Rural Affairs Committee, 05 Oct 1999

Meeting date: Tuesday, October 5, 1999

Official Report 217KB pdf

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Beef on the Bone

Ladies and gentlemen, it is my pleasure to welcome you here today. We have an extensive agenda, which begins with the opportunity to welcome Sir David Carter, the chief medical officer, who will give us the latest evidence on beef on the bone.

We will be delighted to have members of the Health and Community Care Committee with us today. Mary Scanlon has joined us, and it is possible that others will arrive—certainly one other member is expected. Mary Scanlon is welcome to ask questions, and that offer will be extended to other members of that committee.

I invite Sir David Carter to come to the table.

We should consider how the remit of this committee applies to Sir David Carter's evidence, which may be largely based on health issues. It is a matter of respect to the Health and Community Care Committee that members of the Rural Affairs Committee realise that our remit and theirs come up against each other on this. We want to be non-confrontational, and where we stray over our remit, it will be a priority that members of the Health and Community Care Committee should be allowed to comment. We have discussed the remit and are all aware of our position.

I ask Sir David Carter to present the latest evidence on the ban on beef on the bone.

Thank you. I welcome the opportunity to be here today and will be very happy to answer any questions. I am sensitive to the fact that this issue crosses rural affairs and health. It is difficult to deal with one without touching on aspects of the other.

The fact that we are here at all reflects the difficulty that one has to define areas of certainty in the current debate about the beef-on-the-bone ban and the safety of beef in this country. One of our continuing difficulties is that there are still areas in which we do not have hard evidence on which to base advice to Government and Parliament. With every month and year that go by, some of those gaps are being filled in, but it is important to realise that there are still major areas of uncertainty.

I will not rehearse the entire BSE epidemic with you—I realise that you have been briefed and are well aware of the background—but I will touch on one or two salient points. We are all aware that BSE became apparent in 1986. You will be well aware that it rapidly became clear that this was a major epidemic, at the height of which there were 36,000 confirmed cases a year of cattle with BSE. I stress that those are confirmed cases of BSE, and that that number will be an underestimate. It could be argued that Scotland was slower to be affected than other parts of the United Kingdom. It is also clear that the magnitude of the epidemic has been less in Scotland than in other parts of the UK.

About 175,000 cattle with confirmed BSE have been slaughtered. The peak of the epidemic in Great Britain was in 1992. The peak in Scotland was slightly later, in 1993. To nail down a fact, I will say that, as far as we can tell, at the peak of the epidemic in Scotland, the number of affected cattle was 2,208. Since then, there has been a decline in the epidemic, which has been smoother in Scotland than in the rest of Great Britain. In the past few years in Scotland, the number of confirmed cases has gone from 302 to 141 to 85, and the latest figure that we have for this year is 25, but that figure is likely to increase once the final accounting for the year has been done. The epidemic in Scotland is halving year on year.

However, I stress that there has not been a smooth decline in the rest of the UK. In some parts of the UK, there have been years in which the numbers seem almost to have plateaued rather than continued to decline. Why has there been a decline? The main reason is the ban on the feeding of mammalian carcases and protein derived from them to other farm animals and, in particular, to ruminants. That ban was introduced in 1988 but, in retrospect, it is clear that it was never adequately enforced. The date that most people regard as the clean-feed watershed is 1 August 1996.

The evidence this year has been reassuring. The Ministry of Agriculture, Fisheries and Food has looked in great detail at the degree to which the various bans have been enforced. Although there have been some violations—if you wish, we can talk about them later—we can be reassured that the ban on feed derived from mammalian carcases came into effect with vigour on 1 August 1996.

If the ban is effective, why has the BSE epidemic not melted away? As you are well aware, the explanation is that there is a second way in which cattle can get BSE. In the past, most of them got it by eating dead cattle. We now recognise that BSE can also be passed from cow to calf—so-called vertical transmission. The risk of that happening is rated to be about 10 per cent. That is important as it is uncertainty in that area that fuels the uncertainty over whether the beef-on-the-bone ban needs to stay.

I should stress that an additional measure was put in place: from August last year, there was a voluntary cull of any calf whose mother was known to have developed BSE subsequently. With effect from January, that has become compulsory. If a cow develops BSE, or is found to have BSE at the time of slaughter, its calves are culled automatically. I find that reassuring, as it will be a significant step in further eradication of the BSE epidemic in cattle.

I should also point out the importance of the safeguards, over and above that, which are in place. Members will be aware of the ban on specified risk material: brains and spinal cord, for example, are taken out in slaughterhouses. Another key measure has been the introduction of the over-30-months rule, which means that cattle older than 30 months cannot be used for human consumption. Members are probably aware that measures have been introduced recently to increase the confidence with which one can say "That cow is indeed 30 months old". In the past, people have relied on dentition, but the ear-tags scheme and the passport scheme will improve our ability to tell the age of a cow at the time of slaughter.

What is the basis of the over-30-months rule? Why was 30 months selected? Forgive me if I go into a little detail, but I think that it is critical. In a series of so-called pathogenesis experiments, cattle were deliberately infected with BSE by being given the brains of infected cattle to eat. Those cattle were then sacrificed at varying intervals. Material that had been taken from those sacrificed cattle was injected into mice, in a bioassay, and the experiment was continued to discover which mice developed BSE; in other words, which parts of the cattle had been affected by BSE at the time of slaughter.

The infecting dose that is needed for such experiments is 1 g of infected cattle brain—not a huge dose, as it is a very infective disease. I shall inform members of the committee which parts of cows become affected by BSE, and, in turn, become infective. The small intestine becomes infective at six months; the brain and spinal cord become infective at 32 months; clinical signs—when people notice that there is something wrong with a cow, as it is staggering and manifesting the signs of mad cow disease—become apparent at around 35 months.

Recently, evidence became available that suggested that dorsal root ganglion and bone marrow also become infected. Dorsal root ganglion becomes infected at 32 months and bone marrow, in one experiment, became infected at 38 months. I would be happy to enter into details about dorsal root ganglia if members so wish. As the nerves leave and enter the spinal column, there is a swelling on the nerves that is called a dorsal root ganglion. It is an extension of the spinal cord.

I stress that those experimental conditions in which cattle were given BSE-infected material to eat do not necessarily throw the light that could be hoped for on cow-to-calf transmission. We are still not certain what the basis is for cow-to-calf transmission, whether it happens while the calf is still in the womb, at the time of birth, or subsequently. There is no evidence to suggest that milk is responsible, but we still do not know the nature of cow-to-calf transmission. I suggest that, although those pathogenesis experiments are very important, there is still significant uncertainty over the relationship between them and the reality, on the farm, of the transmission of BSE from cow to calf.

Another vital point must be made. I said earlier that those experiments work by injecting bits of sacrificed cattle into mice, then studying the mice to see whether they develop BSE. In doing that, a species barrier is being crossed, and we do not know whether that is a significant barrier; in other words, whether mice are less sensitive to BSE than other cattle would be, were the species barrier not crossed. I hasten to add that experiments that have taken mice out of the loop are now in train—transmission experiments in which the transmission is from cow to cow. However, we still do not have the data from those experiments that would throw light on the issue that we are here to discuss today.

Let me fast-forward to the deliberations of the Spongiform Encephalopathy Advisory Committee, the main committee of experts that advises the Government. The key meeting was that of 2 December 1997, at which SEAC was informed of the infectivity of dorsal root ganglia and bone marrow, and was asked to form a view about how significant a hazard that posed to human health. As the committee is probably aware, SEAC calculated that there was a 95 per cent chance that no case of variant Creutzfeldt-Jakob disease would develop as a consequence of exposure to dorsal root ganglia and bone marrow, and a 5 per cent chance that one case would develop. However, SEAC's range of risk ranged from no cases to 10 cases. Those were cases not of infected cattle, but of human disease. It was that risk estimate that led to the decision to introduce the Beef Bones Regulations, which came into force on 16 December 1997. That is the ban that we are discussing today.

SEAC revisited the issue in November 1998. As on previous occasions, its deliberations were informed by the estimates of a group in Oxford. The Oxford group—of which, I am sure, members have heard—is led by Professor Anderson and is based at the Wellcome Trust Centre for the Epidemiology of Infectious Disease. It is a world-rated group, which is universally regarded as excellent. The Oxford group has been trying to define the effect of the offspring cull on the number of cattle that are incubating BSE and could get into the food chain, because they are younger than 30 months. That is the key information that SEAC has been using.

In November last year, the Oxford group estimated that the total number of cattle incubating BSE that would be slaughtered in 1999 for human consumption was 43. The range of estimate was between 25 and 66. Critically, the number of cattle that might have developed BSE within a year was rated at between one and two, with the range being nought to five.

I should stress again that SEAC was concerned that all the evidence to date had been based on mouse bioassay, and that there was uncertainty about the effects of the species barrier on sensitivity. It is quite possible that some of the other 43 cattle would have a degree of infectivity too low to be detected in the mouse bioassay. Furthermore, with every year that goes by, the groups conducting research in this area are better placed to take back bearings on the information that has become available during the previous year. Looking back, the Oxford group came to the conclusion that its estimates of the previous year had been underestimates. That indicates that there is still a great deal of uncertainty.

SEAC concluded that it was

"still not possible to predict with any degree of precision the risks to human health from dorsal root ganglia and bone marrow".

In fairness, I should say that SEAC was reasonably convinced that the risk would be smaller than it had been a year earlier. I share that conviction, as the risk is undoubtedly diminishing with time. SEAC felt that the risk posed by bone marrow was likely to be very small; I agree with that. It also concluded that the risk posed by dorsal root ganglia was very small—much smaller than it had been at the height of the BSE epidemic, back in 1989 and 1990. I must agree with that, too.

I want to say something about the human version of the condition, variant Creutzfeldt-Jakob's disease. We cannot see BSE in cattle and the beef bones ban in context unless we understand the thinking on new variant Creutzfeldt-Jakob's disease in people. We know that this human form of BSE is caused by the same prion that causes BSE in cattle. There is compelling evidence that there has been transmission from cattle to person by eating infected material.

The disease first became apparent in 1995. It was first reported in 1996. I want to pay tribute to the National CJD Surveillance Unit in Edinburgh: Professor Will and Dr Ironside have been key figures in defining the disease and monitoring its progress. In 1995 there were three cases, then 10 cases in 1996, 10 cases in 1997 and 16 cases in 1998. There have been seven cases so far this year, the total number of cases being 46. All the indications are that we have not seen the last of CJD this year and that the number of cases will increase. We have to wait until next year before we can say with any certainty how many cases occurred this year.

It is important to recognise that there was a significant alarm at the end of last year; of the 16 cases that were reported last year, nine occurred in the last quarter. There was anxiety that we were witnessing a sudden take-off in the epidemic growth curve of variant CJD in people. So far this year, the news is better than we had feared: the number of cases has fallen back to its previous level. However, no one can tell with any certainty the extent of the epidemic in people. We can say that there are a whole host of things that we do not know. We do not know the infecting dose for people, the effect of the species barrier or why some people are more susceptible than others.

Is the disease peculiar to young people? Most people suffering from the disease have been in the 19 to 40 age group; the oldest person was 48 at the time that the disease became manifest. There is an important underlying issue. We still do not understand the incubation period. If a person contracts the disease by eating infected beef, how long is it before the disease becomes apparent?

There are other forms of spongiform encephalopathy. One of those is a disease called kuru, which occurred in Papua New Guinea through cannibalism—eating the brains of dead people. In that situation we can say with some certainty when the index event occurred and we can then define the incubation period. We know that it can be as short as four-and-a-half years, but we also know that it can probably be as long as 40 years. The best estimate at present is that the mean incubation period for such diseases, including BSE and new variant CJD, is of the order of 10 to 15 years.

If one argues that the BSE epidemic began to gather momentum in the late 1980s, peaked in the 1990s and that that was the maximum period of risk, it is clear that there is still some way to go before we reach the peak of the epidemic in people. Current estimates are almost meaningless because we do not have a satisfactory evidence base. Estimates range from a few hundred cases to several million. We simply do not know. It is all very well to say that that the health risk posed by material currently in the food chain is small compared to the one we faced in 1988 to 1999, but we still do not know how large the risk was in that period.

My main message is that the BSE epidemic is subsiding. That delights me, as it should everyone. However, it has not gone away entirely and a significant area of residual uncertainty remains. To my mind, the evidence base is nowhere near secure enough for me to reintroduce a potential health hazard to the human food chain.

I am sure that we will debate the size of the risk. As I said earlier, although the huge wave of risk was posed in the earlier period of the BSE epidemic in cattle, we are not fully out of the woods. With every month that goes by, the evidence base firms up. Another year of statistics on BSE in cattle is almost completed and we are awaiting this year's Oxford estimates, about which there has been a lot of speculation. Oxford is reluctant to give estimates until the data have been worked through. The beef herd in this country has changed its demography. I understand that the estimates from Oxford will be available to SEAC at its meeting on 29 and 30 November.

If we and SEAC have framed our response to the beef-on-the-bone question in relation to those estimates it would be indefensible not to wait for them this year, particularly when uncertainty has surrounded those estimates in the past. I would be reassured if the estimates revealed an absence of BSE in three-year-old cattle in the year 1999-2000. An absence of BSE in four-year-old cattle from mid-2000 would be convincing. However, I hasten to add that the lifting of the beef-on-the-bone ban does not necessarily need to wait until that time.

At the end of August, it seemed to me that the evidence that had been used to frame the ban had not changed significantly, certainly not from the evidence that we had in January and February of this year. I felt that we needed to take account of the data maturing this year, particularly the Oxford estimates.

In this month's debate, nobody has recommended lifting the beef bones ban. It is important to be clear about that. All the chief medical officers in Britain believe that the beef bones ban has to remain in place. All but the chief medical officer in England believe that, until we have further information, the ban on retail sale of beef on the bone should also remain in place—not just because of dorsal root ganglia but because of the anxieties about bone marrow, which is used in stocks, soups, gravy and sauces. Consumer choice is not a relevant factor in dealing with bone marrow in those products.

I apologise if I have gone on longer than you would have liked, but I felt that it was important to outline the evidence base as well as possible.

Thank you very much.

I take this opportunity to welcome Mrs Margaret Smith, Dr Richard Simpson and Mrs Margaret Ewing, who came in at the start of Sir David Carter's speech. For their benefit, I will say that I intend to include all members who are present in the discussion. I will permit members to pursue lines of questioning until they are satisfied that they have got the information that they wanted.

It is only fair that, since Mike Rumbles originally proposed that Sir David Carter come to the committee, he should begin the questioning.

I thank Sir David for coming along today. There has been much controversy about this issue and, while we all recognise that it is a health issue and that Sir David's advice to the Minister for Health and Community Care is essential, the issue impacts directly on rural areas. Many of my constituents have asked me about the latest medical evidence and why the ban cannot be lifted now.

I do not propose to talk about lifting the ban, but you mentioned, Sir David, that there has not been a significant change in the evidence. I want to focus on the word "significant". What change has occurred—in the scientific evidence that is used by you and the chief medical officer in England—that has persuaded your English colleague to change his views while you maintain yours? "Significant" seems to be the key word.

As I see it, the evidence base has not changed. The backdrop of the BSE epidemic is changing as we speak. I have been given evidence, which I find pleasing and reassuring, that the BSE epidemic is declining. In terms of the risk estimates that are posed by bone marrow dorsal root ganglia, the key issue is how many of the cattle that are incubating BSE could pass it on. We have no evidence that is different from what we had in February, when the advice to Government, framed by my colleague in England, was that the ban should remain in place.

So the evidence has not changed; your English colleague has changed his mind?

You would have to ask him that. We are looking at the same evidence base. Neither I nor my colleagues in Wales and Northern Ireland have any evidence that is different from that available to the CMO in England.

The data that I have given are collated on a UK basis, although for the incidence of BSE in cattle they can be broken down and the Scottish figures can be taken out. The figures that I gave for all the other issues are for the UK.

From the statistics that you produced, it strikes me that the problem is much greater south of the border. I am trying to understand the logic. It seems illogical that the CMO for England—where the crisis is bigger—has taken a significantly different view from yours, north of the border where the crisis is not so great.

You are uncovering an important area that I should perhaps have mentioned earlier. It is difficult to think of those things as Scottish or English questions; people cross borders and, more important, meat crosses borders. We will be in a stronger position on knowing the source of each bit of beef that comes into the shops, but we are not there yet. It would be impossible—or at least it would not make much sense—to impose a ban in one part of the UK but lift it in another. We are dealing with a UK context.

I, too, thank the chief medical officer, particularly for the plain way in which he addressed us earlier, which was very easy to understand.

I will continue Mike's line of questioning. As Sir David freely said, there have been 25 cases in Scotland this year. None of those cases has been in the beef herd; every one has been in the dairy herd, none of which—since BSE—gets in to the food chain. Given those facts, and the fact that those 25 cases are from a total of 1,400 or so for the UK, I must continue to ask how the English CMO has reached his conclusion while we cannot.

Sir David mentioned, in his excellent statement, how much more the curve is coming down here and how factors here seem so much more secure.

The answer is the same. I stress again that the Oxford estimates are looking at exactly this issue. It is not just the overall number of cases of BSE in the herd that informs those estimates. The research is examining carefully the demography of the herd and the age spectrum of the cattle concerned. The issue about older versus younger cattle is at the heart of the Oxford estimates. The key issue is what the impact of the offspring cull will be on the risk of cattle under 30 months still being out there incubating BSE, and at risk for human consumption.

I will give members a figure that I did not mention earlier, which is part of the early digest. In Great Britain, 3,670 calves were born between January 1997 and March 1999—they would be still under 30 months old—to dams in the last six months of the incubation period. The cull will have removed an estimated 50 per cent of those cattle, but there remains a significant area of uncertainty.

I return to Alex Fergusson's question, which was essentially, "How can I look at this evidence base and conclude what I have concluded?" My answer is that on the retail sale of beef on the bone, my colleagues in Wales and Northern Ireland come to the same conclusion as I do, whereas my colleague in England comes to a different conclusion—although not about beef bones, as there is still agreement on bone marrow.

Could Scotland go it alone and say that we will lift the ban here because our numbers are much smaller? Nothing would give me greater pleasure than saying that, but the root difficulty is that when people buy beef from the shops, the source of origin cannot be guaranteed, although we are getting into a stronger position as far as that is concerned. I am well aware of the fact that the beef-on-the-bone ban is another layer of difficulty for the beef industry—I am not talking as a chief medical officer but as someone who lives in Scotland.

The best thing that we can do is ensure that beef in Scotland is as wholesome as it can possibly be—that is the best thing that can happen to the beef industry. We are very close to doing that, but I am faced with the difficult question whether I am confident that, by lifting the beef-on-the-bone ban now, we would not reintroduce a significant hazard. I have to say that I do not have that degree of confidence at this moment. The last thing I want to convey is that the matter is decided and that we will not revisit the question. Of course we will—we keep this matter under continual scrutiny.

One of the key events this year will be the Spongiform Encephalopathy Advisory Committee meeting in November. I hope that the committee will receive a new set of data, informed by more reliable estimates from Oxford, set against a firmer backdrop of what is happening with bovine spongiform encephalopathy and the new variant Creutzfeldt-Jakob disease in man. We should not forget that the ban has not yet been in place for two years. If I am to go down in history as the chief medical officer who was criticised, I would rather go down as someone who exercised the precautionary principle for a bit longer than as someone who did something prematurely and unleashed another hazard on the Scottish populace.

I quite understand that response but, in light of the lifting of the beef export ban, my concern is that for some years the general public have had great difficulty believing what politicians say—and politicians rarely agree totally with one another. What worries me now is that our scientists, looking at the same evidence, do not agree. I am worried about the message that that sends out, particularly to potential importers of British beef.

I understand that and I share Alex Fergusson's concern. However, is he asking me whether it would have been better for me to agree with my colleague in England for the sake of uniformity, or whether I should have stuck to what I think is right in terms of framing advice? He would not really ask me that question, as he knows the answer.

, In his report of January this year, Professor Donaldson said:

"It is important to recognise that a decision to lift the ban is a different order of public health intervention than one to put a ban in place."

I think I understand what he is saying. Is he really saying that if we were in this situation without a ban, we would not be thinking of imposing one?

Things have unquestionably got much better in the two years since the ban was imposed. The BSE epidemic is going away and the estimates from Oxford are getting smaller. Things are going in the right direction.

When the CMO in England—as the CMO to Government—framed his advice to the Government, I endorsed the plan in the light of the position that the UK was in during January and February. I endorsed the ban because I agreed with what he said—that it would be a different order of intervention to reintroduce a hazard that we have tried to take out of the human food chain.

I still adhere to that position and I do not think that the evidence base has changed to the significant degree that would allow me to explain to this committee why we should lift the ban now. In February, I thought that it should be retained.

I would love to lift the beef-on-the-bone ban and I would love there to be uniformity throughout the United Kingdom, but I can advise that the ban should be lifted only when I am convinced that we are on firmer ground than we have been on until now.

What statistics are we waiting for? You have said that it will be interesting to see what SEAC says and that you would like all four-year-old cattle to be free of BSE, but that you would not necessarily have to wait until they were to lift the ban.

The main advice to Government on spongiform encephalopathies in general—BSE being one of the diseases in that group—has come from SEAC, which advises not only on the risks posed by beef in the food chain, but on person-to-person risks from those diseases.

Having heeded the advice of SEAC—which is expert in the area—on framing the advice to Government at the end of 1997, and on reassessment at the end of 1998, it seems to me that we should at least hear what it has to say at the end of 1999. We know that what it will say will be informed by the estimates from Oxford, which are based on the most recent assessment of the demography of the beef herd throughout the UK and of the risks that are posed.

I could be sitting here in a different scenario—the committee could be asking how, when I have listened to SEAC's advice until now, can it be possible that I am now not listening to it. SEAC says that it is still not possible to predict with any degree of precision the risk to public health, so the committee could be asking me why I am advocating a lifting of the ban before the most current advice is available.

SEAC will not get you or us off that hook.

No, it will not.

SEAC's original report did not say that there should be a ban on beef on the bone—it offered three recommendations of which that was only one, but which the Government chose to accept.

What will happen in November? Will you still have to make a decision?

Yes. This is a very difficult set of circumstances. I started by saying that no one finds this easy. We can open up this discussion now, when there is still uncertainty, because the evidence base is hardening.

This is not an open-and-shut case. That will be a continuing source of difficulty for me, but that is part of my task. I must inform Government what I consider to be the health hazards posed by this set of circumstances. I must again try to frame a view based on the evidence that becomes available at the end of this year.

It seems that the bone marrow results were significant in leading to the ban, but those results were the product of one experiment, or one set of experiments.

How confident are you in the results of that experiment? Could there have been experimental error? Is that being revisited?

It is one set of results, and a number of people said that it could be a rogue result. They asked whether bone marrow suddenly becomes infected at 38 months. I said that dorsal root ganglia are infected at 32 months and that infection can occur at other points in the chain. There is stronger evidence in those experiments of dorsal root ganglia being infected. I do not, however, think that that can be swept aside. Because of the uncertainties that I mentioned a few minutes ago, all of the experiments are small-number. They have all involved mouse bioassay. We are still uncertain of the sensitivity of the experiments.

If you are asking me if there are any other bits of information that you would like, one of them is the results of the cow-to-cow experiments that are currently running. We are beginning to get results now.

You are right: much hinges on the extent to which bone marrow is truly infected. You cannot ignore, however, the fact that infectivity has been demonstrated. It is a hard call, but you cannot say that you like this bit of evidence but will ignore that bit. I think that we need more evidence—and we are in the process of getting it.

I wish to be clear that one of the problems that you have in wrestling with this difficulty is that we do not know the threshold for the dose infectivity, and that we do not know what reinforcing effect even a small amount of additional prion intake might have on individuals. Are we any closer to understanding that from our knowledge of kuru? Is there anything else that might give us clues on that?

Again, that is a good line of evidence to pursue: there is evidence from acquired Creutzfeldt-Jakob disease and, in particular, from iatrogenic Creutzfeldt-Jakob disease. That refers to cases in which the disease has been transmitted to people through medical procedures. We all know that human growth hormone was infected in the earlier years, and that that transmitted infection from person to person. The evidence suggests that that had a cumulative effect. Nobody knows for sure what the titre of the infecting dose is.

I was stressing, perhaps before you joined us, Dr Simpson, that the infecting dose in cattle is as small as 1 g. It may be much smaller for humans: there may be many doses in that 1 g. I was also making the point that the evidence based on people is still nowhere near firm enough. We do not know what the route of transmission is, although we are beginning to suspect what it is. We are not exactly clear about the circumstances under which some people get the disease and others do not. We do not know if children are more susceptible. However, the fact that this epidemic is affecting young people has to give you cause for thought.

Those questions are part of a raft of intangibles that we do not have the answer to. We have to underline the precautionary principle in all of this. Because there are so many areas of uncertainty, we have to be on firmer ground than we are on at present.

Is it also clear now that the only remaining transmission method is cow-to-calf, or has that not yet been fully determined?

That touches on a vital issue. We eat sheep but do not seem to suffer any adverse consequences from scrapie, which is a disease similar to BSE and has been running for 250 years. Scrapie does not seem to cross the species barrier from sheep to people, but we know that if some scrapie sheep are taken off an area of pasture and a scrapie-free flock are put on that pasture three years later, they will get scrapie.

The evidence that I have for the horizontal transmission of BSE in cattle is extremely reassuring: a number of herds were heavily infected by BSE, with more than 50 cases of infection in the early part of the epidemic. Since the feed ban was introduced, there has been no more BSE in those herds. I think that the evidence is persuasive that there is not a third method of spreading BSE from cattle to cattle.

My reading of the BSE epidemic is that the food ban has bitten. It is now being enforced, and we can see the epidemic tailing away. The residual uncertainty is the maternal-to-calf transmission. That is what the Oxford data are all about. I am sorry that my answer was a rambling one, but it is no: we are not aware of any other transmission method.

That was very helpful. Thank you.

It appears to be clear from the figures that you quoted that we are—we hope—approaching the tail-end of BSE infectivity.

Towards the end of your presentation, you said that the risk is diminishing with time. Is it your expectation that BSE infectivity is likely to cease in a short time?

Yes, it is, and we will all be extremely delighted when that happens: I do not need to go on about that.

Returning to the point that Mr Morgan raised, the interest in what will happen to three-year-old cattle in 1999 and four-year-old cattle in 2000 is not idle speculation. That will be the crunch time as far as the demise of the BSE epidemic is concerned. Once we get rid of BSE, all this discussion will be unnecessary: we will be able to eat whatever we want because BSE will not be in the beef herd. However, we are not quite at that stage.

My position is that just when we are within sight of eliminating the BSE epidemic in cattle, it would be tragic if we allowed any more cases of variant CJD to develop in people. Having got rid of the pool of infectivity in beef cattle, we must do everything we can to ensure that we do not have a pool of infectivity in people.

I wish to pursue that point. What you said with regard to the incubation period of CJD suggested that we are still on the upward slope of CJD infectivity. In your estimation, is it logical to assume that the figure of seven cases for this year so far—if it is not a statistical blip—is likely to increase before the year's figures are complete, and that, given the incubation periods, we should realistically expect a larger number of cases in the coming three or four years?

I agree with that, and it grieves me to say so. Like most people who study the figures regularly, I was deeply concerned by the sudden surge of nine cases in the last quarter of last year. The fact that the number has fallen to only seven cases this year—if I may use only, because any case of new variant CJD is a tragedy—does not mean that we should be complacent. That number does not signify to me that the number of cases is tailing off. All that we know about the incubation periods of these types of diseases—not just kuru, but acquired CJD in people—suggests that the mean incubation period will be 10 years or more. If the height of infectivity was in the earlier years of the BSE epidemic in cattle, and that must be the prediction, we are going to see, sadly, many more cases of variant CJD in people.

I wish to ask a supplementary on that point. You quoted numbers of three, 10, 10, 16 and seven, with regard to new variant CJD. Are those the numbers of deaths, post mortem findings or early diagnoses?

The CJD surveillance unit operates a strict policy—rightly—of releasing the figures only upon absolute confirmation of the diagnosis. Those figures relate to people who have died.

There is a lot of concern about whether we can develop a test for BSE in live cattle. Hopefully, very shortly we will not need one, because there will be no BSE in cattle. The emphasis now is on developing a test for variant CJD in people. At present, the only test that is available is to examine nervous tissue, which essentially means a post mortem diagnosis, although there is evidence that biopsy of the tonsil is a means of detecting prion. Whether that tells one about the patient having CJD is another question.

At present, we do not have a totally reliable test for the diagnosis of variant CJD in life. If we did—this would be relevant to the Health and Community Care Committee—it would throw what we are doing, and what we will have to do with regard to variant CJD in people, into a more rational perspective.

Mike Rumbles has asked me if you can confirm that the figures for CJD that you quoted were UK rather than Scottish figures?

They were UK figures. Rightly, the CJD surveillance unit does not break down the figures. Until now, when there was a relatively small number of cases, there was a desire to respect confidentiality and not to have people speculating about what was going on in specific neighbourhoods. Although we do not get a breakdown by region of the United Kingdom, we should not assume that Scotland is immune to this disease. We know that it is not. Neither do I have any evidence that it is particularly prevalent in Scotland.

I have not seen a breakdown of figures by region of the UK, because there is not such a breakdown. We have had cases in Scotland.

I have one final point. You mentioned the danger of a pool of CJD infectivity and spoke about the risks of person-to-person infection. Does that mean that once this issue has ceased to be of concern to the beef industry, because BSE has ceased to exist, it will continue as a health problem through infectivity in the human population?

There is no question about that.

I thank the Rural Affairs Committee for allowing members of the Health and Community Care Committee to come today. I am grateful for the opportunity to ask this question. What genuine scientific evidence is there—or was there ever—to justify the continuation of the requirement to split ewe carcases in order to remove the spinal column? That has resulted in the destruction of the lucrative trade in surplus UK ewes to France and other European countries.

I was not prepared for that question. As I recall, the evidence is that there is no question that scrapie in sheep is a disease that affects the central nervous system, brain and spinal column. The difficulty was that there was, and still is, considerable speculation about whether BSE in cattle arose because they were eating the brain, spinal column and nerve material of sheep—that somehow the prion protein had been changed in its transit from sheep and had given rise to BSE in cattle.

Conversely, there was anxiety that BSE would affect the sheep flock through the same circular process. If that were the case, there would have been no logic in ensuring that sheep brain was not available in the food chain without ensuring that the spinal cord was also not in the food chain. Brain would have been a major health hazard, and we know that spinal cord is just as infective as brain. That was the reasoning.

Do you still feel that that reasoning is justified?

As long as the uncertainty persists. The years that have gone by since that requirement was introduced have given reassurance in that we are still talking about scrapie in sheep, not about BSE affecting the sheep flock. If we were talking about BSE in sheep, we would be having a much more sombre discussion today. The years that have gone by have suggested that there has not been back transmission of BSE to sheep. That will come up for scrutiny, as all those issues will. When we get to the point of lifting the beef-on-the-bone ban, a series of hurdles will be taken down in the process. All these matters will be subject to reappraisal.

I have some figures, which I dare say most people have, from the National Farmers Union. I was alarmed to learn that, this year, there are 25 cases of BSE in Scotland and 44 in the Republic of Ireland. Does it concern you that the ban does not apply to other countries, where—according to the figures—there is a greater risk?

I would certainly want to watch with great care what is happening in other parts of the EU—not just Ireland. There is a significant amount of BSE in Portugal; you will have seen the European Commission response to that recently. We are aware that there has been a significant problem in Switzerland. There is greater uncertainty about the magnitude of the problem in other parts of the EU.

If you are asking me whether I am concerned to ensure that we eliminate a hazard from the human food chain, the answer is undoubtedly yes. I would be concerned about any countries with incidence of BSE whose meat may be being imported into this country. I am anxious to ensure that we do whatever we can to minimise the risk to human health. This takes us back to the border question. Until now, we have been talking about the border within the UK, rather than the border with the European Union.

We have discussed the differences between you and the chief medical officer in England. Are you satisfied that your counterparts in other European countries are analysing the scientific evidence as rigorously as we in this country are?

I would like to think so. We have faced up to the BSE crisis in a big way. We had no alternative; we had to take it seriously. We are still doing so, and that is the right position. Some people would argue that, because of the concern, British beef must be safer than beef from elsewhere in the EU. That is a legitimate argument. However, the relative position is of no great consequence to me as long as I remain concerned that there is a risk to human health in this country.

You mentioned that there was no regional breakdown of CJD cases in Scotland. That surprises me, given that it is central to the problem. Why is there no such breakdown?

It is for the reasons that I outlined earlier. While the epidemic was still very small, there was a desire to respect confidentiality and families' sensitivity. The National CJD Surveillance Unit has not been putting cases into the public arena. The agreement has been that whenever someone dies with confirmed variant Creutzfeldt-Jakob disease that will be announced.

We have concentrated on variant CJD, but that is only one form of Creutzfeldt-Jakob disease that affects people. Figures for cases of classical CJD have been made available. However, until now CJD has been rare; the incidence of classical CJD stands at about one in a million people. That is another reason to be nervous about breaking down the figures. We do not want people reading something into the fact that there are five cases in one place as opposed to seven in another, when we do not have a database big enough to allow us to make any sense of such differences.

My main question concerns comparative risks. Many people who favour lifting the ban say that we run more risk of, for example, having our health damaged by passive smoking, which is legal at the moment. To what extent do you take into account comparative risks when making your recommendations? How does the risk from BSE compare with other public health risks?

That is a legitimate line of questioning. I am grateful for the indication that the comparison with passive smoking was one that might be offered to me this afternoon, as it has allowed me to do some homework.

If you are asking whether I am concerned about passive smoking, the answer is that I most certainly am. I am pleased that the Health and Community Care Committee has identified smoking as one of its main priorities. Let me provide the committee with a sense of the problem. In this country, a mother who smokes has a 9.8 per cent chance of having a low-birth-weight baby. If she does not smoke, the figure is 4.3 per cent. If proof were needed, that is how early passive smoking starts damaging people. On our best estimates, around 17,000 children under five in the UK are admitted to hospital each year with lung disease, asthma, glue ear and diseases that are attributable to some degree to passive smoking.

You know as well as I do that we are losing the battle in terms of women smoking. The latest figures for deaths from lung cancer in Scotland are 2,747 men and 1,474 women. If one works on the premise that 90 per cent of those deaths are directly attributable to the fact that the person smoked, one is left with a question mark about the other 10 per cent. Some of them may be nothing to do with passive smoking, but the Government white paper "Smoking Kills" puts the risk estimate from passive smoking at something like several hundred cases a year in the UK. It is a huge problem.

I resist any notion to say, "There is the risk of passive smoking. What are you getting concerned about beef on the bone for?" We are still in the threshold phase. For all we know, we are in the foothills of an epidemic of new variant CJD in people. If the bad end of the predictions comes into play, who is going to choose between risks?

I do not see this as an either/or situation. You may have seen the publicity that surrounded the release of my annual report this year. One of the major lines of questioning was, what is all this about cancer? What is happening to lung cancer in this country? We are now firmly in health committee territory. That will be a major area for debate.

I would not like to say that one risk is this big and another is smaller. We know now that passive smoking is a serious risk, while smoking is unquestionably a serious risk. We still have some way to go before we know with certainty how new variant Creutzfeldt-Jakob disease equates to those risks.

I am puzzled about the relevance of the number of cases of new variant CJD. We all know how tragic that is, but I wonder how relevant it is to your decision about when the ban will be lifted. There is the possibility that that number may peak some years hence. We do not know when that will be. Does that mean that there has to be a total elimination of BSE before you say that we can lift the beef-on-the-bone ban? What you have said is that you do not know how little BSE you need to generate X number of cases of new variant CJD.

You are absolutely right. I am not saying that we have to wait until we have seen what happens to new variant CJD in people before we lift the beef-on-the-bone ban. As I said a number of times, each month and each year that goes by gives us a better sense of what these epidemics are doing—it is an informative backdrop to the decisions that we are trying to frame about the immediate issue, which is the beef-on-the-bone ban. While it is an interesting backdrop, in the foreground, if you like, are the firm estimates of what is happening to BSE in cattle and what we know about the impact of the offspring cull on cattle under 30 months that are eligible for slaughter for human consumption. We need more information on that.

Sir David, I was very impressed with your presentation. I listened with bated breath to everything you said, until you started talking about smoking and then I began to drift. You mentioned the statistics and the incidence of BSE recorded over the past few years. You said that last year the incidence of BSE peaked towards the latter quarter of the year. In your opinion, does that have any significance in terms of the fact that most cattle are sold through the mart in the last quarter of the year?

We are slightly at cross-purposes; I may have expressed myself badly. The human form of BSE, new variant Creutzfeldt-Jakob disease, showed a peak last year. That is not directly attributable to anything that has happened with cattle recently. The surge merely reinforces the fact that we should be cautious about making far-reaching predictions based on small data sets. Arguably, the imposition or otherwise of the beef ban would have been irrelevant to the cases of new variant Creutzfeldt-Jakob disease that we are dealing with now. Everything that we know about the disease's incubation period tells us that the people who are suffering now contracted the disease ten years ago.

It is clear that the SEAC meeting and the Oxford report will be important to an assessment of the research information. I would be interested to learn more about the research that is being done; for instance, whether it is purely statistical. You mentioned information coming in from mouse bioassays and attempts to set up a cow bioassay. Presumably, that work will continue after BSE ceases to be a problem. Is there any evidence that the infective agents could affect another species?

The Oxford group is provided with data on the demography—the age structure—of the beef herd, set against which it has data on the latest culls. In addition, it has the information that has become available about the confirmation of BSE in cattle that are slaughtered. One of the things that has reassured me in the past year is that people have examined cattle that were slaughtered as part of the over-30-months scheme and have found only a small number of cattle—perhaps only 0.3 per cent—in which BSE was present but was not manifest in life.

That is the sort of information that Oxford is using in its model. Like all such models, it is fragile and is only as good as the estimates that are fed into it. Each year, we get a back bearing: Oxford looks at what it predicted for the previous year in the light of what happened and finds out if it was right or wrong. I made the point in my presentation that Oxford feels that it underestimated the number of cattle that carry the disease.

To nail down the cattle to cattle thing, it is now easier to do pathogenesis experiments because we do not have to rely on a bioassay. In the past, cattle had to be killed and material from their organs inoculated into mice. It took a year after that to see any results. Now, the same thing can be achieved with histopathology.

You asked about the implications of all that for the broader biology. We now know that there are transmissible spongiform encephalopathies other than BSE and scrapie. We know that quite exotic animals such as kudu suffer from such diseases. We know that cats can also suffer from spongiform encephalopathy.

Ever since Creutzfeldt and Jakob first described the disease in the 1920s, we have known that we have a sporadic form of CJD in the human population. The disease might have been present for millennia, but it was rare; it only came through one time in a million. The incidence of CJD in people may well fall back to that level. That is why the discussion is important. We must ask whether we have magnified something over the last 10 to 15 years, to make it suddenly not such a rare disease.

It is reassuring to note that, if we take the overall incidence of all forms of Creutzfeldt-Jakob disease, we are still not radically out of line with other countries, even allowing for the fact that there have been around 10 cases a year of the new variant CJD. We will have to wait and see.

The new techniques that enable the determination of the existence of the prions in cattle without having to go through the mouse bioassay are a welcome development. I presume that those techniques will allow the results of the research to be reached and interpreted much faster.

You are absolutely right. Watching the experiments evolve has been painfully laborious. Anything that speeds up the process makes a huge difference. However, we still do not have a blood test, or some other less invasive test, for CJD in people who are still alive.

Have we come to the point at which there are no more questions?

I want to ask Sir David about the over-30-months scheme, which he mentioned several times. Last January, we reached a point when any cattle entering the food chain would have been born and reared in a post-BSE regulatory period. Given the fact that it is eight months since we passed that point, do you see a time approaching when you might be able to recommend extending the 30-months scheme to 32 or 33 months? That would be hugely beneficial to those farming Scottish natural breeds, in which the cases of BSE have been almost infinitesimal.

If one assumes that the clean-feed watershed was 1 August 1996, we are now 30 months beyond that. We are reasonably sure—we have evidence from various surveys conducted in the last two years—that the bans are being enforced and so we can be secure in the knowledge that cattle are no longer contracting BSE because we are feeding them infected material. That is great.

The figure of 30 months was not quite empirical, but was plucked out of the air in the light of the experimental data that I went over earlier. There is a margin of error. As more time goes by and as more information becomes available, we will be able to make non-empirical judgments about such matters. I would predict that the 30-months scheme is one of the only things that will be considered and we are not a million miles away from that.

No one has tried to nail me down by saying, "If this happens, will you say that we can do that on 1 December?" You have given me that leeway, but I am sure that you recognise the difficulty. I would love to see the beef-on-the-bone ban revoked, but that will not be the victory that everyone wants. It is one skirmish in a much bigger campaign to get our entire beef industry back on a secure footing.

This is gratuitous and perhaps I should not say it: I have not had any hate mail over the beef-on-the-bone ban. [Laughter.] I may get some now. It has been very salutary to me. Most people recognise that the big prize is to get back to a wholesome industry in which all the ifs, buts and maybes become immaterial.

I want to try and nail you down ever so slightly. You have used phrases such as "we are not a million miles away" and "early". You said earlier that relatives are of little consequence compared to absolutes. I suspect that that is the case for the farming community. Early can mean a lot of things. Have you any idea when we can seriously examine with any reasonable prospect of success the possibility of an extension or a lifting of the over-30-months slaughter scheme?

I think that we are discussing that seriously this afternoon. We are taking a view based on the current evidence and we are expressing the expectation that all those things will be reviewed in a rolling programme.

I would prefer to take this one step at a time and it would be facile of me to say that I think that by, for example, 2 February, we will have lifted this and that by 9 March we will have done that. The only thing that members could be sure of is that I would be wrong. We must take the situation as it comes, so I cannot be drawn into answering such questions.

Have members had all their questions answered at this point? As that is the case, on behalf of the Rural Affairs Committee and those members of the Health and Community Care Committee who have joined us today, I will take this opportunity to express our gratitude to the chief medical officer for Scotland for coming along and exposing himself to our questions, which could—let's face it—have gone anywhere.

I would also like to thank him for the understanding he has given us of the medical evidence relating to the beef-on-the-bone issue in Scotland. It is an issue that this Parliament is very concerned about, and one in which it is essential that we progress with full knowledge of the medical evidence.

I thank you for your contribution, Sir David, and I hope that you have enjoyed the experience. I look forward to the next time that we can act as your host.

This will be gratuitous and I know that I should not say it, but I have enjoyed this afternoon very much indeed. I am grateful to you, convener, and to the committee for the measured way in which business has been conducted.

I take great heart from that and, as I said, it has been a pleasure for me to appear here. I am delighted that we can share the evidence base. We may disagree about bits of it, but this seems to me to be a very good way of doing business. I am very grateful to the committee.

I propose that we suspend the committee for five minutes so that those who wish to leave can do so.

Meeting suspended.

On resuming—

We have an apology from Mike Rumbles, who has been called back to his office and asked us to start without him. He hopes to be back as soon as possible, as does Lewis Macdonald, who I understand is currently being interviewed outside.