APPEAL COURT, HIGH COURT OF JUSTICIARY
Lord Nimmo Smith Lord Clarke Lord Hardie	[2009] HCJAC 69 Appeal No: NO. OPINION OF THE COURT delivered by LORD NIMMO SMITH in NOTE OF APPEAL AGAINST CONVICTION by CRAIG McCREIGHT Appellant; against HER MAJESTY'S ADVOCATE Respondent: _______

Act: Keegan, Solicitor Advocate; Adams Whyte

Alt: Stewart, A.D., Crown Agent

1 April 2009

Introduction

[1] On 18 April 2002, at a sitting of the High Court in Edinburgh, the appellant was convicted after trial of a charge in the following terms:

"[O]n 7 or 8 February 1999 at 5 Fairnsfell, Broxburn, West Lothian, you did assault Yvonne Bessant also known as Davidson, residing there, and did place chloroform at her mouth and nose and cause her to inhale same, render her unconscious, fail to obtain medical assistance for her and place her in the garden at 9 Fairnsfell aforesaid and did murder her and you did previously evince malice and ill-will towards her."

The appellant has now appealed against this conviction. Various grounds of appeal are before this Court. At our invitation, the parties led evidence and addressed us on those grounds which relate to fresh evidence.

The death of the deceased

The background

[2] The deceased Yvonne Bessant was usually known as Davidson, that being the surname of a man with whom she previously had a relationship and by whom she had two children aged 8 and 6 at the time of her death. In 1996 the appellant met the deceased and moved in to live with her at her house at 5 Fairnsfell, Broxburn, about a month after they met. A child was born to them on 13 June 1997. The appellant was generally employed as a fencer but was out of work in February 1999. At that time the deceased had been the tenant of a public house in Broxburn for about two years.

[3] The appellant fathered a child by another woman. The child was born on 11 June 1998. The mother declared to the relevant agencies that the appellant was the father of the child. There then ensued correspondence between the Child Support Agency and the appellant, in the course of which he denied that he was the father of the child. On about 29 January 1999 the mother of the child wrote an unpleasant letter to the deceased setting out the relationship which she had had with the appellant. These events led to difficulties between the appellant and the deceased.

The finding of the deceased's body

[4] The house at 5 Fairnsfell in which the appellant, the deceased and the three children lived was situated in a terrace of four houses. At about 8.00am on Monday 8 February 1999 the occupant of 9 Fairnsfell, the house at the end of the terrace, went out of his house and discovered the clothed body of the deceased lying mainly on garden ground at the side of the house with her right leg extending on to the path. He alerted his neighbour at 7 Fairnsfell. She immediately went to the scene. She recognised the deceased. She formed the impression that the body had been placed there. She telephoned the emergency services. She and her husband then went to tell the appellant what had happened. When he opened the door and was told, he just said, "Oh". Later, after the police had arrived, she noticed a bruise on his left eye.

Pathological and scientific investigations before and during the trial

The locus report

[5] Police officers attended at the locus and, among other things, took photographs of the body of the deceased where it lay. Dr Paul Fineron, a consultant forensic pathologist and senior lecturer at the Forensic Medicine Unit at the University of Edinburgh attended the scene at 11.20am. He prepared a locus report, which included the following passage:

"Rigor mortis is only just beginning to form in the muscles of the fingers. Rigor mortis is not present in the jaws. Hypostasis is present on the back of the body but blanches easily on digital pressure. There is slight warmth on the under surface of the body adjacent to the ground. Professional limited examination reveals no obvious injury. A small amount of tomato stained vomitus is present around the nostrils and the right side of the mouth.

The body is clothed in a long sleeved black denim jacket with four buttons at the front, the lower three of which are buttoned up. Under this is a long sleeved blue cotton top. On the lower part of the body is a pair of black denim jeans, these are fully buttoned up though the zip is located three-quarters of the way up. There is obvious soil scuffing of the clothes.

The temperature adjacent to the body at ground level is 0˚C."

On more detailed examination at the mortuary at St John's Hospital, Livingston at about 1.15pm Dr Fineron noted that the cuff buttons of the jacket were undone, the deceased was wearing a pair of ankle length leather boots, a pair of ankle length white sports socks and underpants. She was not wearing a bra.

The post mortem examination

[6] On the instructions of the Procurator Fiscal at Linlithgow, Dr Fineron then carried out a full post mortem examination and dissection on the body of the deceased, commencing at 1.35pm on 8 February 1999. He prepared a report on the same day. It had not been thought necessary that the examination be carried out by two pathologists. In the course of his external examination he noted that dried vomit was present around both nostrils and on the lower right side of the cheek. There were trivial external injuries, consisting of six bruises on the different parts of the body, and a very faint orange-based abrasion on the point of the chin. Reflection of the scalp revealed a small area of subgaleal bruising in the frontal region in the midline. Otherwise there were no internal injuries. Examination of the stomach led to the following observation:

"[T]he lesser curve shows evidence of acute haemorrhagic gastritis. There are, however, no ulcers or erosions."

The stomach contents were described as "50ml of partially digested food, apparently pizza. No intact tablets or capsules identified." Dr Fineron found no evidence of natural disease to account for the death. In his commentary, he stated:

"Autopsy examination has revealed no evidence of natural disease which can account for death.

Autopsy examination has revealed trivial external injuries and a slight degree of bruising underneath the scalp. There are no internal injuries.

Given the situation in which the deceased was found, namely outdoors following a very cold night with temperatures reported down to -4˚C, it is highly possible that hypothermia has played at least some role in death. There are, however, no specific autopsy signs of hypothermia and hence it is impossible to prove its role in death."

Venous blood, vitreous humour, stomach contents, the liver (weighing 1,590 g) and bile were retained for toxicological analysis. Dr Fineron's opinion at that time as to the cause of the deceased's death was: "1(a) Undetermined (pending toxicology)".

The samples

[7] This is a convenient point at which to set out the conditions in which the samples mentioned above were stored after receipt in the laboratory, and the analyses to which they were subjected:

(1) Blood sample label 1, of venous blood, was stored at 2˚C to 8˚C from 8 to 18 February 1999, and thereafter frozen at -20˚C (or -15˚C). The container was a glass vial. This sample was only used for alcohol analysis.

(2) Blood sample label 3, of venous blood, was stored at 2˚C to 8˚C from 8 to 18 February 1999, and thereafter frozen at -20˚C (or -15˚C). The container was a 25ml Steralin screw capped tube. This sample was used for all analytical investigations other than those for alcohol and chloroform.

(3) Blood sample label 4, of venous blood, was stored at 2˚C to 8˚C from 8 to 18 February 1999 and thereafter frozen at -20˚C (or -15˚C). The container was a 25ml Steralin screw capped tube. This sample was only used for chloroform determination.

(4) Bile sample, which was not used at all for analysis and about which no further information was available from the documents.

(5) Vitreous humour sample for alcohol determination.

(6) The stomach contents, as already noted, consisted of 50ml of partially digested food, apparently pizza. They were stored in a polypropylene tube and frozen until analysis for chloroform.

(7) The liver was placed in a plastic container, which Dr Fineron described as a "yogurt pot", and was kept frozen at -15˚C or -20˚C from receipt. It was sent to the Scottish Agricultural Science Agency for a pesticide determination on 7 December 2000. On receipt there the container was recorded as "leaking", suggesting a thawing of the contents. It was presumably unfrozen to allow samples to be taken for analysis for pesticides, which yielded a negative result. It remained there, presumably re-frozen, until March 2002, when it was returned to the laboratory for analysis for chloroform.

[8] By report dated 18 February 1999 Dr Alan Langford and Dr Howard Okely of the Lothian and Borders Police Forensic Science Laboratory reported that analysis of blood sample label 1 and the vitreous humour sample for alcohol yielded a negative result. Analysis of blood sample label 3 revealed the presence of amphetamine within the blood at a level of 0.05 milligrams per litre ("mg/l"). The blood also yielded a positive preliminary test for cannabinoids, and a negative result for other basic drugs. In a supplementary report dated 11 March 1999 Dr Fineron stated that histological examination of the brain and tissues did not yield any further significant information. The report included the statement that sections from the right ventricle of the heart showed "fairly numerous scattered hyper-oesinophilic fibres and occasional fibres showing contraction band necrosis". Dr Fineron concluded, after considering all the information available to him, that "it seems highly likely that hypothermia has been the final mode of death". He suggested that the entry in the Register of Deaths should be modified to read: "1(a) Presumed hypothermia, (b) Acute amphetamine intoxication. 2 Chronic drug misuse."

[9] Subsequently, the police received information to the effect that the appellant had killed the deceased by administering chloroform to her. This led to further analysis of blood samples labels 1 and 4 and the vitreous humour sample, and re-examination of previous results, by Dr Okely and his colleague Sylvain Denieul. Blood sample label 1 was re-analysed for chloroform, and by report dated 2 August 2000 they reported that "Chloroform was found in the blood (unquantified)". The technique which had been used for the initial examination of that blood sample and the vitreous humour sample for the presence of alcohol was headspace gas chromatography. Although it was not observed at the time, on subsequent re-examination of the chromatogram a small extra peak was detected, which was consistent with the presence of chloroform in the blood sample. By report dated 11 September 2000 they reported that a re-examination of the data obtained from the initial analysis for alcohol "suggests the presence of chloroform". An analysis of blood sample label 4 was thereafter carried out, and by report dated 18 January 2001 they reported that chloroform was present in the sample at a concentration of 31mg/l.

[10] On receipt of this information, Dr Fineron reconsidered his post-mortem findings. In a further supplementary report dated 7 September 2000 he summarised the toxic effects of chloroform on the human body. He went on to write that if a cloth soaked in chloroform were forcibly applied to a victim's nose and mouth, this might result in a degree of suffocation, reducing the amount of oxygen reaching the tissues and allowing carbon dioxide to build up within the body. Both these effects - hypoxia and carbon dioxide retention - were known to predispose to the development of cardiac arrhythmias. Additionally, if the victim were to struggle or panic, this would cause the release of adrenaline in the body and would further increase the risk of cardiac arrhythmias. The presence of amphetamine would further exacerbate the effects of chloroform and these other factors on the heart. He continued:

"However, it must be stressed that death could have occurred due to chloroform administration, even in the absence of Amphetamine."

Referring to his post mortem findings, he wrote that "the dried red mark on the lower lip on the left side could represent the effects of direct contact of chloroform onto the lip". The superficial bruise on the front of the left shoulder "could have been produced by the application of pressure through clothing during forcible gripping". The bruise on the inner aspect of the right upper arm "could have been produced by forceful digital pressure". He stressed, however, that neither of these injuries was entirely specific. He concluded:

"In summary, in the light of information that has now become available to me, it is my opinion that the cause of death given in my initial supplementary report should be recorded as: 1(a) Chloroform intoxication."

[11] It was only in March 2002 that the liver was analysed for chloroform, having been returned for that purpose from the Scottish Agricultural Science Agency. In a report dated 14 March 2002 Dr Okely and Sylvain Denieul reported "Chloroform was found in the liver (unquantified)". On 28 March 2002 (following a suggestion by the defence expert, Dr Flanagan, and during the course of the trial) samples of liver were tested for the presence of chloroform at a temperature of 35˚C. The tests were carried out by Sylvain Denieul, and were verified by Dr Okely. They reported on 2 April 2002:

"In the first quantitation ... the amount of chloroform found was below the level of our lowest standard in the calibration curve, therefore the quantitation was repeated ... using a calibration curve with a mid-point associated with the level found in quantitation 1. This gave the concentration of chloroform in the liver as 1064mg/kg."

The prosecution of the appellant

[12] The reports referred to above, along with the other evidence set out below, provided the Crown with a sufficient basis for prosecuting the appellant for murder. An indictment was served on him. In due course, a trial took place from 26 March to 18 April 2002.

Summary of the Crown case at the trial

[13] In his speech to the jury the Advocate depute summarised the Crown case against the appellant as follows:

"The Crown say that he went to Yvonne Davidson's room where she was lying in bed, he took a rag which [he] had soaked in chloroform, he put it against her mouth and nose, he rendered her unconscious, he took her downstairs, he dressed her and he placed her body outside number 9 Fairnsfell. She may have been dead before she was placed outside. She may, on the other hand, only have been unconscious and the cold air outside caused her to die."

Evidence of a "special knowledge" confession by the appellant

[14] To prove their case, the Crown founded in the first place on evidence from two friends of the appellant, David Stewart and Gary Espie. Stewart gave evidence that sometime between May and August 1998 the appellant referred to trouble he was having with the deceased over his relationship with the other woman, who was then pregnant with his child. According to Stewart, the appellant said that the deceased was "daeing his head in and he'd have to do away with her". He said more than once that he needed to get rid of her. Some time before Christmas 1998 the appellant showed Stewart a small medicine bottle, took the lid off and invited him to smell it. The appellant said that a friend had obtained it for him, that it was chloroform, and "that would do it and they couldn't trace it". The day after the death of the deceased the appellant came to Stewart's house, and said to him, "What a buzz. I had to kick the cup over because she peed the carpet." Stewart noticed that the appellant had a black left eye.

[15] Gary Espie gave evidence that on 10 February 1999 the appellant and another man came to see him. The appellant said that it was he who had killed the deceased. After she had gone to bed he waited for a time and then went upstairs to the bedroom where she was sleeping. He had a rag and chloroform, which he put onto the rag. He then held the rag over the face of the deceased and took it off when she had stopped moving. He picked her up off the bed and carried her down the stairs. He laid her out on the living room floor. She urinated. He went upstairs and got her clothes, then dressed her. He tipped a glass of orange juice over the floor to cover the urine stain. Then he picked the deceased up, took her out into the back garden, carried her to the end of the building and just placed her down there.

[16] The Crown case was that the evidence of Stewart and Espie, taken together, proved that the appellant had made incriminating statements amounting to a special knowledge confession that he had killed the deceased in the manner set out above. The trial Judge gave appropriate directions to the jury in this regard.

Corroboration of a "special knowledge" or "circumstantial" confession

[17] A so-called "special knowledge" confession requires to be proved by two witnesses: Low v HM Advocate 1993 SCCR 493. These witnesses need not accord on each and every element of the confession: Mitchell v HM Advocate 1996 SCCR 97. The Crown relied on the evidence of Stewart and Espie as proving such a confession by the appellant. If the jury accepted that he had made such a confession to Stewart and Espie, they then had to decide whether the only reasonable explanation for the knowledge of the details of the crime disclosed in the confession was that the appellant was the perpetrator: Wilson v HM Advocate 1987 SCCR 217, per Lord Justice-General Emslie at p. 222. It was therefore necessary for the Crown to lead separate evidence about each of the details relied on as showing special knowledge on the part of the appellant.

The evidence of corroboration relied on by the Crown

[18] For corroboration, the Crown relied on the finding of chloroform in the blood and liver of the deceased, and the finding of urine on the carpet. The Crown also founded on a number of adminicles of circumstantial evidence: (1) the position of the body, which according to one witness "just looked as though someone had placed her down"; (2) marks on the face and body of the deceased, particularly the mark on the lower lip, which on the evidence could have been a chemical burn caused by a rag containing chloroform being placed against her mouth; (3) the state of the appellant's clothing, which could be regarded as consistent with the appellant's having dressed the deceased; (4) the place where the deceased's body was found, which according to one witness was not where she would normally have gone; (5) evidence that lights were on in the deceased's house in the early hours of the night during which she died; (6) evidence about the finding of vomit on the deceased's clothing in a position consistent with her having vomited before the clothing was pulled onto her; and (7) the bruising to the appellant's eye.

[19] It is clear, however, that by far the most important aspect of the Crown's case related to the finding of chloroform in the deceased's blood and liver and the other findings at the autopsy, from which the jury were invited to conclude that it had been proved that the deceased died as the result of the inhalation of chloroform, that is to say, by breathing it in in vapour form. The defence sought to counter this by raising the possibility of ingestion of the chloroform, that is to say, by swallowing it in liquid form. As to this, the Advocate depute said in his speech to the jury:

"There is no evidence that Yvonne Davidson ingested chloroform. ... I suggest to you, ladies and gentlemen, that the whole theory of ingestion of chloroform involves speculating from the word go. Now, we begin to depart from what we know for a fact. I suggest to you that if you use your common sense then you will see how unlikely this scenario is. ... I suggest that we can discount ingestion because it involves speculation. There is no evidence that she ingested it and there's no signs at post mortem. That leaves us with inhalation. ... You have heard evidence that the accused confessed to using a rag soaked in chloroform and you know that the medical and the forensic evidence is consistent with that. Does the fact that the accused said that he used chloroform and the finding of chloroform in the blood not make it difficult to escape the conclusion that he put it there? Don't separate the engine from the carriages. Don't separate the confession from the medical and the scientific evidence. Put the two together and I suggest that you have a very powerful case against Mr McCreight."

[20] The solicitor advocate for the appellant addressed the jury at length on the possibility of ingestion. In the course of his submissions he said:

"But things came to a sudden halt when it appeared from the liver reading that indeed this death occurred not as the drug-infested Mr Stewart would have it or the fugitive Espie would have it by smothering with a chloroform rag, but by another means of ingestion. So that the theory that emanates from Stewart in the beginning and Espie later on, is debunked."

[21] In the course of his charge to the jury, the trial Judge said:

"The defence have raised the question of possible ingestion of chloroform .... Obviously, if you accept that what occurred here was ingestion, in other words the consuming or drinking of chloroform by the deceased, whether it was accidental or otherwise, then you could not convict of the charge. The reason for that is that the Crown case is as set out in the charge, and appears to be based on the evidence principally of Gary Espie - was that the chloroform was placed at her nose and mouth and that the deceased was caused to inhale it; so the Crown case is of inhalation based on the evidence of David Stewart and also on the absence of internal damage to the body of the deceased at post mortem, which the Crown say shows that there was no drinking or swallowing."

It might be added that, as was made clear elsewhere in his charge, the trial Judge may be taken to have directed the jury that if, after considering the evidence bearing on the ingestion hypothesis, they entertained a reasonable doubt whether the Crown had proved its case of inhalation, the jury were also bound to acquit.

Chloroform

[22] To assist in understanding the remainder of this opinion, we propose at this stage to set out what appears to us to be uncontroversial material relating to chloroform, principally derived from evidence led before us.

[23] The definition of chloroform given in the Oxford English Dictionary (2^nd edition) is:

"The common name of a thin colourless liquid (sp. gr. 1.5), having a pleasant ethereal odour, and pungent sweetish taste, the vapour of which when inhaled produces insensibility; hence it is much used as an anaesthetic in surgical and obstetrical operations. Chemically, it is a triatomic haloid ether of the methyl series = trichloromethane, or methenyl trichloride, Cl₃CH."

[24] The eminent toxicologist Professor Dr Fritz Pragst, who gave evidence at the appeal (see paragraphs [51] to [56]), provided the following information. Chloroform was first used as an inhalation narcotic in 1847. Later, it was replaced by ether and other substances because of the relatively high risk of fatal complications. The anaesthetic effect of chloroform is based on its interaction with the membranes of nervous cells of the central nervous system and occurs in four recognised stages, the third of which is divided into four planes. There is a clear difference between drop-wise application for anaesthesia and the application of a cloth pad soaked in chloroform over the mouth and nose. In most cases of homicide, suicide or other intentional abuse resulting in death, the method of application has been inhalation, though there have also been cases of oral intake. The standard textbook, Baselt, Disposition of Toxic Drugs and Chemicals in Man (8^th ed., 2008) ("Baselt") reports on concentrations of chloroform in blood and tissues as well as its toxicity. Post mortem blood concentrations ranged from 10 to 834 mg/l in these cases.

[25] Generally, there are two ways in which the action of chloroform by inhalation may be lethal. In the first, which is similar to narcosis (anaesthesia), the vapour is inhaled for a longer time at moderate concentration. The substance is absorbed by the lungs and slowly distributed in the body including the nervous system. No severe effect on the heart action occurs during this time. If there are no other complications, for example, asphyxiation or aspiration of vomit, the concentration in blood and tissues may increase to very high levels until death occurs by paralysis of respiration. Since there is sufficient time, chloroform can equilibrate between blood and tissues, and the concentrations in the tissues, such as the liver, may be considerably higher than in blood because of the high affinity of chloroform to lipids contained in the tissues. If in addition to the effect of chloroform there is a deficiency of oxygen, caused for example by a cloth wetted with chloroform being firmly held over the mouth and nose, death may occur earlier and at lower blood concentrations, and the tissue concentrations are lower in comparison to blood since there has been insufficient for equilibration.

[26] The second possibility is that, by breathing through a cloth wetted with chloroform, air with a very high chloroform concentration is inhaled. This leads to a sudden stream of blood with very high concentration of the substance from the lung to the left heart ventricle. In this case, the effect on the autonomic nervous system of the heart dominates, leading to cardiac arrhythmia and sudden cardiac arrest. In this case, the post mortem blood concentrations in venous blood and in tissues remain low and would not be interpreted as being lethal according to the anaesthetic narcosis scheme.

[27] The following information was provided by Professor Alexander Forrest, who gave evidence at the appeal (see paragraphs [57] to [62]). Chloroform is not a corrosive. It is an irritant and, if rubbed on the skin, it can produce an irritant effect with a reddening of the skin. It also tends to remove grease from the skin. If applied to the skin, it can certainly cause reddening and a rough appearance of the skin which would persist into the post mortem period. It is not uncommonly the case that when a person has been inhaling non-irritant solvents, such as toluene, and has died in consequence, there may be reddish discolouration around the mouth. Chloroform can be regarded as being a solvent.

[28] With respect to the effect of ingestion of chloroform on the stomach, Professor Forrest quoted from Taylor's Principles and Practice of Medical Jurisprudence (9^th ed., 1934), edited by Professor Sydney Smith, which contains the following statement at Vol. 2, pp. 620-1:

"On opening of the cadaver there is very likely to be a smell of Chloroform, and when the drug is swallowed, the stomach may show signs of irritation in patches; beyond these two signs, which, it must be noted, are neither of them constant, and both may be absent, nothing is to be noticed and only a critical analysis will reveal the cause of death. ... As Chloroform is much less volatile than Ether, and its odour is not so pungent, it is not so easily detected in the dead body by the smell. The body should be inspected as soon as possible, and any solids or liquids intended for examination should be kept in well closed glass vessels."

The presence of chloroform in the deceased's blood and liver

[29] It is now necessary to examine in more detail the evidence which was led at the trial relating to the presence of chloroform in the deceased's blood and liver, and the competing hypotheses of inhalation and ingestion. As the trial Judge reports, Dr Fineron gave his evidence on 4 and 5 April 2002. He was immediately followed by Professor Busuttil, who completed his evidence on the latter date. Because he was not available at a later date, the evidence of the defence expert, Dr Flanagan, was interposed in the Crown case. He gave evidence on 9 and 10 April 2002. He was immediately followed by Dr Okely, who completed his evidence on the latter date. The trial Judge reports that the suggestion of ingestion of chloroform as accounting for the large concentration of it in the liver was not known to the Crown until Dr Flanagan gave his opinion to that effect in the witness box. He therefore granted an unopposed motion by the Advocate depute to recall Dr Fineron to give further evidence on that point. He did so on 12 April 2002. Professor Busuttil was recalled by the defence on 16 April 2002. When Dr Fineron and Professor Busuttil were recalled they commented on the possibility of ingestion raised by Dr Flanagan in the course of his evidence. We shall now set out the features of the evidence of these witnesses.

Dr Paul Fineron

[30] At the time of the trial Dr Fineron had recently ceased to be consultant forensic pathologist at the University of Edinburgh and had become consultant pathologist at the Western General Hospital in Edinburgh. He gave evidence on 4 and 5 April 2002. He spoke to his locus and post mortem reports. He confirmed that he had found evidence of haemorrhagic gastritis, and said that this was a very common condition, could be caused by a variety of agents and was essentially of no significance. He also referred to his histological examination of various samples, including sections from the heart. He said that there were features of contraction band necrosis, which he described as a non-specific finding often found in a variety of causes of death, but thought to be associated with high adrenalin levels within the body (right ventricle). Following receipt of the results of the toxicological analysis of a blood sample, which showed the presence of amphetamine, his hypothesis for the sequence of events leading to the deceased's death "was amphetamine intoxication possibly leading to disturbed behaviour ... in the heart rhythm precipitating a collapse and then possibly hypothermia had played a role".

[31] Dr Fineron said that once he had received information that chloroform was present in the samples obtained at post mortem, he regarded this as highly significant. It totally altered his opinion as to the cause of death. Once he had received information from the forensic scientists that the concentration of chloroform in the blood sample was 31mg/l, he re-examined his findings on post mortem examination. Among other signs, he decided that the red mark on the left side of the lower lip could be a "contact burn due to chloroform". Other signs could have been the result of force used in applying a chloroform-soaked cloth to the deceased's face. If the deceased had taken amphetamine, and if through fear adrenalin was released within her body, these could have exacerbated the effects of the chloroform on her heart. He then gave the opinion that the cause of death should be recorded as chloroform intoxication. He said in evidence:

"I consider the presence of finding a significant quantity of chloroform - and certainly the concentrations as detailed in the toxicology report - indicates that it has been administered from outwith. ... It is an abnormal finding and in line with the subtle signs round the mouth would indicate or suggest that the deceased has had chloroform administered to her by being in contact with the face. Given that inhalation of chloroform by this mechanism in my opinion is a totally adequate cause of death, I felt it was entirely appropriate that I should modify my opinion as to the cause of death".

[32] The Advocate depute asked him to comment on the information which had become available from the forensic scientists, in their report dated 2 April 2002, that chloroform had been found in the liver at a concentration of 1064mg/kg. Dr Fineron said that he was not aware of any reliable scientific literature which allowed him to place an accurate interpretation on the quantity of chloroform found in the liver. Comparing it with the concentration found in the blood, he said he was not sure how one could interpret that. He rejected the possibility of chronic abuse of chloroform:

"It certainly indicates that the deceased has died relatively rapidly, or having consumed in some way chloroform, and I think that is possibly the only interpretation one could place on it."

[33] In cross-examination he said that the concentration of chloroform in the liver was high, and this indicated acute intoxication, but that was all he could say. He was referred to the then current edition of Baselt, and accepted that the figure of 1064mg/kg which had been given for the concentration of chloroform in the liver was greatly in excess of the range given in the textbook in cases of deaths from acute chloroform intoxication. The cross-examiner used this as a basis for suggesting that the concentration in the liver was attributable to chronic abuse of chloroform, rather than an acute intoxication. Dr Fineron rejected this possibility. He said:

"The fact - again I think one has to be very cautious in interpreting these levels - but the fact that it was such a high level may suggest that death followed a very brief but massive exposure to chloroform".

His opinion therefore remained that death was directly due to chloroform intoxication.

Professor Anthony Busuttil

[34] At the time of the trial Professor Anthony Busuttil was Regius Professor of Forensic Medicine at the University of Edinburgh. He was a highly experienced consultant pathologist. He had no direct involvement in the investigations following the death of the deceased, but he had discussed the case with Dr Fineron, the police and the procurator fiscal. He first became involved when evidence of toxicological analysis came to light.

[35] When he gave evidence on 5 April 2002, he was taken through Dr Fineron's reports. He gave general evidence about the effects of chloroform. He was asked about Dr Fineron's final conclusion, that in the light of information that had become available to him, in his opinion the cause of death given in his initial supplementary report was incorrect and it was now his opinion that the cause of death should be recorded as chloroform intoxication. Professor Busuttil said that he thought that chloroform was a major component in relation to the death of the deceased. It was present in the blood in quantities consistent with toxicity, and in quantities which were fully consistent with its having been related to the mechanism of death. He postulated that the chloroform and the amphetamine which had been found in the deceased's body and the hypothermia at least interacted. If he were certifying the death, he would have stated that death was caused by the combined effects of chloroform intoxication, amphetamine intoxication and hypothermia. Even without the amphetamine intoxication and the hypothermia as causative factors, the amount of chloroform which had been found in the deceased's blood could have killed her. The Advocate Depute asked him questions based on the figure given in the forensic scientists' report dated 2 April 2002. In the course of these questions the Advocate Depute said:

"We know that 106[4]mg[/kg] is found in the liver; do you have anything to say about that, what does that suggest?"

Professor Busuttil replied that this was a very large amount going by standards which toxicologists refer to. "It suggests an acute inhalation of chloroform." When asked again about his opinion as to the cause of death, he said that he believed that chloroform had "a major if not the most important impact in terms of causing this lady's death". But there were also the presence of amphetamine, and the very cold temperatures. He concluded:

"So my view would be that chloroform had a very major part to play in her death, which may have been attributable to the presence of amphetamine and the exposure to a low temperature; and the three together certainly caused her death with chloroform perhaps being the more important of the (inaudible) of things that caused her death."

[36] In cross-examination, Professor Busuttil said that the amount of chloroform which had reportedly been found in the liver was much too high to suggest chronic exposure. The liver was otherwise normal, and the reported concentration of chloroform in it was high. These two findings made it more than likely that there had been "an acute massive exposure", though he could not rule out the possibility of chronic exposure.

Dr Robert Flanagan

[37] Dr (as he then was) Robert Flanagan was a consultant clinical toxicologist at Guy's Hospital in London. His evidence, which was given on 9 and 10 April 2002, was interposed during the Crown case. He had previously seen the reports prepared by Dr Okely and colleagues. Additional material had been provided following a consultation with Crown counsel about one week previously. He had expressed caution about the interpretation of their findings because of the possibility of contamination after samples had been collected, the possibility that another substance had been metabolised in the body of the deceased, and the possibility that that metabolite had been converted into chloroform if the analysis was performed at the normal temperature of 60ºC. To avoid this conversion, the analysis required to be carried out at 30 to 35ºC. Following his expressions of concern, the forensic scientists had carried out an analysis of a liver sample at the lower temperature, and had reported on 2 April 2002 that chloroform had been found at a concentration of 1064mg/kg. He himself had received this information in the morning of the day when he first gave evidence. He described that as "a massive amount". It proved chloroform exposure. Under reference to the then current edition of Baselt, he said:

"Well, the only thing I can think of to try and reconcile not only the blood, the blood of 31 and the liver of 1064, is if exposure has been by ingestion as opposed to inhalation. That is the only way I can think that these figures can be reconciled, unless I am missing something, because the amount in the liver is so large of 1064mg/kg. ... Having at least got the liver to analyse, we now have this massive exposure documented in the liver and a relatively small amount in the blood. All I can think of, it has gone by mouth into the stomach and then into the liver. ... That is all I can think of to try to reconcile the results relating to the bodies of concentration in blood and the massive amount in the liver. ... I think this has come through the mouth, in my opinion."

He went on to say that that concentration in the liver could not have been produced by inhalation. Explaining what he meant by ingestion, he said:

"I was trying to not say that it was deliberately the person that drank it themselves. It could have been somebody else giving them something to drink. It could even have been somebody else making them drink it, but I think exposure was by the oral route as opposed to the inhalation route, is all I am saying."

The concentrations of chloroform reported to have been found on analysis of the blood and liver samples meant that it must have been a major contributory factor in the death of the deceased. The analyses which had been carried out did not, however, give the full picture. If the gastric contents had been analysed for chloroform that might have provided more information as to whether the exposure had been by the oral route.

[38] In cross-examination by the Advocate depute he repeated his opinion that the most likely explanation for the results was an acute ingestion by mouth, and not by inhalation. "I would suggest that we could look at the stomach contents even now during the trial because that might give some more information." Later he said:

"Toxicologists are paranoid about not over-interpreting. In this case with the chloroform being so high in the liver it is I think dramatic - it is 0.1 of liver weight. Exposure must have been massive and I cannot see how that can be achieved by inhalation .... I think it has got to be ingestion in my opinion."

Dr Flanagan said repeatedly that he was not a pathologist, and he could not give evidence about the signs which would be found on post mortem examination if chloroform had been ingested. The Advocate depute put it to him, in a series of questions, that the information from the pathologists was that they would expect to have seen discolouring or burning in the gullet and in the stomach, and that none had been found. According to the pathologists therefore, "they have had no evidence that chloroform was drunk". In the course of his replies Dr Flanagan said:

"I suggest to look at the stomach contents because that might give us more information, and put it to the pathologist and see how he answers your questions. ... I am just saying that I think it has gone by the oral route, the stomach, intestines and the liver. That is the only way I can think of explaining this massive amount in the liver and the relatively small amount in the blood. When we met before I did explain that I thought that the blood concentration on its own was equivocal. ... I suggested that we need to get more information to complement this solitary result. Having got this liver result that points me to the oral route. How it got in by the oral route I cannot tell you."

Shortly after this, the following exchange took place:

"Q. If there is no pathological evidence to suggest that somebody drank chloroform, are you still maintaining that this lady ingested chloroform?

A.    Unless you can give me any other evidence, yes."

[39] The Advocate Depute also cross-examined Dr Flanagan on the possibility that the results obtained by analysis of the blood and the liver could be explained by post mortem redistribution "from other parts of the body into the liver". Dr Flanagan explained that post mortem redistribution normally occurred from major organs into blood. He therefore thought it unlikely that that was the explanation for the results in the present case.

Dr Howard Okely

[40] Dr Okely gave evidence on 10 April 2002 about various investigations which he and his colleagues had undertaken before and during the trial, as set out above at paragraphs [8] to [11]. He said that the concentration of chloroform in the blood of 31mg/l lay within the range which had been found in fatal poisonings, but was also associated with anaesthesia. He described it as a potentially fatal concentration. He said that the concentration of chloroform in the liver of 1064mg/kg appeared to be high, indeed higher than any of the concentrations in cases of fatal chloroform poisoning which had, to his knowledge, been published. This was only the second case of alleged fatal chloroform poisoning that he had encountered in 27 years of toxicology. Under reference to the then current edition of Baselt he said that the range for concentrations of chloroform in the liver given there was much less than in the present case. The concentration he had found must have arisen from acute poisoning. He said that the concentration in the liver seemed to be quite high in relation to the concentration in the blood, and that this could be for a number of reasons.

[41] He referred in particular to the possibility that this was attributable to post mortem redistribution:

"That is to say that after death the drugs which are stored in tissues are released to a greater or lesser extent, and this is one of the reasons why we do not generally examine drug levels in the liver, because they tend to be rather unreliable. ... We generally rely on the concentration in the blood."

He went on to say that rapid death would ensue from the application of a cloth soaked in chloroform to the mouth and nose and consequent inhalation. He continued:

"In this case [as just described] I would have expected a relatively high concentration of chloroform in the blood but a relatively low concentration in the liver, whereas if death had ensued after some hours of unconsciousness, then I would expect the reverse scenario whereby there would be a low concentration in the blood and a higher concentration in the liver."

[42] In support of the hypothesis of post mortem distribution he said that a number of papers had been published about it. Although it had not been lodged as a production, he referred to one published by Professor Pounder as being particularly significant. (The reference appears to have been to Pounder DJ, The nightmare of postmortem drug changes, Legal Medicine 1993 (ed. Wecht CH), 163-191; Salem, Butterworths, 1993.)

Dr Fineron (recalled)

[43] Dr Fineron was recalled to give evidence on 12 April 2002. The Advocate Depute informed him that Dr Flanagan had expressed the view in the course of his evidence that the chloroform entered the deceased's body by way of ingestion. He was asked what he would have expected to find at post mortem, if chloroform was ingested. He said:

"Chloroform is - as we know - an organic solvent like carbon tetrachloride which is used for dry cleaning. While the skin is quite resistant to these compounds because it has this layer of dead cells on the surface, the oesophagus or gullet does not, so it is more susceptible to injury. So, if somebody actually swallowed a quantity of chloroform into their mouth and it went down the oesophagus or gullet, we may well see that the lining has been stripped off and it would appear either congested or possibly with a dry whiteish appearance. Once the chloroform reaches the stomach, the cells lining the stomach are different and they are very vulnerable. Now, normally the stomach cells secrete a protective layer of mucus that protects the cells from acid and other compounds within the stomach. However, chloroform will very rapidly dissolve this away and expose the underlying cells and these would be very rapidly damaged. So, we would expect to see a blackened stomach where there was bleeding into the stomach wall and these black areas, not the speckled appearance I saw on initial autopsy due to gastritis but large areas of black discolouration of the skin. Also, if somebody had ingested chloroform and subsequently died, I would be able to smell it. I would expect to smell the chloroform or similar compound actually within the stomach contents and in this case, I saw none of these changes nor did I detect the smell of chloroform at all".

[44] Asked whether if chloroform had been drunk, one would see anything on the lips, he said:

"Yes, one certainly may see lesions on the lips area drying [sic]. In the initial autopsy, we did see the sort of appearance one would see on the outside of the lip but no lesions, no drying on the inside of the lip or in the inside of the mouth itself which I would expect to see if somebody had swallowed chloroform and had been in contact with the lining of the mouth for a period of time".

The acute haemorrhagic gastritis which he had found was a very common acute reaction to a whole host of insults. If chloroform had been drunk neat, he would expect to see more florid changes, as described. He went on to say:

"I would be quite confident I would detect the smell of chloroform had it been within the stomach contents".

Asked whether he thought that the chloroform entered the deceased's body by way of inhalation or ingestion, he said that in his opinion it was inhalation. This was "because there was absolutely no evidence in autopsy to support the hypothesis that the chloroform was ingested, for the reasons I have already stated".

[45] In cross-examination, Dr Fineron was asked about the reported concentration of chloroform in the liver. He agreed that this was a "massive amount". He said:

"I do not think we have enough knowledge to interpret the levels and as I have already indicated in my evidence in past, levels of drugs within blood certainly changes after death and will change another organ [sic]. ... So, I do not know how to interpret this and I am not prepared to interpret the levels found in an attempt to make an assessment of how the chloroform was taken or how much".

He was asked what he thought of Dr Flanagan's recommendation that the stomach contents be examined by a toxicologist for the presence of chloroform. He replied:

"If chloroform was present - was in the stomach contents - that would imply it was ingested but that it is all it would tell. ... Simply, one cannot make any conclusions about concentrations of drugs within stomach contents because the drug is in the stomach, it is not actively in the body. If a drug is present within the stomach contents, the implication is it has been swallowed rather than reached the body by another route".

He was asked about the possibility that the reported concentration of chloroform in the liver was attributable to post mortem redistribution by leakage from the stomach to the surrounding organs. In the course of his reply he said:

"Well, obviously if the drug is not present within the stomach, it cannot leak out of the stomach after death which is what that statement is saying".

He accepted that if chloroform had been inhaled, there could not be post mortem redistribution of it from the stomach. The following exchange then took place:

"Q. Because you see, your colleague - Dr Okely - seemed to suggest ... that that was one possible explanation for a higher concentration in the liver - post mortem distribution?

A.    Yes, but as I indicated earlier, determined post mortem redistribution does not just refer to leakage from the stomach. There are a lot of other causes of redistribution."

Professor Busuttil (recalled)

[46] On 16 April 2002 Professor Busuttil was recalled and further cross-examined (1) on the question whether Dr Fineron's findings during the post mortem examination were consistent with ingestion of chloroform by the deceased; and (2) the issue of post mortem redistribution of chloroform. He explained that chloroform is irritant, not corrosive. If ingested, it might produce irritant effects, and its smell might be detected (or might be missed) on post mortem examination. The finding of haemorrhagic gastritis was consistent with the presence of an irritant in the stomach. He disagreed with Dr Fineron's evidence that if chloroform had been ingested he would have expected to see blackening: this was usually a feature of corrosive effect and in Professor Busuttil's opinion chloroform was not sufficiently irritant to cause this. On the topic of post mortem redistribution, Professor Busuttil explained that, where there was a gradient of concentrations, the drug or chemical would diffuse from an organ where there was a high concentration to other parts of the body which had a lower concentration of that particular substance. He was not aware of any experimental data relating to the diffusion of chloroform. In general, if there was a high concentration of a substance in blood, this might diffuse from the blood into the adjacent tissues, such as the liver, but it was not possible for post mortem redistribution of a substance from blood into adjacent tissues to result in a higher concentration of the substance in the latter.

Scientific investigations after the trial

[47] Extensive efforts were made after the conviction of the appellant to secure fresh evidence which might lead to the quashing of the conviction. The evidence itself which was thus secured is set out below. At this stage, there are only two matters which require mention, both of them arising from investigations carried out at the prompting of those advising the appellant.

[48] First, by report dated 30 March 2006 Sunella Brahma and Jane Officer, of the Lothian and Borders Police Forensic Science Laboratory reported that the stomach contents taken at autopsy had been examined, and that chloroform had been found in them at a concentration of approximately 162mg/kg.

[49] Secondly, by letter dated 9 October 2006 Dr Okely reported that he had reviewed the quantitation of chloroform carried out on the liver. He had re-calculated the concentration of chloroform from the original data and had found there was an error in the reported result. He wrote:

"The reported result should in fact be approximately 1.0 milligram of chloroform per kilogram of liver [precisely 1.064 mg/kg], not 1064 milligram of chloroform per kilogram of liver as stated in the document produced by myself and Sylvain Emile Denieul during the trial. ...

The error in the calculation occurred while extrapolating from the concentration of chloroform in the liver samples used in the quantitation to obtain a final result expressed in milligram per kilogram (usual units of concentration measurement for liver). This resulted in an incorrect translation of units giving rise to a 1000 fold magnification of the true result." (Emphasis added)

Evidence at the appeal

[50] We now turn to consider the evidence led at the appeal, so far as salient. For clarity of presentation, we shall set the evidence out in a different order to that in which it was led before us. We shall set out the evidence led from witnesses who did not give evidence at the trial. We shall then set out the evidence led from witnesses who did give evidence at the trial. We should emphasise that the witnesses in both categories gave evidence before us on the basis of (1) the concentration of chloroform in the blood of 31mg/l reported on 18 January 2001 (see paragraph [9] above); (2) the concentration of chloroform in the stomach contents of approximately 162mg/kg reported on 30 March 2006 (see paragraph [48] above) ); and (3) the concentration of chloroform in the liver of approximately 1.0mg/kg reported on 9 October 2006 (see paragraph [49] above. Of these, (2) and (3) were not available at the trial, and the then reported concentration of chloroform in the liver was 1064mg/kg (see paragraph [11] above). Witnesses in the latter category gave evidence, moreover, in knowledge of the evidence which had been or would be led from those in the former during the course of the appeal.

Professor Dr Fritz Pragst

[51] Professor Dr Fritz Pragst is a highly experienced forensic toxicologist. From 1989 to 2006 he was head of the Department of Toxicological Chemistry of the Institut für Rechtsmedizin (Institute of Legal Medicine) of Charité-Universitätsmedizin Berlin. Since retirement in 2006 he has continued working at the Institute of Legal Medicine as a Guest Scientist. Among the numerous deaths and acute intoxications he has been involved in investigating is one case of homicide by forced inhalation of chloroform, which became the subject of a paper published in 1996, of which he was one of the authors.

[52] From his review of the papers in the present case Professor Pragst compiled a useful summary of information about the collection and storage of materials used for toxicological analysis in the present case, which we have adapted and set out in paragraph [7] above. He provided the following commentary about the collection and storage of the samples. The Steralin containers used for collection and storage of the samples consisted of polypropylene. This substance absorbs chloroform, leading to noticeable swelling of the polymer material. With a melting temperature of -63˚C, chloroform is able to diffuse even within frozen sample material slowly to the surface and can be absorbed directly by the polypropylene walls of the container. If the container is not completely filled with the sample, so that some air remains in the headspace between the sample and the lid, chloroform, which has a remarkable vapour pressure at -20˚C, can evaporate from the sample surface and be absorbed from the air by the polypropylene of the container. It can penetrate the polypropylene and can finally evaporate to the surrounding air. This would not be possible with glass vessels, although the usual plastic cover can also lead to losses. Over a long time of storage, contraction and expansion of the gas volume within the container caused by temperature variations of the refrigerator can lead to leakage of chloroform after evaporation, since the container is not usually absolutely tightly closed. Such loss is even more pronounced if the container is warmed up to room temperature and opened for taking out parts of the sample. The rates of loss have been the subject of reports in two papers referred to by Professor Pragst. In his opinion, taking into account the long storage time of between 18 and 86 months before the analyses, it was very probable that a considerable part of any chloroform which was present had been lost, this loss increasing with increasing storage time. Given that the liver was sent to another institution between the autopsy and analysis for chloroform, it could be assumed that it was at room temperature for some time and that the container was opened and the material intermediately removed in order to separate some liver tissue for pesticide analysis. Professor Pragst expected that this would have led to a further loss of chloroform in addition to the foregoing reasons.

[53] Professor Pragst examined in some detail the analytical methods which had been used in the course of the various investigations which were documented in the papers before him. This led him to express the following opinions. Chloroform was unambiguously identified in blood sample label 4 and the quantification was accurately performed. No essential analytical errors could be found. A concentration close to 31mg/l at the date of analysis must be accepted. It was very probable from the results, though not entirely proved, that the small peaks found in the chromatograms of the alcohol assay carried out on 9 February 1999 originated from chloroform, taking into account the unambiguous identification in blood at a later time and the presence in liver and gastric content.

[54] Professor Pragst found no errors in the preparation of the standards, the performance of the measurement and the calibration in respect of the liver sample. Chloroform was unambiguously identified by the mass spectrum in six portions of the liver sample. He did, however, criticise the calibration, which in his opinion should have been performed with spiked liver tissue samples, and the same sample amount should always have been used in order to obtain correct results. It could not, in his opinion, be concluded without experiments whether this error led to a positive or negative deviation of the results from the real value. A second error was that in the calculation the higher specific weight of liver as compared to the aqueous standard solutions was not taken into account. Since the specific weight of liver tissue is higher than 1.00 the result in mg/l corresponds to a lower concentration in mg/kg. These two errors were, however, with a high probability, small in comparison to that caused by the loss of chloroform during the time between sampling and measurement. It could be accepted that a concentration of around 1mg/kg chloroform was contained in the liver at the time of investigation. An error of e.g. - 50% or + 100% would not essentially change the interpretation.

[55] Of the analysis for gastric content, reported on 30 March 2006 as yielding a chloroform concentration of 162mg/kg, Professor Pragst was prepared to assume that chloroform was unambiguously identified, although the method of analysis was not described in the documents before him.

[56] After considering the interpretation of the chloroform concentrations in blood, liver and gastric content in the present case, and under relevance to the relevant literature, Professor Pragst concluded, in part 7 of his report, as subsequently amended by him:

"7.1 Chloroform was unambiguously detected in blood, liver tissue and gastric content.

7.2 The concentration in venous blood of 31 mg/l can be regarded as a minimum concentration at the time of death. Probably the concentration was considerably higher but this cannot be proved.

7.3 The chloroform concentration of about 1 mg/kg in liver measured 38 months after sampling is not compatible with the venous blood concentration. The value is by far too low. Losses, occurred probably mainly during using the sample for other analytical investigations. No profound interpretation from this value is possible.

7.4 In the same way, the chloroform concentration in the gastric content of 162 mg/kg proves only its presence.

7.5 The concentration of 31 mg/l in venous blood is not necessarily lethal. Death at this concentration can have occurred:

- by cardiac arrest after inhalation of a high concentration with a very short survival time

- by combination of narcotic effect and suffocation, also with short survival time. However there was no evidence for suffocation found in the documents which came to my attention.

- by combination of the narcotic effect with hypothermia with longer survival time. In this case ingestion, alone or in combination with inhalation, would also be possible.

It cannot be distinguished between these possibilities from the analytical data available. Additional evidence, particularly an estimation of the time of death and of the survival time after chloroform application, which would be helpful, is missing. Furthermore, it cannot be distinguished from the analytical data between self-application and forced application from second hand.

7.6 The detection of the relatively low concentration of chloroform in gastric content neither proves nor completely exclude[s] the possibility [of] oral ingestion.

7.7 From the whole of the evidence which was contained in the papers and disposed to my attention ..., a fast death after inhalation of chloroform (e.g. from a cloth wetted by chloroform over mouth and nose) by cardiac arrest and in combination with suffocation seems to me most probable. However, there was no evidence for suffocation found in the documents which came to my attention.

7.8 A volatile screening should be involved in the routine of the every general unknown toxicological analysis. At latest after specific suspicion to chloroform, not only blood but all other samples should have been analysed for this substance. This would have avoided much uncertainty and speculation in the present case."

Professor Alexander Forrest

[57] Professor Alexander Forrest, a registered medical practitioner and chartered chemist, with numerous qualifications and memberships of learned bodies, was Honorary Professor of Forensic Chemistry at Sheffield University and Visiting Professor in the Faculty of Health and Welfare at Sheffield Hallam University. He also held appointments as Assistant Deputy Coroner in two jurisdictions in Yorkshire. He stated that he had never himself investigated a case of ingestion or inhalation of chloroform himself, such cases being very rare in the United Kingdom. The expertise he brought to assist the Court was derived from his general knowledge of toxicology, reading widely in the relevant literature, including nineteenth century literature, and sharing experience with colleagues, in particular in the United States, at scientific meetings.

[58] Chloroform is volatile and will be lost by evaporation from blood samples, particularly blood samples contained in plastic containers, and particularly if the containers were not full to the brim. Professor Forrest believed that there was a significant probability that the chloroform concentration, as measured in a blood sample which had been collected in a 25ml Steralin container, had been affected by evaporation. Volatile substances had a tendency to disappear more rapidly from plastic containers, such as the plastic "universal" type of container in which the quantitative analysis of blood obtained by Dr Fineron from the deceased's body at post mortem was collected. This would be even more so if, as might have been the case, the Steralin container was made from polystyrene rather than polypropylene. Consequently, the concentration of chloroform in the blood sample when it was first obtained from the deceased could have been considerably higher than when it was measured.

[59] Professor Forrest was not aware of data relating to the loss of chloroform from frozen liver or stomach content, though from first principles he expected that a frozen liver sample might be less likely to lose chloroform rapidly than would be the case from a frozen blood sample. He thought that the only certain conclusion one could draw from the finding of chloroform, at a concentration of 162mg/kg of stomach content, was simply that there was chloroform present in the stomach at the time of death. It was probable that the concentration found in 2006 when a sample was analysed was lower, possibly much lower, than that which would have been present at the time of death. If the chloroform was ingested, it was not possible to estimate from the levels of chloroform detected in the liver and the blood the quantity which had been ingested. Any such calculations were likely to produce results so imprecise as to potentially be misleading. It was very likely that there had been considerable changes, which it was not possible to quantify, in the concentration of chloroform in stomach content, liver and tissue between the time of the death and the time at which the analyses were carried out.

[60] Chloroform was formerly used as a general anaesthetic. The inhalation of chloroform would first of all have produced drowsiness and then unconsciousness. Vomiting could occur and, in the presence of depressed consciousness, this could lead to obstruction of the upper part of the airway. One cause of death could simply be depression of consciousness to the level that the individual concerned could no longer breathe. When chloroform by inhalation was used for homicidal purposes, by the placing of a chloroform-soaked cloth over the victim's mouth and nose, it might be combined with firm pressure, which itself could obstruct the airways. The combination of intoxication with chloroform and obstruction of the airways was likely to be rapidly fatal. Once unconsciousness had supervened, which would occur rapidly, there would not be much of a struggle. In the absence of a struggle, when a person already unconscious had their airway obstructed, characteristic changes of asphyxia, in particular petechial haemorrhages, might not be seen. There was frequently a cardiac component involved when a person died as a result of the inhalation of chloroform. Chloroform could cause increased irritability of the heart muscle and of the electrical conducting system of the heart. Particularly under conditions of stress, when adrenaline was released from the adrenal glands, this could precipitate fatal disorders of the heart beat. The finding reported by Dr Fineron of contraction band necrosis in the muscle on the right side of the heart suggested that the deceased might have died rapidly rather than with a slow decline into unconsciousness over a period of many minutes or hours; although it might simply indicate a rapid terminal event after an extended period of unconsciousness. The concentration of amphetamine found in the deceased's blood was a relatively low one, but it was sufficient to cause pharmacological activity and, as such, would be expected to potentiate the potential adverse effects of chloroform on the heart. Amphetamine was a stimulant and would stimulate and potentiate the effects of natural adrenaline in the body. Taking all of these findings together, Professor Forrest felt that on balance the deceased was more rather than less likely to have died rapidly, that is to say, within a very few minutes, or less, of the initiation of the process that led to her death rather than over an extended period of many minutes or even hours.

[61] Professor Forrest said that ingestion and inhalation of chloroform were not mutually exclusive. Much depended on the method of administration. It was entirely possible that with pure inhalation chloroform could enter the stomach. It would be present in the upper part of the airway in high concentrations. It would tend to dissolve in saliva and be swallowed. In addition the swallowing of some chloroform-laden air would occur. The concentration in stomach content in the present case could reflect either ingestion or inhalation, or a combination of both. On balance, he favoured its primarily reflecting ingestion, or a combination of inhalation and ingestion, but he could not be certain. He did not think that the orange material in and around the opening of the deceased's nostrils could be attributed specifically to the effects of chloroform. Ingestion or inhalation of chloroform could result in vomiting, so the colouration could be attributable to the deceased's having vomited following her last meal. Taking the information overall, it was his opinion that the available information was compatible with, and in no way excluded, the hypothesis that the deceased might have ingested chloroform shortly before her death. The data were also compatible with the hypothesis that she both inhaled and ingested chloroform shortly before her death. The data were less compatible with the hypothesis that death was a result of the inhalation of chloroform alone with or without asphyxia associated with obstruction of the airway. There was nothing in the data he had seen which made him believe that her death was due to any factor other than the toxic effects of chloroform. At the very least, chloroform had made a more than minimal contribution to her death.

[62] In a statement dated 19 October 2006, prepared once the revised result for the concentration of chloroform in the liver had been communicated, Professor Forrest wrote:

"Having reviewed this result together with all of the other information available to me, I would agree that the analytical results obtained ... are entirely typical of the results that one would expect to be found were the deceased to have inhaled chloroform shortly before her death. Further, the results are typical, taking into account the delay between the time of death and the various analyses that have been carried out, of the results one would expect following the lethal inhalation of chloroform."

In a report dated 12 January 2009 Professor Pounder (whose evidence is set out next) commented that Professor Forrest had in this passage not commented on the possibility of ingestion. In the course of his evidence Professor Forrest accepted that this was a valid criticism. He did not exclude ingestion alone, or a combination of ingestion and inhalation. It was possible to formulate a hypothesis of ingestion alone, but unfortunately this was not testable, as toxicology data could only be interpreted in knowledge of all the circumstances.

Professor Derrick Pounder

[63] Professor Derrick Pounder, Professor of Forensic Medicine at the University of Dundee, had many years of experience in forensic pathology. He had a special interest and expertise in drug and poison related deaths and had conducted original research and published extensively on a phenomenon known as post mortem drug redistribution. Professor Pounder prepared two reports, the first dated 31 March 2008 and the second, incorporating all relevant matters contained in the first report, dated 12 January 2009.

[64] Having reviewed the information available at the latter date, Professor Pounder stated that the concentration of chloroform in the blood of the deceased was within the range found in chloroform-related fatalities. He agreed with the witnesses who gave evidence at the trial that the death was, with reasonable medical certainty, attributable to chloroform. This view was not dependent upon the chloroform concentration in liver and consequently was unaffected by the disclosure of the error in calculation of the chloroform concentration in liver. This view was based on a number of facts: (a) there was no trauma sufficient to account for death; (b) there was no natural disease to account for death; (c) the presence of chloroform and specifically its concentration in the blood was sufficient to account for death; (d) hypothermia as a cause of death could not stand alone and must necessarily be secondary to some other incapacitating condition; and (e) amphetamine intoxication was only a remote possibility as a cause of death and was entertained originally because of the absence of any more likely alternative. The mechanism by which chloroform caused the death could only be a matter of speculation. The same was true of the contribution, if any, of amphetamine and hypothermia. Although the precise mechanism of death might be unclear, there was reasonable certainty on the issue of cause of death, namely that it was the result of the effects of chloroform.

[65] Professor Pounder commented on the evidence given by Dr Fineron at the trial, in particular the statements that there was absolutely no evidence at autopsy to support the hypothesis that the chloroform was ingested, and that if chloroform had been ingested he would expect to find damage to the gullet, a blackened stomach, and would expect to smell the chloroform on opening the stomach. Professor Pounder stated that the medical literature did not support these statements. While they reflected one extreme end of the spectrum of possible findings following a fatal ingestion of chloroform, they did not fairly reflect the usual or the full range of possible findings following fatal chloroform ingestion. Dr Fineron failed to advise the Court that the absence of any noteworthy changes to the inside of the mouth and gullet of the deceased, and the presence of a haemorrhagic gastritis in the stomach, were consistent with the ingestion of a fatal dose of chloroform. He failed to advise the Court that the presence of gastritis, although an entirely non-specific irritant effect, could be viewed as corroborative of ingestion of chloroform, an irritant. He further failed to advise the Court that ingestion as a route of administration could not be excluded on the basis of the anatomical findings at autopsy. The literature did not support the view that Dr Fineron would have expected to smell the chloroform on opening the stomach. In the single case of which Professor Pounder had personal experience, he detected only an extremely fleeting unusual odour of a volatile compound. Had he not been alerted to the possibility that the compound was present he would certainly not have smelt it. In any event, the issue was now definitively settled by the analysis of the stomach contents. Thus the opinion of Dr Fineron on this issue was proved to be wrong.

[66] Professor Pounder proceeded to consider the evidence relating to the marks found upon the deceased's face. He described as "balanced" Dr Fineron's view at the trial that although non-specific these findings "could be due to a chloroform-soaked pad, for example, being placed on the face". Professor Pounder said that the fair presentation of non-specific findings to the face being consistent with the prosecution proposition of the placement of a chloroform-soaked rag over the nose and mouth was not matched with an equally fair acceptance that the non-specific finding of an acute haemorrhagic gastritis could be due to the ingestion of chloroform. His report contained this statement:

"In my opinion the presentation at trial of the scientific evidence with respect to the possibility of ingestion was erroneous as a matter of science, carried the flavour of bias when seen in the context of the totality of the scientific evidence, and was seriously misleading on a critical matter for consideration by the jury."

[67] Professor Pounder went on to consider the evidence given at trial about the possibility that post mortem redistribution could account for the remarkable and unexpectedly high (and in fact erroneous) reported concentration of chloroform in the liver relative to that of the blood. He stated that, in general, the interpretation of post mortem blood and tissues levels of drugs and poisons presented considerable difficulties, not least of all because the concentration of drugs and poisons in blood and tissues changed with time after death. These temporal changes in drug and poison levels in the body post mortem were commonly encompassed within the term "post mortem drug redistribution". The proposition of the Crown pathologists and toxicologist that the unexpectedly high chloroform concentration in the liver might be explained not by ingestion but by inhalation followed by post mortem redistribution from the blood to the liver had no scientific foundation, to the best of his knowledge and belief. The discounting of the significance of the finding of the high chloroform level in the liver, on the basis that there had been post mortem redistribution from blood to liver, had

"the flavour of an ill-considered, on-the-hoof reaction to a new evidential fact, potentially devastating to the prosecution position, in what was already a scientifically challenging case in which the experts had made errors during the investigation".

[68] Professor Pounder went on to say that there was no need to consider this matter further, given that the concentration of chloroform in the liver as discussed at trial was erroneous. The true concentration of chloroform found in the liver was itself problematic to interpret since it was significantly less than the lowest reported concentration of chloroform in the liver in a series of deaths attributed to chloroform inhalation, where the range was from 6mg/kg to 201mg/kg. Such a very low concentration of chloroform in liver when contrasted with blood possibly reflected substantial loss of chloroform from the liver sample sometime between autopsy and analysis. Whatever the cause of this prior to analysis, the analytical result for the chloroform concentration in the liver must be regarded as anomalously low when contrasted with the blood level. In his view the concentration of chloroform in the liver was best regarded as so unreliable that it should be discounted.

[69] By contrast with the liver sample, both the blood sample and the stomach contents which were analysed were stored under very similar conditions until the time of analysis. There were no available scientific data on the relative losses of chloroform from blood as opposed to stomach content samples under the conditions of storage in this case, and speculations on such matters were futile in his opinion. What was undeniable was that the two samples were taken at autopsy, the blood was analysed so that the results were reported on 18 January 2001 and the stomach contents were analysed so that the results were reported on 30 March 2006. The interval between autopsy and sample analysis was four times greater for the stomach contents than for the blood and if, as was reasonably likely, loss of chloroform from any sample was time-dependent, then there was an expectation that any fall in concentration in chloroform in blood would be mirrored by an even greater fall of concentration of chloroform in stomach contents.

[70] Following the ingestion of chloroform, the chloroform would be found in high concentrations in the stomach until it was absorbed, when only traces would remain. Following inhalation of chloroform, some chloroform could be expected to be found in the stomach contents, if only as a result of diffusion from the blood into the stomach contents in life. Additionally, during inhalation of chloroform, the swallowing of air and saliva contaminated with chloroform would introduce chloroform into the stomach. The limited data which were available suggested that the chloroform concentration in stomach contents might be up to twice that in blood in cases of presumed chloroform inhalation. In the present case, there was an approximately five-fold difference between the concentration in stomach contents and the concentration in blood, without correcting for any storage-time differential loss of chloroform. This was compelling evidence that chloroform was ingested. In Professor Pounder's opinion, the analytical results clearly indicated that there had been ingestion of chloroform and the analytical results in their entirety could be accounted for as a consequence of ingestion of chloroform without inhalation. On the other hand, a combination of both the ingestion and inhalation of chloroform was an open possibility, but inhalation of chloroform without ingestion of chloroform could be excluded with reasonable certainty. Taking the analytical results in blood and stomach contents alone (or together with liver) it was not possible to indicate the relative probability of ingestion alone as against ingestion combined with inhalation (or inhalation combined with ingestion). In his view, the autopsy findings did not assist in assessing the relative probability of these two possibilities.

[71] Professor Pounder addressed the scientific propositions advanced by the Crown at the trial in support of the argument that inhalation rather than ingestion was the primary method of chloroform administration: (1) that the autopsy findings which would be expected if chloroform had been ingested were not present; (2) that the toxicological findings, including those in the liver, were consistent with inhalation of chloroform without ingestion of chloroform; and (3) that there were autopsy findings corroborative of inhalation of chloroform. He reported:

"In summary, the pathology and toxicology in this death make it a difficult case. These difficulties were compounded by the fact that the true nature of the cause of death, chloroform intoxication, escaped detection initially. The failure to analyse the liver and stomach contents prior to trial further compounded the problem of interpreting the significance of the findings. The medical opinion offered at trial that the autopsy findings excluded the possibility of ingestion of a lethal dose of chloroform was wrong as a matter of science ... [T]he autopsy findings are consistent with ingestion of chloroform and ... the concentration of chloroform now found in the stomach contents is irrefutable evidence that ingestion of chloroform took place. The evidence now available indicates that at least some, if not all, of the chloroform was ingested. It can no longer be said that ingestion of chloroform as a possibility can be excluded, it is now a fact. Of the three scientific propositions advanced by the prosecution to counter the defence argument that chloroform could have been ingested ... the Crown pathologist has resiled from the first, the analysis of stomach contents has put paid to the second, and the third can only stand if it is qualified by an acceptance that some chloroform was ingested. The Crown case on the now available scientific evidence could only be advanced on the basis that there was both inhalation and ingestion of chloroform.

As the trial Judge noted in the charge to the jury ..., an acceptance that the chloroform was ingested would mean that the jury could not convict of the charge. Thus the erroneous scientific advice offered to the jury to the effect that ingestion of chloroform could be excluded as a possibility was on a critical issue."

[72] Professor Pounder had published more papers about post mortem redistribution than anyone else in Europe, and probably in the world. The more abnormal the case, the greater was the necessity to perform more extensive analysis. In the present case he would have analysed all the samples as soon as there was a suggestion that chloroform was involved in the death. Professor Pounder said that he would agree with Professor Forrest's views about the means by which chloroform could reach the stomach following inhalation (see paragraph [61] above). He added that chloroform in the body would diffuse from the blood into the stomach contents. But here the concentration in the stomach contents was compelling evidence that at last some chloroform had been ingested. The possibility of swallowing a few drops from a cloth pressed against the face was lay speculation and was not found in the literature.

Professor Flanagan

[73] At the time of the appeal, Professor Flanagan, as he had become, was a consultant clinical scientist in the department of toxicology at King's College Hospital, London. He was Honorary Professor in Analytical Toxicology at the University of London. Before us, he said that if he had been in charge of the investigation into the death of the deceased he would have wanted to analyse all available fluids, tissues and body samples for chloroform, using the method most likely to detect it at a temperature of 35ºC. He was shocked when he received the information that the liver analysis had yielded a concentration of chloroform of 1064mg/kg for the first time on the morning of the day when he had been due to give evidence. The only explanation he could think of was that a large part or all of the chloroform in the deceased's body had entered it by ingestion. Although the workings which produced this figure were not there, it looked like a thorough piece of work and he took it at face value. In retrospect he should have spotted something flawed in the analysis. This led to his giving the evidence in the passages quoted above. He had not had time to look in the literature, and it had all come as such a shock.

[74] He subsequently learned that Dr Fineron had given evidence about the gross effects of the ingestion of chloroform and about post mortem redistribution. Contrary to what Dr Fineron said, chloroform was not a corrosive poison, it was an irritant which could cause reddening or bleaching of the skin. He himself had been asked about post mortem redistribution in the course of cross-examination. This was based on information provided by Dr Okely. When Dr Okely came to give evidence, what he said was wrong. A substance such as chloroform could not be concentrated from one tissue to another after death against the concentration gradient. Professor Flanagan described the process by which post mortem redistribution might occur where a substance had been ingested. He disagreed with Dr Okely's redistribution hypothesis, given that the Crown disallowed the possibility of oral ingestion. Once he had been informed in 2006 of the analysis of the stomach contents, where the concentration of chloroform was reported as being 163mg/kg, in his view this provided support for the most likely route being ingestion of a significant proportion if not all of the dose of chloroform. At that time it was still understood that the concentration of chloroform in liver was 1064mg/kg. Thereafter it was discovered that the true figure was 1000 times less. This gave rise to different considerations. Given what could be established about the conditions in which the liver had been stored and manipulated, he thought that a significant amount of chloroform must have been lost from it, but he could not say how much. There were then two possibilities. Either the original concentration was so low that chloroform had nothing to do with the death; or the loss of chloroform from the liver was so great that the liver was of no evidential value.

[75] In a report dated 20 December 2006, prepared following receipt of information about the recalculation of the liver chloroform concentration, Professor Flanagan wrote:

"In my opinion it remains possible that either ingestion of chloroform for whatever reason, or a combination of inhalation and ingestion, could be the origin of the chloroform found in the blood - notwithstanding speculation as to changes in chloroform concentration since the samples were collected, the chloroform concentration reported in stomach contents ... is considerably higher than that measured in the blood sample .... However, given that the liver chloroform concentration now reported ... is so low, I do not feel confident in ascribing death either to chloroform poisoning alone, or to chloroform poisoning in the presence of a low concentration of amphetamine. Indeed, it could be that the finding of chloroform is incidental to the actual cause of death."

[76] Before us, Dr Flanagan stated emphatically that, had the true figure for the concentration of chloroform in the liver, and the figure for concentration of chloroform in the blood, been available prior to the trial, he would at the trial have had a much stronger basis for saying that at least part of the dose had entered the deceased's body by ingestion. He would have been far less confident in saying that ingestion was the only route, because the liver concentration was so low. If he had been called after the Crown case had closed, he could have disputed the unsound explanation that what was then understood to be a high concentration of chloroform in the liver was attributable to post mortem redistribution. He would also have been in a position to dispute the evidence which had been given that chloroform was corrosive, when it was in fact irritant.

Professor Busuttil

[77] By the time of the appeal Professor Busuttil had retired from his academic post, but continued to work as a pathologist. Before us, he said that, now knowing the correct figure for the concentration of chloroform in the liver, and the figure for the concentration of chloroform in the stomach contents, he did not depart from his view that chloroform was a major cause of the deceased's death. Hypothermia had no bearing on the toxicological findings, and might have been a contributory cause. It would have taken a massive dose of chloroform to produce a concentration of 1064mg/kg in liver, but if the true figure was 1.064mg/kg that would not reflect a massive dose. Given that chloroform had been found in the stomach contents, this could have produced irritation, but not blackening, of the stomach lining. Chloroform from the upper air passages could have reached the stomach mixed with saliva which had been swallowed. The presence of chloroform in the stomach meant either that it must have been ingested, or that it had been swallowed mixed with saliva.

[78] Professor Busuttil had seen Professor Pragst's report, which he described as "very impressive". Professor Pounder was, he said, a worldwide expert in post mortem redistribution. There was nothing he disagreed with in his report. Toxicology was not his own expertise, so he had no basis on which he could disagree with Professor Flanagan. He believed, however, that the only value of toxicology so long after the event was qualitative not quantitative. The blood analysis (which had been available at the trial) was the most accurate. He would be very circumspect about taking a particular value and building a circumstantial case on it.

Dr Okely

[79] By the time of the appeal Dr Okely was section leader in toxicology at the Scottish Police Services Laboratory, Edinburgh. He explained that all the samples which had been taken at the post mortem examination were received at the laboratory on 8 February 1999. With the exception of the liver, they were refrigerated. The liver was placed in the freezer. On 7 December 2000 the liver was taken from the freezer and sent in a cool box to the Scottish Agriculture Science Agency for a pesticide determination. It was received back about two years later. In their report dated 14 March 2002 he and Sylvain Denieul stated that the liver and the vitreous humour were further examined, and chloroform (unquantified) was found in each. Each was examined for other chlorinated hydrocarbons with a negative result. Following a suggestion by Dr Flanagan that other chlorinated hydrocarbons might give rise to a finding of chloroform on analysis, this test had been carried out. Dr Flanagan had suggested that the chloroform found during the initial analysis might be due to the conversion of trichloroacetic acid to chloroform, which occurs when the acid is heated at 40ºC. It was found that if during the analysis the samples were heated at the lower temperature of 35ºC this conversion did not take place. The quantitation of chloroform in the liver was performed at the lower temperature and gave a concentration (as they reported) of 1064mg/kg. He gave evidence to that effect at the trial. He was not aware before the trial that the Crown case was that the chloroform had been inhaled, and the defence case that it had ingested, otherwise he would have taken a different approach to analysis. It was not general practice to analyse stomach contents, and this was not done before the trial, as there was no indication to do so.

[80] Asked about the evidence he had given at the trial about post mortem redistribution, he said that he was aware of this but had no specialist knowledge: he knew too little to comment and he wished to withdraw that evidence, which was clearly erroneous. Had he been aware of the true result he would not have postulated post mortem redistribution. The picture was complicated by the conditions of storage of the samples and the length of time for which they had been stored. It was very difficult to interpret the figures. The concentration which had been found in the blood sample was consistent with that which had been found in fatal cases. But there was insufficient blood in the glass container in which the sample for analysis for alcohol had been stored, so they used a sample from one of the plastic containers. It was not possible to back-calculate because of the number of unknowns. This was especially so with the liver.

[81] Had he known at the time of the trial of the concentration of chloroform in the stomach contents and the true figure for the concentration of chloroform in the liver, he would not have been able to express an opinion as to whether the deceased died comparatively quickly or slowly. Looking at the matter now, it was not within his area of expertise to offer any opinion as to the route by which chloroform had entered the deceased's body. He now accepted that ingestion could not be ruled out.

Dr Fineron

[82] By the time of the appeal Dr Fineron was a consultant histopathologist in the Department of Laboratory Medicine at the Western General Hospital, Edinburgh. He was taken over his locus and post mortem reports, and the evidence which he gave at the trial. By the time of the appeal he had been made aware of the correct figure for the concentration of chloroform in the liver, and of the figure for concentration of chloroform in the stomach contents. He had also had occasion to reconsider the evidence that he gave at the trial about the signs which he would have expected to find if chloroform had been ingested. He said: "I think it is fair to say I overstated the case in the initial trial". He referred in particular to the evidence he had given about blackening of the stomach. He now accepted that blackening might not be present if death ensued very rapidly. He had reached this view on the basis of reflection, thinking more deeply about the matter. Acute haemorrhagic gastritis could be consistent with the ingestion of chloroform, but this was in no way specific. He had been supplied with copies of reports by Professors Pounder and Flanagan. In giving evidence at the trial on the basis of a reported concentration of chloroform in the liver of 1064mg/kg, and in the view he expressed about post mortem redistribution, he accepted that he had no expertise apart from reading literature and he was contending with what was understood to be a grossly high level in the liver by comparison by blood. Overall, he said:

"On reflection I accept I mis-stated the position. The explanation I gave the court [in the passages quoted at paragraphs [43] to [45] above] was incorrect".

He was confident that chloroform was a major cause of the deceased's death, but ultimately he could not say how it entered her body.

[83] In summary, Dr Fineron said that as a pathologist he would like every sample to be analysed. That would have been of substantial help in the present case. He accepted the presence of chloroform in the stomach, though he did not smell it at autopsy. It followed that the significance of not smelling it was overstated. He accepted that he was wrong about the blackening of the stomach and the other signs which he said at the trial would have been produced by the ingestion of chloroform, but were not present. He said:

"I was trying to be as helpful as possible. With hindsight, based on very scanty literature, we were all somewhat grappling in the dark".

While his view remained that chloroform was the sole or the main cause of the deceased's death, he accepted that there was no way of establishing the exact mechanism of the death. He concluded:

"I have to concede that, knowing what we do today, the trial would have been conducted entirely differently by both the prosecution and the defence".

Fresh evidence and the law

The legislation

[84] By section 106(1) of the Criminal Procedure (Scotland) Act 1995 any person convicted on indictment may, with leave, inter alia appeal against such conviction. Subsection (3) provides that by such an appeal a person may bring under review of this Court any alleged miscarriage of justice, which may include such a miscarriage based on inter alia "(a) subject to subsections (3A) to (3D) below, the existence and significance of evidence which was not heard at the original proceedings". By subsection (3A) such evidence may found an appeal only where there is a reasonable explanation of why it was not so heard. Subsection (3B) is not relevant for present purposes. Subsection (3C) provides inter alia that where evidence such as is mentioned in subsection (3)(a) is evidence which is from a person who gave evidence at the original proceedings, and which is different from, or additional to, the evidence so given, it may not found an appeal unless there is a reasonable explanation as to why the evidence now sought to be adduced was not given by that person at those proceedings, which explanation is itself supported by independent evidence. Subsection (3D) provides that for the purposes of subsection (3C) "independent evidence" means evidence which (a) was not heard at the original proceedings, (b) is from a source independent of the person referred to in subsection (3C), and (c) is accepted by the court as credible and reliable.

The authorities

[85] The following passages in the authorities to which reference was made in the course of the hearing appear to us to be of relevance for present purposes. In Megrahi v HM Advocate 2002 JC 99, Lord Justice-General Cullen, in delivering the opinion of the court, and under reference to Cameron v HM Advocate 1991 JC 251 and Kidd v HM Advocate 2000 JC 509, said at paragraph 219:

"We summarise the approach adopted in those cases in the following propositions: (1) The court may allow an appeal against conviction on any ground only if it is satisfied that there has been a miscarriage of justice. (2) In an appeal based on the existence and significance of additional evidence not heard at the trial, the court will quash the conviction if it is satisfied that the original jury, if it had heard the new evidence, would have been bound to acquit. (3) Where the court cannot be satisfied that the jury would have been bound to acquit, it may nevertheless be satisfied that a miscarriage of justice has occurred. (4) Since setting aside the verdict of a jury is no light matter, before the court can hold that there has been a miscarriage of justice it will require to be satisfied that the additional evidence is not merely relevant but also of such significance that it will be reasonable to conclude that the verdict of the jury, reached in ignorance of its existence, must be regarded as a miscarriage of justice. (5) The decision on the issue of the significance of the additional evidence is for the appeal court, which will require to be satisfied that it is important and of such a kind and quality that it was likely that a reasonable jury properly directed would have found it of material assistance in its consideration of a critical issue at the trial. (6) The appeal court will therefore require to be persuaded that the additional evidence is (a) capable of being regarded as credible and reliable by a reasonable jury, and (b) likely to have had a material bearing on, or a material part to play in, the determination by such a jury of a critical issue at the trial."

At paragraph 249 the court said, of a circumstantial case:

"The assessment of the significance of the additional evidence must, therefore, in our view, be conducted in the context of the whole circumstantial evidence laid before the trial court."

[86] In Fraser v HM Advocate 2008 SCCR 407 Lord Justice-Clerk Gill said at paragraphs 131 to 134:

"[131] Sections 106(3) and 106(3A) of the 1995 Act regulate fresh evidence appeals in the context of the single ground of appeal that the 1995 Act allows, namely miscarriage of justice. Before new evidence can be considered by the court, the appellant must furnish a reasonable explanation why it was not heard at the trial. Unless there is a reasonable explanation, the appeal cannot succeed, no matter how significant the proposed new evidence may be (Campbell v HM Advocate 1998 JC 130 at pp. 150, 176-178; Barr v HM Advocate 1999 SCCR 13, at pp. 17-18).

[132] If the appellant provides such an explanation, the onus being on him, the court must consider whether the new evidence would have been capable of being regarded by a reasonable jury as credible and reliable. If the court is so satisfied, it must next consider the cogency of the new evidence. The new evidence must be important evidence of such a kind and quality that it was likely to have been found by a reasonable jury, under proper directions, to have been of material assistance in their consideration of a critical issue that emerged at the trial (Cameron v HM Advocate 1991 JC 251, per Lord Justice-General Emslie at p 262).

[133] At that stage the appeal can succeed only if the court is satisfied that if the jury had heard the new evidence, it would have been bound to acquit; or that the new evidence is of such significance that it is reasonable to conclude that the verdict of the jury, reached in ignorance of its existence, must be regarded as a miscarriage of justice (section 103(3)(a); Cameron v HM Advocate, supra, at pp. 261-262). Since there is a danger that fresh evidence may assume greater strength than it would have had if it had been led at the trial (Gallacher v HM Advocate 1951 JC 38, at p. 47), it is essential that this Court should assess it in the context of the whole evidence led at the trial (Megrahi v HM Advocate 2002 JC 99, at para. 249; c.f. Lyon v HM Advocate 2003 SCCR 692).

[134] These principles are based, in my view, on the assumption that the proposed new evidence, if available to the defence at the trial, would in fact have been led. In this case I am not persuaded that we should make that assumption; but if we are required to make it for the purposes of section 106, it follows, in my view, that we must consider that evidence in its entirety, taking into account those elements that were unfavourable as well as those that were favourable to the appellant."

[87] Reference may also be made to Smith v HM Advocate 2001 SCCR 143. In that case the medical evidence at trial was that the deceased had died from a head injury consistent with his having been kicked on the head while he was lying on the floor. The fresh medical evidence at the appeal was that death had been caused by the deceased being knocked over and the back of his head striking the floor. The Crown accepted that there had been a miscarriage of justice, but submitted that in setting aside the verdict of guilty of murder the Court should substitute a verdict of guilty of culpable homicide. The court held that the conviction must be quashed unless the court was satisfied that, on the basis of all the relevant evidence, a reasonable jury, properly instructed, would have found that the Crown had proved that the appellant was guilty of culpable homicide. At paragraphs 23 to 24 the Court said:

"[23] The contention of the advocate-depute was that, even though the original proceedings had been affected in this way, nevertheless we could simply use the appropriate parts of the evidence as it came out at the trial and supplement that evidence with the facts as now agreed between the parties in the joint minute. If that were done, he said, the court could reach the view that the Crown evidence taken as a whole was such that a reasonable jury would have rejected the defence of self-defence and would have convicted the appellant. In advancing that submission the advocate-depute at one point argued that we should consider the new agreed facts but should take the other evidence frozen into the form in which it emerged at the flawed trial. While it will often - and indeed perhaps usually - be appropriate to proceed in this way, we are satisfied that such an approach would be inappropriate, and would indeed be productive of manifest injustice, in this particular case. That approach presupposes that the area of new evidence, or in this case the area of the new agreed factual basis, can simply be regarded as 'additional' to the rest of the evidence in the case. Here, however, as we have sought to explain, the evidence of Professor Harland and Dr Watson did not form a discrete chapter but, rather, it influenced the way in which other witnesses were examined and cross-examined and indeed played a role in counsel's advice that the appellant should not give evidence. Therefore the new facts do not just add to the evidence led at the trial: they actually replace the medical evidence which lay at its heart. That being so, it would in this particular case be artificial to pretend that justice could be done by testing matters simply on the basis of the other parts of the evidence at the original trial with the addition of the new agreed facts.

[24] In these circumstances, when we ask ourselves whether we are satisfied that a reasonable jury properly directed would have convicted the appellant of culpable homicide, we must reply in the negative since we are unable to say what the evidence before that jury would have been, far less how they might have reacted to it. ... [I]n any trial based on the true medical position the position of self-defence would have been explored against the wholly different background provided by that evidence. That background would indeed have fitted with certain of the points made by the appellant in his voluntary statement and might therefore have led the reasonable jury to take a favourable view of the parts of the statement where the appellant claimed that he had acted in self-defence. We cannot know. But precisely because we cannot know, it is impossible for us to affirm that a reasonable jury properly directed would in any event have convicted the appellant of culpable homicide. That being our conclusion, we must reject the Crown's contention. ..."

The effect of the fresh evidence in this appeal

[88] The Crown concede, as is inevitable, that there is a reasonable explanation why the fresh evidence we have heard was not heard at the original trial. The requirements of section 106(3A) of the 1995 Act are therefore met. Several of the witnesses who gave evidence before us - Dr Fineron, Dr Okely, Professor Busuttil and Dr (now Professor) Flanagan - also gave evidence at the trial, and accordingly fall into the category of persons to whom subsection (3C) applies. It is not in dispute that the requirements of a reasonable explanation and support by independent evidence provided by that subsection and subsection (3D) are met. More generally, and uniquely in our experience, there is no issue about the credibility or reliability of the evidence of the witnesses before us. Applying head (6) of the passage from Megrahi v HM Advocate quoted above, it is not therefore in dispute that the additional evidence is capable of being regarded as credible and reliable by a reasonable jury. The issue before us is whether it is likely to have had a material bearing on, or a material part to play in, the determination by such a jury of a critical issue at the trial.

[89] In considering this issue we have been greatly assisted by the fact that the solicitor advocate for the appellant also appeared for him at the trial, so that his argument was informed throughout by his own direct experience of the course of the trial. This should be standard practice, especially in complex cases, unless there is good reason to the contrary. We do not of course intend by this to criticise the Advocate depute who appeared before us, since the Advocate depute who appeared at the trial has subsequently demitted office.

Submissions for the appellant

[90] The solicitor advocate for the appellant submitted that at the trial the jury was misled in respect of material evidence. He relied on the fact that the two key witnesses for the Crown, Dr Fineron and Dr Okely, had admitted, in light of subsequent developments, that their evidence at the trial was wrong and misled the jury. He also relied on the evidence of Professors Pragst, Forrest and Pounder. The consensus of expert opinion was now that ingestion could not be excluded. There could, he submitted, be no doubt that the preparation and presentation of the defence would have been completely different had the true facts been known at the time of the trial. It was difficult, he submitted, to see how it could be argued that the presentation of the appellant's defence was not prejudiced in the whole circumstances. Everything pointed to there having been a miscarriage of justice.

Submissions for the Crown

[91] The Advocate depute sought to argue that the significance of the fresh evidence had to be assessed in the context of the evidence led and arguments advanced by the Crown and the defence. The starting point was the evidence of Stewart and Espie, who spoke to a special knowledge confession by the appellant. Corroboration was provided by the finding of chloroform in the blood of the deceased and urine on the carpet. The Crown also relied on other facts and circumstances, as set out above at paragraph [18]. Had the fresh evidence, in the form of the correct figure for the concentration of chloroform in the liver, and the presence of chloroform in the stomach contents, been available at the trial, the Crown could have responded by arguing that inhalation and ingestion were not mutually exclusive. Proof of ingestion was incidental to proof of inhalation. The presentation at the trial came to suggest an artificial distinction between ingestion and inhalation. Ingestion, in the sense of drinking, was advanced as a result of the explanation suggested by Dr Flanagan as to the apparently heavy concentration of chloroform in the liver. It did not arise out of any other element of the defence case. No evidence was led suggesting that the deceased actually had ingested chloroform, through the malice of another, or her own state of mind, or propensity on her part. The precise mechanism of death, as opposed to the cause of death, could not be ascertained before or after the fresh evidence had come to light. It could not be said that the fresh evidence was of such significance that it was reasonable to conclude that the verdict of the jury, reached in ignorance of its existence, must be regarded as a miscarriage of justice. The fresh evidence did not impact directly upon the confession in its essentials - the confession to killing the deceased, and that chloroform was used - and did not open up lines of cross-examination of Crown witnesses as to fact. The theory of ingestion was unsupported by any evidence to the effect that the deceased, or anyone else, would drink it, or that the deceased had drunk it. There was no incrimination by the appellant, no evidence was led of proclivity on the part of the deceased to take chloroform and there was no evidence of her feeling suicidal. The trial Judge's charge, in the passage quoted above at paragraph [21], tended to raise the Crown's hurdle higher than it should have been (see Fraser v HM Advocate at paragraphs 107, 174 and 185). The miscalculation of the concentration of chloroform in the deceased's liver provided a line of defence where none had existed before. This miscalculation, and the absence of any analysis of the stomach contents for the presence of chloroform, did not constrain the defence. The defence at the trial were not prevented from relying on any other line of defence, by their adoption of the argument relating to ingestion of chloroform. This position was not contradictory of any other position which was adopted, or which might have been adopted. The consequences of the miscalculation of the concentration of chloroform in the deceased's liver were that the defence were given a basis for an argument which did not exist on the basis of the true figures. An artificial distinction arose between inhalation and ingestion, based on explanations given for the liver concentration figure, which was apparently important given the unnecessary precision with which the Crown had libelled the murder charge on the indictment. Alternatives to the administration of chloroform to the deceased in the manner libelled in the indictment were fanciful and speculative. The fresh evidence of the concentration of chloroform in the liver and the presence of chloroform in the stomach contents would not have assisted the jury to a material extent in their consideration of whether the appellant murdered the deceased, in the context of the other evidence available. It was enough to corroborate the evidence of the special knowledge confession by evidence that chloroform was found in the body of the deceased. In the course of discussion, however, the Advocate depute accepted two things. Firstly, he conceded, that knowing what was now known, the trial would have been conducted entirely differently by both the prosecution and the defence. Secondly, he did not seek to contradict Professor Pounder's opinion that the jury were seriously misled.

Discussion

[92] In our opinion the position of the Crown is untenable. The charge on which the Crown proceeded to trial libelled that the appellant placed chloroform at the deceased's mouth and nose and caused her to inhale it. The efforts of the Crown were directing to proving that averment, among others, and in due course the Advocate depute at the trial invited the jury to hold that averment proved: see the passage from the Advocate depute's speech quoted at paragraph [13] above. The defence did not of course require to prove anything. It was enough for them if the jury entertained a reasonable doubt as to whether the Crown case was proved. They did this in various ways, including the canvassing of the ingestion hypothesis. There was no need for them to explain how or why the deceased might have ingested chloroform. It was enough for them if the ingestion hypothesis raised a reasonable doubt in the minds of the jury as to whether the Crown case, based on inhalation, was proved. It was precisely for that reason that the Advocate depute, in the passage in his speech to the jury quoted at paragraph [19] above, felt obliged to invite them to reject the ingestion "scenario". The defence position was encapsulated in the short passage from the Solicitor Advocate's speech quoted at paragraph [20] above. It was because of these competing positions that the trial Judge directed the jury very clearly, in the passage quoted at paragraph [21] above, on the Crown case based on inhalation and the defence case based on ingestion. In this situation, it is simply not open to the Crown to argue now that it did not matter whether the route by which the chloroform entered the deceased's body was inhalation or ingestion. Had the indictment been so framed as to cover either hypothesis, and had the trial been conducted accordingly, it would have been an entirely different trial from the one which took place.

[93] At the trial, the Crown relied to a large extent on the evidence of Dr Fineron in support of the inhalation hypothesis. The information at that time was that the deceased's blood contained 31mg/l of chloroform on analysis, and that the liver contained 1064mg/kg of chloroform on analysis. Dr Fineron gave evidence that chloroform was corrosive and, if ingested, would have left gross signs such as blackening of the stomach. He also gave evidence that the high liver reading could be accounted for by post mortem redistribution. He rejected the ingestion hypothesis. The fresh evidence that we have heard establishes the following: (1) the figure for the concentration of chloroform in the liver was overstated by a factor of 1000: the true figure was 1.064mg/kg; (2) the stomach contents have been analysed and found to contain 162mg/l of chloroform, and this is consistent with ingestion; (3) Dr Fineron's evidence that chloroform was corrosive and would have left gross signs was erroneous: the signs actually found were consistent with ingestion. His evidence about post mortem redistribution was also erroneous. (The figures for the concentration of chloroform in the liver and in the stomach contents only represent of course the concentration at the time of analysis.)

[94] We entirely agree with Professor Pounder's robust criticism: the presentation at trial of the scientific evidence with respect to the possibility of ingestion was erroneous as a matter of science, carried the flavour of bias when seen in the context of the totality of the scientific evidence, and was seriously misleading on a critical matter for consideration by the jury. The investigations conducted before the trial fell far short of what, on any reasonable view, should have been done. Dr Fineron appears to have regarded it as sufficient that there was, in his view, evidence consistent with the hypothesis of inhalation, without considering any alternative hypothesis, such as ingestion, and the means by which each might, in accordance with basic scientific principles, be tested. It is remarkable that the liver was not analysed for chloroform until after the start of the trial, and then only at Dr Flanagan's suggestion. The calculation was then botched. As a result the reported concentration of 1064mg/kg was dramatically high (and must in itself for that reason have impressed the jury), and pressure of time resulted, not in re-checking the calculation, but in ill-thought-out and erroneous attempts to explain the concentration. It is also remarkable that, despite a suggestion by Dr Flanagan in the course of his evidence at the trial, the stomach contents were not analysed for chloroform until a much later stage. Had the result (which might have been higher at an earlier date) been known at the time of the trial, not one witness would have been able to reject the ingestion hypothesis, as Dr Fineron in particular did in giving evidence. Bad theories were erected on wrong and incomplete facts.

[95] It is accepted by both the solicitor advocate for the appellant and the Advocate depute that had the true state of the facts, as they are now known, been known at the time of the trial then, subject to such opportunity as might have been needed for further investigation, the trial would have been conducted on an entirely different basis by both Crown and defence. It is not our task to decide what the outcome of the trial would have been: in a case such as this, that would involve fruitless speculation. It is enough to say that we are entirely satisfied that the statutory test, read in light of the authorities set out above, has been met in the present case, and that a miscarriage of justice has occurred.

Result

[96] The appeal must accordingly be allowed on the first ground of appeal, and the conviction for murder quashed. In the circumstances it is unnecessary for us to dispose of the second ground of appeal.

[97] We should add that we announced that the appeal was to be allowed, giving brief reasons for doing so, on the date which this Opinion bears. We said that we would issue full reasons at a later date, which we now do. Once we had quashed the conviction, we heard submissions, under reference to sections 118(1)(c) and 119 of the 1995 Act, on the question whether we should grant authority to the Crown to bring a new prosecution. We decided by a majority that in the whole circumstances it was not in the interests of justice that we should grant the Crown application.