% subtracted to account for radiative
heat loss
- An emission factor of 114 mg/s/MW for
acrolein for all stages of the fire, compared against an odour threshold
of 0.38 µg/m³ and a health threshold of 146 µg/m³
- An emission of 600 mg/s/MW for total
aldehydes for all stages of the fire, compared against a health threshold
of 500 µg/m³
- PM10 emission factors of 27.5
g/kg for Stage 2 and 12.5 g/kg for Stages 1 and 3 of the fire, compared
against the COMEAP High trigger value of 107 µg/m³. Assuming 0.8%
contamination, as specified by the Mr Justice Jay, the PM10
emission factors used are 27.61 g/kg for Stage 2 and 12.73 g/kg for Stages
1 and 3
- PM2.5 emission factors of 22.6
g/kg for Stage 2 and 10.25 g/kg for Stages 1 and 3 of the fire, compared
against the COMEAP High trigger value of 74 µg/m³. Assuming 0.8%
contamination, as specified, the PM2.5 emission factors used
are 22.64 g/kg for Stage 2 and 10.39 g/kg for Stages 1 and 3
- The agreed meteorological data, of Dr Wild
and Mr Lynagh (Lynagh/Wild dataset). CERC and Envirobods agreed that in
order to make full use of the Lynagh/Wild dataset, hourly inputs for the
model should be derived by calculating hourly averages from the 10-minute
data recorded every 15 minutes, as detailed in CERC’s supplementary report
dated 22nd September 2014. The Lynagh/Wild dataset only
provides data until 1st July 2011, therefore to consider whole
period of the fire meteorological data from the Met Office Crosby station
were used from the 1st July 2011, up to and including the 7th
July 2011
- Modelled PM10 and PM2.5
concentrations include background concentrations using values measured at
the Briery Hey monitoring site. This monitoring data includes a 43 hour
gap in PM2.5 monitoring between the 10th June 2011
and 12th June 2011. PM2.5 concentrations for this
period were estimated from the measured PM10 concentrations,
assuming a PM2.5/PM10 ratio of 0.45. This ratio is
the ratio of the mean concentrations over the period of the fire, where
both PM2.5 and PM10 concentrations are recorded.
Based
on this model set-up, specified by Mr Justice Jay and outstanding elements
agreed between the dispersion modelling experts, the following outputs are
provided:
- Document 1: Contour maps of the number of
hours exceeding the odour threshold for acrolein and the COMEAP High
trigger values for PM10 and PM2.5. Contours for
exceedences of the health thresholds for acrolein and total aldehydes
could not be plotted because modelled concentrations are not sufficiently
high.
- Document 2: Tables of number of hours
exceeding the thresholds of PM10, PM2.5, acrolein
and total aldehydes at the locations of the 20 Test Claimants, along with
modelled maximum hourly concentrations at these locations.
- Document 3: Tables of modelled PM10
and PM2.5 concentrations for particular days and Test Claimant
locations, as specified by Mr Justice Jay.
- Document 4: Time series histograms of
hourly ‘unit discharge’ concentrations compared against the specified
acrolein and total aldehydes thresholds for the locations of the 20 Test
Claimants.
- Document 4a: Time series histograms of
hourly ‘unit discharge’ concentrations, plotted for a lower concentration
range than used in Document 4, to show modelled concentrations more
clearly and allow better comparison against the acrolein odour threshold.
- Document 5: Time series histograms of
hourly PM2.5 concentrations for the locations of the 20 Test
Claimants, compared with the COMEAP High trigger value of 74 µg/m³.
- Document 6: Time series histograms of
hourly PM10 concentrations for the locations of the 20 Test
Claimants, compared with the COMEAP High trigger value of 107 µg/m³.
Sonae GLO: Further Modelling
1. Contour maps of number of hours exceeding threshold values
This
document presents the following contour maps of modelled number of hours for
which hourly average concentrations exceed specified threshold values:
·
Acrolein
concentrations exceeding the odour recognition threshold of 0.38 µg/m³
·
PM10
concentrations, including background concentrations using measured data from
the Briery Hey monitoring site, exceeding the COMEAP High trigger value of
107 µg/m³.
o Two plots are presented for PM10:
the first is based on 100 m resolution model output for an output area of 9.4
km x 6.6 km; and the second is based on 50 m resolution model output for
an output area of 5 km x 4 km, producing better resolution of the modelled
exceedence area.
·
PM2.5
concentrations, including background concentrations using measured data from
the Briery Hey monitoring site, exceeding the COMEAP High trigger value of
74 µg/m³.
o Two plots are presented for PM2.5:
the first is based on 100 m resolution model output for an output area of 9.4
km x 6.6 km; and the second is based on 50 m resolution model output for
an output area of 5 km x 4 km, producing better resolution of the modelled
exceedence area.
Contour
maps for the acrolein health threshold of 146 µg/m³ and the total aldehydes
threshold of 500 µg/m³ have not been produced because these thresholds are not
exceeded beyond the boundary of the Sonae factory.
The
maximum modelled acrolein concentration across the output area is 95.6 µg/m³,
below the health threshold, therefore a contour map cannot be produced since
there are no exceedences of the threshold across the model output area.
The
maximum modelled total aldehydes concentration across the output area is
502.6 µg/m³, just above the threshold of 500 µg/m³. This maximum
concentration is modelled with the 50 m resolution output and is the only point
across the output area above the threshold value. This output point is located
within the boundary of the Sonae factory.
To
minimise differences in the appearance of contour plots due to contouring
methodology, CERC and Envirobods agreed to use Golden Software’s Surfer package
for contour plotting, using the Inverse Distance Weighting interpolation
method.
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