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You are here: BAILII >> Databases >> England and Wales High Court (Queen's Bench Division) Decisions >> Saunderson & Ors v Sonae Industria (UK) Ltd [2015] EWHC 2264 (QB) (30 July 2015) URL: http://www.bailii.org/ew/cases/EWHC/QB/2015/2264.html Cite as: [2015] EWHC 2264 (QB) |
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Neutral Citation Number: [2015] EWHC 2264 (QB)
Case No: 2MA90124
IN THE HIGH COURT OF JUSTICE
QUEEN'S BENCH DIVISION
MANCHESTER DISTRICT REGISTRY
“SONAE GROUP LITIGATION”
Liverpool Civil and Family Court
35 Vernon Street
Liverpool L2 2BX
Date: 30/07/2015
Before:
MR JUSTICE JAY
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Between:
|
MRS SUSAN SAUNDERSON & OTHERS |
Claimants |
|
- and - |
|
|
SONAE INDUSTRIA (UK) LTD |
Defendant |
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- - - - - - - - - - - - - - - - - - - - -
Mr Michael Redfern QC, Mr Pepin Aslett and Miss Alice Dobbie (instructed by Camps Solicitors) for the Claimants
Mr Michael Kent QC and Mr Michael Jones (instructed by Clyde & Co Claims LLP) for the Defendant
Hearing dates: 3rd – 5th, 8th – 12th, 15th – 19th, 22nd – 26th June 2015
- - - - - - - - - - - - - - - - - - - - -
Judgment
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.
“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)”
THE DEFENDANT’S PLANT AND MODUS OPERANDI
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.
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.
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.
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.
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
(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.
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.
The Quantity of Woodchips in the Bunkers
“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”
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.
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.
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.
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.
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.
“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.
Heat Release Rates
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).
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.
“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.
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.
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.
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).
“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.”
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.”
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.”
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.
“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.”
“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.”
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.
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.
Ash and Dust Deposition
“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.
“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.”
TOXICOLOGY
“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.”
“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.
(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.
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.”
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.
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.”
· 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).
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.
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.
THE METEOROLOGICAL EVIDENCE
“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.”
THE PLUME MODELLING
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.
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.
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.
GOVERNING LAW
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.”
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.
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.
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.”
“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.”
THE EVIDENCE FROM THE CLINICIANS
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.
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.
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.
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.
“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.”
“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.”
“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.”
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.
“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.”
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.
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.
THE TEST CLAIMANTS
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.
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.
Mrs Tracey Beatham
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.
“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”
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.
Ms Jessica Alexander
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
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.
“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. ”
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 …”
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.
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.
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.
Mr Terence Dunn
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.
Ms Julie Carney
“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.
“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
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.
“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.
Mrs Annette Farrell
320. She is a light smoker and had pre-existing problems with bronchitis and shingles.
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.
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.”
Mr James Reece
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
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.
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 …”
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.
Mr Paul McLoughlin
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.
“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.”
“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.”
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
357. Mr Shaw is a non-smoker who had no chest symptoms of any note for a number of years.
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.
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
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.
Mr Francis Glascott
“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 …”
Mr Leon Swift
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.
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.
“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.”
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”
“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
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.”
Mrs Kathleen Tully
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 …”
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.
Master Bradley Woods
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.
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
“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.
THE REMODELLING BY THE PLUME MODELLERS: RESULTS AND DISCUSSION
FINAL ANALYSIS, SYNTHESIS AND CONCLUSIONS
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.
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.
“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.
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.
468. These claims must all be dismissed, and judgment must be entered for the Defendant.
APPENDIX 1
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:
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:
Sonae GLO: Further Modelling
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.[1]
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.
Sonae GLO: Further Modelling
Table 1 lists the locations of 20 Test Claimants. Two tables then follow presenting the model outputs for the locations of the 20 Test Claimants:
Table 2 presents the number of hours exceeding the COMEAP High trigger values for PM10 and PM2.5 and the maximum predicted hourly concentrations for these pollutants. The number of exceedences and maximum hourly concentrations include the modelled contribution from the fire and background concentrations using measured data from the Briery Hey monitoring site.
Table 3 presents the number of hours exceeding acrolein thresholds for odour (0.38 µg/m³) and health (146 µg/m³), and the health threshold for total aldehydes (500 µg/m³).
Table 1: Locations of the 20 Test Claimants
ID |
Name |
Postcode |
Coordinates of location (Ordnance Survey British National Grid) |
|
Eastings (m) |
Northings (m) |
|||
2 |
Jessica Alexander |
L32 8TX |
341941 |
397952 |
3 |
Tracey Beatham |
L33 2DE |
340940 |
399888 |
7 |
Dawn Bunting |
L33 6XB |
342398 |
399215 |
10 |
Julie Ann Carney |
L32 9PQ |
341428 |
397883 |
13 |
Kelly Colebourn |
L32 7PZ |
341955 |
397276 |
14 |
Karen Court |
L33 4DH |
341351 |
401049 |
17 |
Terence Dunn |
L33 4DP |
341193 |
400972 |
18H |
Annette Farrell (home) |
L33 1UW |
341158 |
400143 |
18W |
Annette Farrell (workplace) |
L32 9PP |
340868 |
397737 |
20 |
Francis Glascott |
L32 9QD |
341311 |
397760 |
23 |
Edmund Kenny |
L33 1YF |
341130 |
399991 |
24 |
Gary Mangan |
L33 9XF |
342431 |
399666 |
25 |
Paul McLoughlin |
L33 1WD |
341259 |
399931 |
27 |
Teri O’Brien |
L32 2AR |
340096 |
399491 |
28H |
James Reece (home) |
L32 4SP |
339918 |
398434 |
28W |
James Reece (workplace) |
L34 9HN |
343241 |
396479 |
30 |
Peter Shaw |
L33 7TJ |
343172 |
398968 |
33 |
Leon Swift |
L33 7UY |
343654 |
399545 |
35 |
Kathleen Tully |
L33 1UG |
341606 |
400205 |
37 |
Shaun West |
L33 9UJ |
342477 |
399612 |
39 |
Bradley Woods |
L33 1RF |
342181 |
400231 |
40H |
Steven Woolvine (home) |
L32 7RP |
341239 |
397200 |
40W |
Steven Woolvine (workplace) |
L33 7RX |
342549 |
397466 |
Table 2: Number of hours exceeding COMEAP High trigger values for PM10 and PM2.5, together with modelled maximum concentrations, at the test case locations. Modelled concentrations include background concentrations from the Briery Hey monitoring site.
ID |
PM10 (including background concentration) |
PM2.5 (including background concentration) |
|||
Number of hours exceeding COMEAP High trigger value (107 µg/m³) |
Maximum hourly concentration (µg/m³) |
Number of hours exceeding COMEAP High trigger value (74 µg/m³) |
Maximum hourly concentration (µg/m³) |
||
2 |
0 |
100.0 |
0 |
66.0 |
|
3 |
0 |
100.0 |
0 |
66.0 |
|
7 |
0 |
100.0 |
0 |
66.0 |
|
10 |
0 |
100.0 |
0 |
66.0 |
|
13 |
0 |
100.0 |
0 |
66.0 |
|
14 |
0 |
100.5 |
0 |
66.0 |
|
17 |
0 |
100.3 |
0 |
66.0 |
|
18H |
0 |
100.0 |
0 |
66.0 |
|
18W |
0 |
100.0 |
0 |
66.0 |
|
20 |
0 |
100.0 |
0 |
66.0 |
|
23 |
0 |
100.0 |
0 |
66.0 |
|
24 |
2 |
114.8 |
2 |
79.9 |
|
25 |
0 |
100.0 |
0 |
66.0 |
|
27 |
0 |
100.0 |
0 |
66.0 |
|
28H |
0 |
100.0 |
0 |
66.0 |
|
28W |
0 |
100.0 |
0 |
66.0 |
|
30 |
1 |
140.1 |
1 |
112.2 |
|
33 |
0 |
100.0 |
0 |
66.0 |
|
35 |
0 |
100.1 |
0 |
66.0 |
|
37 |
5 |
135.8 |
6 |
96.4 |
|
39 |
0 |
101.0 |
0 |
66.0 |
|
40H |
0 |
100.0 |
0 |
66.0 |
|
40W |
0 |
100.0 |
0 |
66.0 |
Table 3: Number of hours exceeding odour and health thresholds for acrolein, and health threshold for total aldehydes at the test case locations. Modelled maximum concentrations for these pollutants are also presented.
ID |
Acrolein |
Total aldehydes |
|||
Number of hours exceeding threshold value |
Maximum hourly concentration (µg/m³) |
Number of hours exceeding health threshold (500 µg/m³) |
Maximum hourly concentration (µg/m³) |
||
Odour (0.38 µg/m³) |
Health (146 µg/m³) |
||||
2 |
6 |
0 |
0.74 |
0 |
3.9 |
3 |
16 |
0 |
1.37 |
0 |
7.2 |
7 |
10 |
0 |
1.40 |
0 |
7.4 |
10 |
10 |
0 |
1.05 |
0 |
5.5 |
13 |
2 |
0 |
0.59 |
0 |
3.1 |
14 |
3 |
0 |
0.82 |
0 |
4.3 |
17 |
4 |
0 |
1.17 |
0 |
6.2 |
18H |
14 |
0 |
1.29 |
0 |
6.8 |
18W |
4 |
0 |
0.96 |
0 |
5.1 |
20 |
9 |
0 |
0.97 |
0 |
5.1 |
23 |
18 |
0 |
1.45 |
0 |
7.6 |
24 |
36 |
0 |
7.78 |
0 |
41.0 |
25 |
18 |
0 |
1.55 |
0 |
8.2 |
27 |
3 |
0 |
0.66 |
0 |
3.5 |
28H |
0 |
0 |
0.25 |
0 |
1.3 |
28W |
0 |
0 |
0.30 |
0 |
1.6 |
30 |
14 |
0 |
12.01 |
0 |
63.2 |
33 |
17 |
0 |
2.21 |
0 |
11.6 |
35 |
11 |
0 |
1.83 |
0 |
9.6 |
37 |
44 |
0 |
9.48 |
0 |
49.9 |
39 |
9 |
0 |
1.46 |
0 |
7.7 |
40H |
2 |
0 |
0.39 |
0 |
2.1 |
40W |
2 |
0 |
0.49 |
0 |
2.6 |
Sonae Group Litigation: Final Modelling
3. Tables of modelled hourly PM10 and PM2.5 concentrations for specific days and Test Claimants
This document presents tables of PM10 and PM2.5 concentrations for the day and Test Claimant combination specified in Table 1. Hourly concentrations and 24-hour mean concentrations are presented along with background concentrations from the Briery Hey monitoring site.
Table 4: Summary of daily PM10 and PM2.5 concentrations tables presented in this document
Test Claimant ID |
Day |
Table number |
24 |
10th June 2011 |
2 |
12th June 2011 |
3 |
|
30 |
10th June 2011 |
4 |
11th June 2011 |
5 |
|
27th June 2011 |
6 |
|
33 |
11th June 2011 |
7 |
15th June 2011 |
8 |
|
20th June 2011 |
9 |
|
37 |
10th June 2011 |
10 |
12th June 2011 |
11 |
|
17th June 2011 |
12 |
|
39 |
10th June 2011 |
13 |
12th June 2011 |
14 |
|
17th June 2011 |
15 |
Table 5: Modelled hourly PM10 and PM2.5 concentrations for Test Claimant 24, 10th June 2011
10/06/2011 |
Test Claimant 24 |
|||
Hour (hour ending BST) |
Modelled concentrations including background (µg/m³) |
Briery Hey background (µg/m³) |
||
PM10 |
PM2.5 |
PM10 |
PM2.5 |
|
1 |
18.3 |
6.9 |
16.0 |
5.0 |
2 |
16.0 |
10.0 |
16.0 |
10.0 |
3 |
18.0 |
1.0 |
18.0 |
1.0 |
4 |
32.6 |
20.8 |
17.0 |
8.0 |
5 |
20.0 |
5.0 |
20.0 |
5.0 |
6 |
31.5 |
9.4 |
31.0 |
9.0 |
7 |
22.0 |
8.0 |
22.0 |
8.0 |
8 |
30.0 |
6.0 |
30.0 |
6.0 |
9 |
26.0 |
1.0 |
26.0 |
1.0 |
10 |
28.0 |
11.0 |
28.0 |
11.0 |
11 |
13.6 |
7.1 |
11.0 |
5.0 |
12 |
12.0 |
8.0 |
12.0 |
8.0 |
13 |
15.0 |
6.8 |
15.0 |
6.8 |
14 |
6.0 |
2.7 |
6.0 |
2.7 |
15 |
17.0 |
7.7 |
17.0 |
7.7 |
16 |
19.0 |
8.6 |
19.0 |
8.6 |
17 |
20.0 |
9.0 |
20.0 |
9.0 |
18 |
19.0 |
8.6 |
19.0 |
8.6 |
19 |
3.0 |
1.4 |
3.0 |
1.4 |
20 |
7.0 |
3.2 |
7.0 |
3.2 |
21 |
13.0 |
5.9 |
13.0 |
5.9 |
22 |
9.0 |
4.1 |
9.0 |
4.1 |
23 |
5.0 |
2.3 |
5.0 |
2.3 |
24 |
19.0 |
8.6 |
19.0 |
8.6 |
24-hour mean concentration (µg/m³) |
17.5 |
6.8 |
16.6 |
6.1 |
24-hour mean concentration excluding background (µg/m³) |
0.9 |
0.7 |
Table 6: Modelled hourly PM10 and PM2.5 concentrations for Test Claimant 24, 12th June 2011
12/06/2011 |
Test Claimant 24 |
|||
Hour (hour ending BST) |
Modelled concentrations including background (µg/m³) |
Briery Hey background (µg/m³) |
||
PM10 |
PM2.5 |
PM10 |
PM2.5 |
|
1 |
16.0 |
7.2 |
16.0 |
7.2 |
2 |
21.0 |
9.5 |
21.0 |
9.5 |
3 |
20.0 |
9.0 |
20.0 |
9.0 |
4 |
18.0 |
8.1 |
18.0 |
8.1 |
5 |
21.0 |
9.5 |
21.0 |
9.5 |
6 |
20.0 |
9.0 |
20.0 |
9.0 |
7 |
32.9 |
16.9 |
27.0 |
12.2 |
8 |
64.4 |
28.2 |
36.0 |
5.0 |
9 |
42.9 |
17.9 |
32.0 |
9.0 |
10 |
103.6 |
68.4 |
26.0 |
5.0 |
11 |
114.8 |
79.2 |
30.0 |
10.0 |
12 |
101.9 |
71.9 |
15.0 |
1.0 |
13 |
49.2 |
42.2 |
11.0 |
11.0 |
14 |
68.1 |
47.8 |
23.0 |
11.0 |
15 |
32.0 |
20.4 |
18.0 |
9.0 |
16 |
35.3 |
28.4 |
14.0 |
11.0 |
17 |
22.1 |
6.0 |
16.0 |
1.0 |
18 |
75.3 |
46.8 |
18.0 |
0.0 |
19 |
82.7 |
63.1 |
14.0 |
7.0 |
20 |
87.9 |
65.4 |
20.0 |
10.0 |
21 |
95.5 |
71.3 |
18.0 |
8.0 |
22 |
109.2 |
79.9 |
26.0 |
12.0 |
23 |
59.0 |
45.1 |
16.0 |
10.0 |
24 |
10.4 |
7.3 |
10.0 |
7.0 |
24-hour mean concentration (µg/m³) |
54.3 |
35.8 |
20.2 |
8.0 |
24-hour mean concentration excluding background (µg/m³) |
34.1 |
27.8 |
Table 7: Modelled hourly PM10 and PM2.5 concentrations for Test Claimant 30, 10th June 2011
10/06/2011 |
Test Claimant 30 |
|||
Hour (hour ending BST) |
Modelled concentrations including background (µg/m³) |
Briery Hey background (µg/m³) |
||
PM10 |
PM2.5 |
PM10 |
PM2.5 |
|
1 |
16.0 |
5.0 |
16.0 |
5.0 |
2 |
16.0 |
10.0 |
16.0 |
10.0 |
3 |
18.0 |
1.0 |
18.0 |
1.0 |
4 |
17.0 |
8.0 |
17.0 |
8.0 |
5 |
20.0 |
5.0 |
20.0 |
5.0 |
6 |
31.0 |
9.0 |
31.0 |
9.0 |
7 |
22.0 |
8.0 |
22.0 |
8.0 |
8 |
30.0 |
6.0 |
30.0 |
6.0 |
9 |
26.0 |
1.0 |
26.0 |
1.0 |
10 |
28.0 |
11.0 |
28.0 |
11.0 |
11 |
11.0 |
5.0 |
11.0 |
5.0 |
12 |
23.3 |
17.2 |
12.0 |
8.0 |
13 |
33.5 |
21.9 |
15.0 |
6.8 |
14 |
140.1 |
112.2 |
6.0 |
2.7 |
15 |
90.2 |
67.4 |
17.0 |
7.6 |
16 |
19.6 |
9.1 |
19.0 |
8.6 |
17 |
53.4 |
36.3 |
20.0 |
9.0 |
18 |
25.5 |
13.9 |
19.0 |
8.6 |
19 |
14.0 |
10.3 |
3.0 |
1.3 |
20 |
7.1 |
3.3 |
7.0 |
3.2 |
21 |
17.8 |
9.8 |
13.0 |
5.9 |
22 |
9.2 |
4.2 |
9.0 |
4.1 |
23 |
5.2 |
2.4 |
5.0 |
2.3 |
24 |
20.5 |
9.8 |
19.0 |
8.6 |
24-hour mean concentration (µg/m³) |
28.9 |
16.1 |
16.6 |
6.1 |
24-hour mean concentration excluding background (µg/m³) |
12.3 |
10.1 |
Table 8: Modelled hourly PM10 and PM2.5 concentrations for Test Claimant 30, 11th June 2011
11/06/2011 |
Test Claimant 30 |
|||
Hour (hour ending BST) |
Modelled concentrations including background (µg/m³) |
Briery Hey background (µg/m³) |
||
PM10 |
PM2.5 |
PM10 |
PM2.5 |
|
1 |
17.0 |
7.7 |
17.0 |
7.7 |
2 |
8.0 |
3.6 |
8.0 |
3.6 |
3 |
11.0 |
5.0 |
11.0 |
4.9 |
4 |
18.1 |
8.2 |
18.0 |
8.1 |
5 |
18.0 |
8.1 |
18.0 |
8.1 |
6 |
15.0 |
6.8 |
15.0 |
6.7 |
7 |
19.1 |
8.6 |
19.0 |
8.6 |
8 |
26.0 |
12.1 |
25.0 |
11.2 |
9 |
28.1 |
12.7 |
28.0 |
12.6 |
10 |
19.6 |
9.0 |
19.0 |
8.6 |
11 |
15.0 |
7.8 |
12.0 |
5.4 |
12 |
20.1 |
9.1 |
20.0 |
9.0 |
13 |
20.6 |
9.5 |
20.0 |
9.0 |
14 |
22.1 |
12.2 |
16.0 |
7.2 |
15 |
12.6 |
5.9 |
12.0 |
5.4 |
16 |
26.8 |
15.6 |
17.0 |
7.6 |
17 |
16.3 |
8.1 |
14.0 |
6.3 |
18 |
12.2 |
5.5 |
12.0 |
5.4 |
19 |
28.5 |
19.6 |
10.0 |
4.5 |
20 |
17.2 |
8.5 |
15.0 |
6.8 |
21 |
15.5 |
8.3 |
12.0 |
5.4 |
22 |
16.1 |
9.1 |
11.0 |
5.0 |
23 |
11.0 |
5.0 |
11.0 |
5.0 |
24 |
12.0 |
5.4 |
12.0 |
5.4 |
24-hour mean concentration (µg/m³) |
17.7 |
8.8 |
15.5 |
7.0 |
24-hour mean concentration excluding background (µg/m³) |
2.2 |
1.8 |
Table 9: Modelled hourly PM10 and PM2.5 concentrations for Test Claimant 30, 27th June 2011
27/06/2011 |
Test Claimant 30 |
|||
Hour (hour ending BST) |
Modelled concentrations including background (µg/m³) |
Briery Hey background (µg/m³) |
||
PM10 |
PM2.5 |
PM10 |
PM2.5 |
|
1 |
37.1 |
32.1 |
37.0 |
32.0 |
2 |
26.0 |
18.0 |
26.0 |
18.0 |
3 |
36.0 |
28.0 |
36.0 |
28.0 |
4 |
29.0 |
21.0 |
29.0 |
21.0 |
5 |
29.0 |
18.0 |
29.0 |
18.0 |
6 |
37.3 |
21.3 |
37.0 |
21.0 |
7 |
43.2 |
35.1 |
32.0 |
26.0 |
8 |
35.0 |
14.0 |
35.0 |
14.0 |
9 |
33.0 |
10.0 |
33.0 |
10.0 |
10 |
35.0 |
7.0 |
35.0 |
7.0 |
11 |
31.0 |
14.0 |
31.0 |
14.0 |
12 |
45.0 |
32.0 |
45.0 |
32.0 |
13 |
41.1 |
37.1 |
41.0 |
37.0 |
14 |
37.0 |
14.0 |
37.0 |
14.0 |
15 |
29.1 |
5.0 |
29.0 |
5.0 |
16 |
27.3 |
15.2 |
27.0 |
15.0 |
17 |
21.5 |
7.4 |
21.0 |
7.0 |
18 |
19.3 |
15.2 |
19.0 |
15.0 |
19 |
22.3 |
7.3 |
22.0 |
7.0 |
20 |
17.0 |
18.0 |
17.0 |
18.0 |
21 |
23.5 |
5.4 |
23.0 |
5.0 |
22 |
17.0 |
9.0 |
17.0 |
9.0 |
23 |
25.0 |
15.0 |
25.0 |
15.0 |
24 |
21.1 |
4.1 |
21.0 |
4.0 |
24-hour mean concentration (µg/m³) |
29.9 |
16.8 |
29.3 |
16.3 |
24-hour mean concentration excluding background (µg/m³) |
0.6 |
0.5 |
Table 10: Modelled hourly PM10 and PM2.5 concentrations for Test Claimant 33, 11th June 2011
11/06/2011 |
Test Claimant 33 |
|||
Hour (hour ending BST) |
Modelled concentrations including background (µg/m³) |
Briery Hey background (µg/m³) |
||
PM10 |
PM2.5 |
PM10 |
PM2.5 |
|
1 |
17.0 |
7.7 |
17.0 |
7.7 |
2 |
8.0 |
3.6 |
8.0 |
3.6 |
3 |
11.0 |
5.0 |
11.0 |
4.9 |
4 |
18.0 |
8.1 |
18.0 |
8.1 |
5 |
31.2 |
18.9 |
18.0 |
8.1 |
6 |
15.0 |
6.8 |
15.0 |
6.7 |
7 |
19.1 |
8.6 |
19.0 |
8.6 |
8 |
25.1 |
11.3 |
25.0 |
11.2 |
9 |
29.8 |
14.1 |
28.0 |
12.6 |
10 |
19.8 |
9.2 |
19.0 |
8.6 |
11 |
12.4 |
5.8 |
12.0 |
5.4 |
12 |
36.5 |
22.5 |
20.0 |
9.0 |
13 |
24.7 |
12.8 |
20.0 |
9.0 |
14 |
16.1 |
7.3 |
16.0 |
7.2 |
15 |
13.0 |
6.2 |
12.0 |
5.4 |
16 |
17.0 |
7.7 |
17.0 |
7.7 |
17 |
14.4 |
6.6 |
14.0 |
6.3 |
18 |
14.6 |
7.6 |
12.0 |
5.4 |
19 |
10.0 |
4.5 |
10.0 |
4.5 |
20 |
15.0 |
6.8 |
15.0 |
6.8 |
21 |
12.0 |
5.4 |
12.0 |
5.4 |
22 |
11.0 |
5.0 |
11.0 |
4.9 |
23 |
11.0 |
5.0 |
11.0 |
4.9 |
24 |
12.0 |
5.4 |
12.0 |
5.4 |
24-hour mean concentration (µg/m³) |
17.2 |
8.4 |
15.5 |
7.0 |
24-hour mean concentration excluding background (µg/m³) |
1.7 |
1.4 |
Table 11: Modelled hourly PM10 and PM2.5 concentrations for Test Claimant 33, 15th June 2011
15/06/2011 |
Test Claimant 33 |
|||
Hour (hour ending BST) |
Modelled concentrations including background (µg/m³) |
Briery Hey background (µg/m³) |
||
PM10 |
PM2.5 |
PM10 |
PM2.5 |
|
1 |
19.0 |
9.0 |
19.0 |
9.0 |
2 |
19.0 |
13.0 |
19.0 |
13.0 |
3 |
40.0 |
28.0 |
40.0 |
28.0 |
4 |
33.0 |
17.0 |
33.0 |
17.0 |
5 |
21.0 |
14.0 |
21.0 |
14.0 |
6 |
22.0 |
12.0 |
22.0 |
12.0 |
7 |
26.0 |
18.0 |
26.0 |
18.0 |
8 |
22.0 |
10.0 |
22.0 |
10.0 |
9 |
19.0 |
13.0 |
19.0 |
13.0 |
10 |
17.0 |
8.0 |
17.0 |
8.0 |
11 |
22.0 |
9.0 |
22.0 |
9.0 |
12 |
17.0 |
15.0 |
17.0 |
15.0 |
13 |
8.3 |
5.9 |
6.0 |
4.0 |
14 |
7.0 |
3.0 |
7.0 |
3.0 |
15 |
9.0 |
7.0 |
9.0 |
7.0 |
16 |
25.1 |
13.1 |
20.0 |
9.0 |
17 |
12.7 |
7.6 |
12.0 |
7.0 |
18 |
12.9 |
8.7 |
12.0 |
8.0 |
19 |
18.5 |
7.0 |
16.0 |
5.0 |
20 |
10.0 |
4.0 |
10.0 |
4.0 |
21 |
19.2 |
9.7 |
11.0 |
3.0 |
22 |
26.8 |
9.0 |
17.0 |
1.0 |
23 |
23.8 |
8.9 |
19.0 |
5.0 |
24 |
30.2 |
12.1 |
24.0 |
7.0 |
24-hour mean concentration (µg/m³) |
20.0 |
10.9 |
18.3 |
9.5 |
24-hour mean concentration excluding background (µg/m³) |
1.7 |
1.4 |
Table 12: Modelled hourly PM10 and PM2.5 concentrations for Test Claimant 33, 20th June 2011
20/06/2011 |
Test Claimant 33 |
|||
Hour (hour ending BST) |
Modelled concentrations including background (µg/m³) |
Briery Hey background (µg/m³) |
||
PM10 |
PM2.5 |
PM10 |
PM2.5 |
|
1 |
43.7 |
30.2 |
19.0 |
10.0 |
2 |
44.0 |
28.6 |
20.0 |
9.0 |
3 |
22.0 |
18.0 |
22.0 |
18.0 |
4 |
21.8 |
9.1 |
18.0 |
6.0 |
5 |
17.7 |
9.6 |
17.0 |
9.0 |
6 |
21.3 |
8.3 |
21.0 |
8.0 |
7 |
21.0 |
15.0 |
21.0 |
15.0 |
8 |
41.0 |
2.0 |
41.0 |
2.0 |
9 |
32.0 |
5.0 |
32.0 |
5.0 |
10 |
18.6 |
7.5 |
18.0 |
7.0 |
11 |
26.1 |
5.1 |
26.0 |
5.0 |
12 |
21.7 |
6.6 |
21.0 |
6.0 |
13 |
16.4 |
9.3 |
16.0 |
9.0 |
14 |
21.8 |
10.7 |
21.0 |
10.0 |
15 |
21.4 |
25.2 |
20.0 |
24.0 |
16 |
19.2 |
16.0 |
18.0 |
15.0 |
17 |
12.0 |
5.0 |
12.0 |
5.0 |
18 |
15.0 |
13.0 |
15.0 |
13.0 |
19 |
17.0 |
16.0 |
17.0 |
16.0 |
20 |
21.0 |
10.0 |
21.0 |
10.0 |
21 |
19.0 |
19.0 |
19.0 |
19.0 |
22 |
31.0 |
15.0 |
31.0 |
15.0 |
23 |
25.0 |
17.0 |
25.0 |
17.0 |
24 |
32.0 |
22.0 |
32.0 |
22.0 |
24-hour mean concentration (µg/m³) |
24.2 |
13.5 |
21.8 |
11.5 |
24-hour mean concentration excluding background (µg/m³) |
2.4 |
2.0 |
Table 13: Modelled hourly PM10 and PM2.5 concentrations for Test Claimant 37, 10th June 2011
10/06/2011 |
Test Claimant 37 |
|||
Hour (hour ending BST) |
Modelled concentrations including background (µg/m³) |
Briery Hey background (µg/m³) |
||
PM10 |
PM2.5 |
PM10 |
PM2.5 |
|
1 |
17.9 |
6.6 |
16.0 |
5.0 |
2 |
16.0 |
10.0 |
16.0 |
10.0 |
3 |
18.0 |
1.0 |
18.0 |
1.0 |
4 |
43.3 |
29.5 |
17.0 |
8.0 |
5 |
20.0 |
5.0 |
20.0 |
5.0 |
6 |
31.3 |
9.3 |
31.0 |
9.0 |
7 |
22.0 |
8.0 |
22.0 |
8.0 |
8 |
30.0 |
6.0 |
30.0 |
6.0 |
9 |
26.0 |
1.0 |
26.0 |
1.0 |
10 |
28.0 |
11.0 |
28.0 |
11.0 |
11 |
13.2 |
6.8 |
11.0 |
5.0 |
12 |
12.0 |
8.0 |
12.0 |
8.0 |
13 |
15.0 |
6.8 |
15.0 |
6.8 |
14 |
6.0 |
2.7 |
6.0 |
2.7 |
15 |
17.0 |
7.7 |
17.0 |
7.7 |
16 |
19.0 |
8.6 |
19.0 |
8.6 |
17 |
20.0 |
9.0 |
20.0 |
9.0 |
18 |
19.0 |
8.6 |
19.0 |
8.6 |
19 |
3.0 |
1.4 |
3.0 |
1.4 |
20 |
7.0 |
3.2 |
7.0 |
3.2 |
21 |
13.0 |
5.9 |
13.0 |
5.9 |
22 |
9.0 |
4.1 |
9.0 |
4.1 |
23 |
5.0 |
2.3 |
5.0 |
2.3 |
24 |
19.0 |
8.6 |
19.0 |
8.6 |
24-hour mean concentration (µg/m³) |
17.9 |
7.1 |
16.6 |
6.1 |
24-hour mean concentration excluding background (µg/m³) |
1.3 |
1.0 |
Table 14: Modelled hourly PM10 and PM2.5 concentrations for Test Claimant 37, 12th June 2011
12/06/2011 |
Test Claimant 37 |
|||
Hour (hour ending BST) |
Modelled concentrations including background (µg/m³) |
Briery Hey background (µg/m³) |
||
PM10 |
PM2.5 |
PM10 |
PM2.5 |
|
1 |
16.0 |
7.2 |
16.0 |
7.2 |
2 |
21.0 |
9.5 |
21.0 |
9.5 |
3 |
20.0 |
9.0 |
20.0 |
9.0 |
4 |
18.0 |
8.1 |
18.0 |
8.1 |
5 |
21.0 |
9.5 |
21.0 |
9.5 |
6 |
20.0 |
9.0 |
20.0 |
9.0 |
7 |
41.6 |
24.1 |
27.0 |
12.2 |
8 |
87.3 |
46.9 |
36.0 |
5.0 |
9 |
54.7 |
27.5 |
32.0 |
9.0 |
10 |
128.3 |
88.5 |
26.0 |
5.0 |
11 |
135.8 |
96.4 |
30.0 |
10.0 |
12 |
119.9 |
86.6 |
15.0 |
1.0 |
13 |
72.2 |
60.9 |
11.0 |
11.0 |
14 |
89.5 |
65.3 |
23.0 |
11.0 |
15 |
44.4 |
30.5 |
18.0 |
9.0 |
16 |
51.8 |
41.8 |
14.0 |
11.0 |
17 |
29.9 |
12.3 |
16.0 |
1.0 |
18 |
94.8 |
62.7 |
18.0 |
0.0 |
19 |
94.9 |
73.0 |
14.0 |
7.0 |
20 |
104.7 |
79.1 |
20.0 |
10.0 |
21 |
111.6 |
84.4 |
18.0 |
8.0 |
22 |
122.3 |
90.6 |
26.0 |
12.0 |
23 |
64.8 |
49.8 |
16.0 |
10.0 |
24 |
10.2 |
7.2 |
10.0 |
7.0 |
24-hour mean concentration (µg/m³) |
65.6 |
45.0 |
20.3 |
8.0 |
24-hour mean concentration excluding background (µg/m³) |
45.4 |
37.0 |
Table 15: Modelled hourly PM10 and PM2.5 concentrations for Test Claimant 37, 17th June 2011
17/06/2011 |
Test Claimant 37 |
|||
Hour (hour ending BST) |
Modelled concentrations including background (µg/m³) |
Briery Hey background (µg/m³) |
||
PM10 |
PM2.5 |
PM10 |
PM2.5 |
|
1 |
26.0 |
10.0 |
26.0 |
10.0 |
2 |
22.0 |
18.0 |
22.0 |
18.0 |
3 |
20.0 |
10.0 |
20.0 |
10.0 |
4 |
24.0 |
7.0 |
24.0 |
7.0 |
5 |
24.0 |
12.0 |
24.0 |
12.0 |
6 |
27.0 |
12.0 |
27.0 |
12.0 |
7 |
31.0 |
11.3 |
27.0 |
8.0 |
8 |
23.5 |
7.2 |
22.0 |
6.0 |
9 |
31.2 |
17.9 |
24.0 |
12.0 |
10 |
41.1 |
17.9 |
40.0 |
17.0 |
11 |
32.7 |
13.2 |
30.0 |
11.0 |
12 |
85.6 |
11.3 |
84.0 |
10.0 |
13 |
44.0 |
12.8 |
43.0 |
12.0 |
14 |
81.7 |
15.2 |
79.0 |
13.0 |
15 |
64.7 |
6.4 |
63.0 |
5.0 |
16 |
100.9 |
13.7 |
100.0 |
13.0 |
17 |
27.5 |
6.0 |
25.0 |
4.0 |
18 |
21.5 |
8.3 |
20.0 |
7.0 |
19 |
17.8 |
2.6 |
17.0 |
2.0 |
20 |
18.3 |
12.7 |
15.0 |
10.0 |
21 |
28.0 |
13.1 |
18.0 |
5.0 |
22 |
27.3 |
13.6 |
18.0 |
6.0 |
23 |
31.6 |
21.8 |
22.0 |
14.0 |
24 |
31.6 |
32.8 |
22.0 |
25.0 |
24-hour mean concentration (µg/m³) |
36.8 |
12.8 |
33.8 |
10.4 |
24-hour mean concentration excluding background (µg/m³) |
3.0 |
2.4 |
Table 16: Modelled hourly PM10 and PM2.5 concentrations for Test Claimant 39, 10th June 2011
10/06/2011 |
Test Claimant 39 |
|||
Hour (hour ending BST) |
Modelled concentrations including background (µg/m³) |
Briery Hey background (µg/m³) |
||
PM10 |
PM2.5 |
PM10 |
PM2.5 |
|
1 |
16.0 |
5.0 |
16.0 |
5.0 |
2 |
16.0 |
10.0 |
16.0 |
10.0 |
3 |
18.0 |
1.0 |
18.0 |
1.0 |
4 |
17.0 |
8.0 |
17.0 |
8.0 |
5 |
20.0 |
5.0 |
20.0 |
5.0 |
6 |
35.5 |
12.7 |
31.0 |
9.0 |
7 |
22.0 |
8.0 |
22.0 |
8.0 |
8 |
30.1 |
6.1 |
30.0 |
6.0 |
9 |
26.4 |
1.3 |
26.0 |
1.0 |
10 |
28.0 |
11.0 |
28.0 |
11.0 |
11 |
19.0 |
11.5 |
11.0 |
5.0 |
12 |
12.0 |
8.0 |
12.0 |
8.0 |
13 |
15.0 |
6.8 |
15.0 |
6.8 |
14 |
6.0 |
2.7 |
6.0 |
2.7 |
15 |
17.0 |
7.7 |
17.0 |
7.7 |
16 |
19.0 |
8.6 |
19.0 |
8.6 |
17 |
20.0 |
9.0 |
20.0 |
9.0 |
18 |
19.0 |
8.6 |
19.0 |
8.6 |
19 |
3.0 |
1.4 |
3.0 |
1.4 |
20 |
7.0 |
3.2 |
7.0 |
3.2 |
21 |
13.0 |
5.9 |
13.0 |
5.9 |
22 |
9.0 |
4.1 |
9.0 |
4.1 |
23 |
5.0 |
2.3 |
5.0 |
2.3 |
24 |
19.0 |
8.6 |
19.0 |
8.6 |
24-hour mean concentration (µg/m³) |
17.2 |
6.5 |
16.6 |
6.1 |
24-hour mean concentration excluding background (µg/m³) |
0.5 |
0.4 |
Table 17: Modelled hourly PM10 and PM2.5 concentrations for Test Claimant 39, 12th June 2011
12/06/2011 |
Test Claimant 39 |
|||
Hour (hour ending BST) |
Modelled concentrations including background (µg/m³) |
Briery Hey background (µg/m³) |
||
PM10 |
PM2.5 |
PM10 |
PM2.5 |
|
1 |
16.0 |
7.2 |
16.0 |
7.2 |
2 |
21.0 |
9.5 |
21.0 |
9.5 |
3 |
20.0 |
9.0 |
20.0 |
9.0 |
4 |
18.0 |
8.1 |
18.0 |
8.1 |
5 |
21.0 |
9.5 |
21.0 |
9.5 |
6 |
21.2 |
10.0 |
20.0 |
9.0 |
7 |
27.0 |
12.2 |
27.0 |
12.1 |
8 |
36.0 |
5.0 |
36.0 |
5.0 |
9 |
32.0 |
9.0 |
32.0 |
9.0 |
10 |
27.0 |
5.8 |
26.0 |
5.0 |
11 |
31.8 |
11.5 |
30.0 |
10.0 |
12 |
19.5 |
4.7 |
15.0 |
1.0 |
13 |
11.1 |
11.1 |
11.0 |
11.0 |
14 |
23.3 |
11.2 |
23.0 |
11.0 |
15 |
18.0 |
9.0 |
18.0 |
9.0 |
16 |
14.0 |
11.0 |
14.0 |
11.0 |
17 |
16.0 |
1.0 |
16.0 |
1.0 |
18 |
18.7 |
0.5 |
18.0 |
0.0 |
19 |
20.9 |
12.6 |
14.0 |
7.0 |
20 |
21.2 |
11.0 |
20.0 |
10.0 |
21 |
20.1 |
9.7 |
18.0 |
8.0 |
22 |
29.7 |
15.0 |
26.0 |
12.0 |
23 |
32.3 |
23.3 |
16.0 |
10.0 |
24 |
24.5 |
18.9 |
10.0 |
7.0 |
24-hour mean concentration (µg/m³) |
22.5 |
9.8 |
20.2 |
8.0 |
24-hour mean concentration excluding background (µg/m³) |
2.3 |
1.9 |
Table 18: Modelled hourly PM10 and PM2.5 concentrations for Test Claimant 39, 17th June 2011
17/06/2011 |
Test Claimant 39 |
|||
Hour (hour ending BST) |
Modelled concentrations including background (µg/m³) |
Briery Hey background (µg/m³) |
||
PM10 |
PM2.5 |
PM10 |
PM2.5 |
|
1 |
26.0 |
10.0 |
26.0 |
10.0 |
2 |
22.0 |
18.0 |
22.0 |
18.0 |
3 |
25.0 |
14.1 |
20.0 |
10.0 |
4 |
24.1 |
7.1 |
24.0 |
7.0 |
5 |
24.0 |
12.0 |
24.0 |
12.0 |
6 |
27.3 |
12.3 |
27.0 |
12.0 |
7 |
28.8 |
9.5 |
27.0 |
8.0 |
8 |
23.6 |
7.3 |
22.0 |
6.0 |
9 |
24.2 |
12.2 |
24.0 |
12.0 |
10 |
41.1 |
17.9 |
40.0 |
17.0 |
11 |
31.0 |
11.8 |
30.0 |
11.0 |
12 |
85.0 |
10.9 |
84.0 |
10.0 |
13 |
44.0 |
12.8 |
43.0 |
12.0 |
14 |
80.0 |
13.8 |
79.0 |
13.0 |
15 |
64.0 |
5.8 |
63.0 |
5.0 |
16 |
101.0 |
13.8 |
100.0 |
13.0 |
17 |
26.0 |
4.8 |
25.0 |
4.0 |
18 |
21.3 |
8.1 |
20.0 |
7.0 |
19 |
18.5 |
3.2 |
17.0 |
2.0 |
20 |
16.5 |
11.2 |
15.0 |
10.0 |
21 |
18.2 |
5.2 |
18.0 |
5.0 |
22 |
18.6 |
6.5 |
18.0 |
6.0 |
23 |
22.1 |
14.1 |
22.0 |
14.0 |
24 |
22.2 |
25.2 |
22.0 |
25.0 |
24-hour mean concentration (µg/m³) |
34.8 |
11.2 |
33.8 |
10.4 |
24-hour mean concentration excluding background (µg/m³) |
0.9 |
0.8 |
Sonae GLO: Further Modelling
4. Histograms of modelled hourly concentrations for the 20 Test Claimants
i) Unit discharge concentrations with equivalent thresholds for acrolein and total aldehydes
This document presents time series of hourly average concentrations for a ‘unit discharge’ at the locations of the 20 Test Claimants.
The ‘unit discharge’ rate of 1 g/s is used for peak heat release rate of 358 MW, equivalent to an emission factor of 2.793 mg/s/MW. Since the emission factors for acrolein and total aldehydes are assumed to be constant throughout the lifetime of the fire, thresholds equivalent to the exceedence thresholds for these pollutants can be displayed on the unit discharge time series.
The equivalent thresholds are derived using the following formula:
unit discharge emission factor (2.793 mg/s/MW) |
x pollutant exceedence threshold (µg/m³) |
pollutant emission factor (mg/s/MW) |
The table below shows the equivalent thresholds for acrolein and total aldehydes based on emission factors of 114 mg/s/MW and 600 mg/s/MW, respectively. These equivalent threshold values are also shown in the following 23 time series histograms for the locations of the 20 Test Claimants.
Pollutant |
Emission Factor (mg/s/MW) |
Pollutant exceedence threshold (µg/m³) |
Equivalent threshold for unit discharge modelling (µg/m³) |
Acrolein |
114 |
0.38 (odour threshold) |
0.0093 |
146 (health threshold) |
3.577 |
||
Total aldehydes |
600 |
500 |
2.328 |
Sonae GLO: Further Modelling
4a. Histograms of modelled hourly concentrations for the 20 Test Claimants
ii) Unit discharge concentrations showing only the equivalent threshold for the acrolein odour threshold
This document presents time series of hourly average concentrations for a ‘unit discharge’ at the locations of the 20 Test Claimants.
Since the maximum modelled hourly unit discharge concentration across the Test Claimant locations is 0.29 µg/m³, the 23 histograms shown in Document 4 are presented again in this document with a larger scale on the ‘y’ axis (maximum concentration is set to 0.3 µg/m³). Consequently only the equivalent threshold for the acrolein odour threshold of 0.38 µg/m³ (equivalent to a unit discharge concentration of 0.0093 µg/m³) can be shown on these histograms.
Sonae GLO: Further Modelling
5. Histograms of modelled hourly concentrations for the 20 Test Claimants
iii) Modelled PM2.5 concentrations compared against the COMEAP High trigger value of 74 µg/m³
The 23 time series histograms in this document show modelled hourly average concentrations of PM2.5 at the locations of the 20 Test Claimants. Modelled concentrations include the modelled contribution from the fire and background concentrations using measurements from the Briery Hey monitoring site.
The PM2.5 measurements from Briery Hey contain a 43-hour period between the 10th June 2011 and 12th June 2011 where no PM2.5 data are recorded. For this period, PM2.5 concentrations have been estimated from PM10 concentrations assuming a PM2.5/PM10 ratio of 0.45. This ratio is based on the ratio of mean PM2.5 and PM10 concentrations over the period of the fire where both PM10 and PM2.5 concentrations are recorded at Briery Hey.
This methodology for estimating PM2.5 concentrations for the period of missing data was agreed between CERC and Envirobods
Sonae GLO: Further Modelling
Modelled PM10 concentrations compared against the COMEAP High trigger value of 107 µg/m³
The 23 time series histograms in this document show modelled hourly average concentrations of PM10 at the locations of the 20 Test Claimants. Modelled concentrations include the modelled contribution from the fire and background concentrations using measurements from the Briery Hey monitoring site.
[1] A contour map is produced interpolating changes in values in between the model output points. This calculation cannot be performed by the contouring software if all the output points are equal.