The Safety Of Gelatin, Its
Production, & Mad Cow/vCJD
Prion Theory
By Roland Heynke, Germany <>
Gelatin Without BSE-Infectivity can ONLY be produced from healthy animals
The agents of scrapie and BSE are extremely resistant to physical and chemical influences. Compared with the conditions during gelatin production, in experiments they withstood an acidity, which was ten times as high, an alkaline concentration twenty times as high and a drying temperature that was about 220°C higher. As the procedures of gelatin production can not be tightened up without significant losses of yield and quality, gelatin can only be produced safely from healthy animals. In order to get a reliable test for the agent in man, animal, and raw material, it has to be shown, whether the altered prion protein is identical with the agent. Therefore a simple experiment has been proposed, by which the prion theory can be proved or refuted within a few days.
Gelatin is everywhere
Gelatin is a primary product with an extraordinary wide field of application, used for quality improvement of innumerable foodstuffs and medicaments. It serves for supplementary source of protein, carrier material, bonding agent, stabiliser and emulsifier. It is also used as an aid for frothing up, flavour enhancement, common salt replacement, clearing of drinks and as a collagen source for dietetics.
It can be found in jelly, jellied meat and aspic, in ice cream, some margarines, sweets like gummy bears, soft caramels, marshmallows, meringues, liquorice and cream-filled chocolate cakes, in gateau fillings and desserts, in milk products like yoghurt and crmes as well as in pies and convenience food. Cream and foam are often made of jelly with beaten egg white, whipped cream or cream cheese.
Quality-tested wines, cider, apple juice and in some countries also beer, are freed from blurrings, tannin agent and bitter constituents with the help of gelatin. From fizzy drinks it is not removed at all. In milk-shakes with fruit or vegetable additives gelatin prevents the milk from curdling. Vegetable juices are thickened with gelatin and enriched with vitamins and minerals. In tinned meat gelatin binds the meat juice. In some cases salami and pepper sausage are protected from drying up by gelatin.
The pharmaceutical industries use gelatin in soft and hard medicament capsules, for binding in tablets and dragees, in form of sponges for treating wounds and as a colloid to expand the plasma after severe losses of blood. They are also included in vitamin compounds and cosmetics. People having problems with their nail growth or with their joints and cartilage are treated with gelatin. Animal food industries sometimes use gelatin in substitute milk products for calves.
As gelatin is so omnipresent, nobody in the industrial nations can avoid its assimilation. Therefore even vegetarians have to doubt whether the production of gelatin from slaughter wastes of pigs and cattle totally removes BSE infectivity.
BSE safety disputed
The World Health Organization writes in its data sheet 113 and in the report WHO/EMC/DIS/96.147 about the conference on April, 2 and 3 1996 in Geneva they held together with the FAO and the OIE (Office International des Epizooties) on human and outher transmissible spongiform Encephalopathies: "Gelatin in the food chain is considered to be safe if produced by a manufactoring process utilizing production conditions which has been demonstrated to significantly inactivate any residual infectiviy". This is as true as it is trivial. Unfortunately there is no sensitive test for low titers of infectivity, so that this condition can not be fulfilled. The reasons are the short lifespan of rodent recipients and the necessity to overcome the species barrier between cattle and rodents.
The Press Release WHO/28 - 3 April 1996 (Rev.1 15 April 1996) garbles this insignificant but true assessment to a misleading and scientifically untenable contention: "Gelatin is considered safe for human consumption since its preparation involves a chemical extraction process that destroys BSE infectivity". BSE-infectiousness is also destroyed during cooking and baking, but nevertheless anyone with a bit of sense would not eat the cooked brain from a cow which died of BSE. This attitude is especially questionable, as WHO knew about a scottish study which had been ordered by the European gelatin industries in Scotland in 1993. A scaled-down simulation of the acid and the lime treatment, the two chemical key stages in the manufacturing process of gelatin, did not reveal any reduction of scrapie infectivity.
Likewise in the report WHO/EMC/DIS/96.147 it is explicitly pointed out, that parts of cattle destined for the pharmaceutical industries should only be bought from practically BSE-free countries. The reason is the fact that the applicable inactivating procedures can only reduce the risk of infection with the BSE agent, which is extremely resistant to physical and chemical influences. The European Agency for the Evaluation of Medical Products in London decided, that gelatin for medicaments should not come from cattle slaughtered in Britain.
British slaughter wastes contain considerable amounts of infectivity and there is no manufactoring process utilizing production conditions which has been demonstrated to significantly inactivate any residual infectiviy. Nvertheless EU-commissioner Franz Fischler pushed through a lifting of the export ban for British gelatin, on condition that it is produced according to the procedure applied by the German gelatin factories Stoess AG [6]. Therefore it is interesting to compare the conditions of this procedure with those of the experiments, which the agents have demonstrably withstood.
The raw material in gelatin production
About 65 % of the world-wide produced gelatin comes from hidesplits, connective tissue and the bones of cattle [6]. Otherwise pigs serve for source material [6]. Only in Australia, South Africa and New Zealand also sheep are used [6]. The quality of the gelatin is influenced by the source of supply, which in Europe traditionally is mainly from pigs in the case of gelatin for food and medicaments [6].
There is such a huge demand of raw material, that a limitation to very young or especially natural living animals is not possible [6]. But at least in Germany only slaughter wastes from animals, which are released for human consumption, are used for the production of gelatin for food and medicaments. Because however, up to now BSE can only be diagnosed very lately, most of the infected animals are not identified. Thus the veterinarian's check-up before slaughtering does not provide a remarkable protection against BSE and scrapie.
It is obvious, that hidesplits, connective tissues and bones of BSE-infected animals are far less infectious than the central nervous system. But as long as the agents are not definitely identified and not detectable by any sensitive test, not any tissue and body liquid can seriously be declared free of infectivity. Skin and bones from infected animals must also be supposed to be infectious, because they are well supplied with blood and nerves. The infectivity of blood has been demonstrated as early as 1962 with a goat [5] and among others in 1992 with human beings [7]. That this did not work with cattle until now, is due to the very low sensitivity of the common functional test and absolutely insufficient efforts made in this concern.
The 10-15 kg raw material from one cow disappear in production batchs of 20,000 to 100,000 kg. It is then diluted with other gelatin about the factor 10-100 to achieve the final products [6]. Thus the agent is certainly diluted to a great extent, but at the same time it is distributed to a very large number of end products.
The infectivity withstands acidulation and alkaline treatment
Bones are splintered into pieces of less than 12 mm diameter. Their fat content becomes reduced to below 2% with hot water and then they are dried for a minimum of 30 minutes at a temperature of well over 100°C [6]. This procedure removes much of the infectiousness of the raw material, but certainly not all of it.
The cleaned pieces of bone are freed from phosphate minerals with 4% hydrochloric acid, at a pH below 1.5, so that only the collagen structure remains [6]. This procedure takes five days, but begins with an already used, more diluted hydrochloric acid, which becomes replaced by a fresh one only toward the end of the treatment [6]. The finally reached pH 1.5 corresponds to a concentration of less than 0.1 M hydrochloric acid. Unfortunately, the effect of this long-lasting treatment with a weak acid on the BSE agent has never been published yet. According to one publication however, the effect of acids in contrast to strong caustic solutions seems to be only temporary [3]. In an experiment the treatment with 1 M hydrochloric acid turned out to be insufficient [2]. This indicates, that the acid treatment during the gelatin production is quite probably not adequate to inactivate the agent.
More than 90 % of the gelatin won from cattle receives an additional treatment. It normally takes about 50 days with pH higher than 12.5 to open cross connections between the collagen molecules [6]. Even a pH 13 corresponds to a sodium hydroxide concentration of only 0.1 M. Sometimes the incubation time is being shortened from 50 to 14 days by increasing the concentration up to 0.3 M (6(. As the infectivity is not fully inactivated by 2 M sodium hydroxide (8(, this lime treatment cannot be considered to be safe. The non published scottish study which had been ordered by the European gelatin industries demonstrated no measurable reduction of scrapie infectivity after days of treatment with acid or lime (personal communication(. Furthermore the lime treatment is only applied for raw material from cattle (6(. The delicate skin of young pigs is not treated with the caustic solution. For them an acid treatment during one day is sufficient. The effect on BSE agents however is comparable to the demineralization of bones.
Heat resistence of the infectious agent
After having been extracted step by step with water of increasing temperature, the gelatin is sterilized at 140°C for 4 seconds. Of course, also this treatment is not suitable to fully inactivate the BSE-agent. This was demonstrated by an experiment, in which brain samples with an average weight of 340 g were autoclaved during 1 hour at 134°C or for at least 18 minutes at temperatures of 135oC or 134-138oC. This was not sufficient either to inactivate scrapie- and BSE agents. So 14 out of 22 mice fell ill from the brain of hamsters which had been autoclaved during 1 hour at 134oC. Hamster brain that had been autoclaved at 134-138oC during 18 minutes, killed all of 19 mice. It is interesting that a longer period of time of autoclaving does not result in a more efficient inactivation. Although autoclaving reduced the infectiousness by 7 orders of magnitude, it was still fit for lethal infections. Drying material is even more difficult to sterilise. Amylid fibrils from scrapie-infected brains of hamsters remained infectious after autoclaving and partially even after one hour at 360°C (1(.
Total inactivation impossible
On the whole the procedures used for gelatin production certainly are suited to reduce the infectiousness of BSE-contaminated raw material. But it is just as certain, that hereby a complete inactivation is not possible.
There is not any indication that a minimun dose is required for the transmission of BSE to other species. On the contrary, the characteristic stability of the agent and the defenselessness of the immune system seem to indicate, that extremely small doses up to only one single molecule could be enough for an infection. On the other hand, from all the cattle that got infected foodstuff and the thousands of recipients of infectious growth hormone, only comparatively few fell ill. Thus there must be an individually different, but unknown lethal dose. Not mortally infected human beings and animals can nethertheless represent sources of infection. Therefore it is important to distinguish lethal from sublethal infections, and at the same time the non-mortal infections have to be recognized much more as a problem.
Open questions
From the scientific pont of view it is surprising, that until now there has been published no simulation of the gelatin manufacturing process with highly infectious material. This would be necessary to calculate the degree of agent inactivation. To detect even very low levels of infectivity, we need a for example immunologic system, that directly marks the agent instead of functional tests with the injection of test material into the brains of mice. Beforehand however, the agent has to be identified. Therfore scientists have been searching for a scrapie virus since decades. This approach was without success and by combining available facts, the virus-theory can already be excluded [4].
Proof or disproof of the prion theory
If the prion theory was right, we would already know quite a lot about the agents and we could immediately detect them with available antibody-tests. Unfortunately this already fairly old theory has not been proved or refuted despite of numerous attempts. However, this could be done within a few days, with an experiment, which in principle has been published repeatedly. It only has to be carried out and analyzed somewhat more sophisticated. Therefore one has to mix radioactively labelled prion proteins with infectious material in a test tube and to record the increase of amount of protease resistant and labelled prion protein. According to the virus-hypothesis this increase would be at most linear, because only driven by the added infectious material, which could not reproduce. In accordance with the prion-theory the newly transformed prion protein would contribute to conversion of the rest. In that case an accelerating increase of the protease resistant and radioactive prion protein could be observed, until the reserves of normal prion protein will run out.
Reference list:
1) Brown,P.; Liberski,P.P.; Wolff,A.; Gajdusek,D.C. - Resistance of scrapie infectivity to steam autoclaving after formaldehyde fixation and limited survival after ashing at 360 degrees C: practical and theoretical implications. - Journal of Infectious Diseases 1990 Mar; 161(3): 467-72 2) Brown,P.; Rohwer,R.G.; Gajdusek,D.C. - Newer data on the inactivation of scrapie virus or Creutzfeldt-Jakob disease virus in brain tissue - Journal of Infectious Diseases 1986 Jun; 153(6): 1145-8 3) Gasset,M.; Baldwin,M.A.; Fletterick,R.J.; Prusiner,S.B. - Perturbation of the secondary structure of the scrapie prion protein under conditions that alter infectivity - Proceedings of the National Academy of Sciences of the United States of America 1993 Jan 1; 90(1): 1-5 4) Heynkes,R. - Rinderwahnsinn - Durch die moderne Medizin erst gefährlich - Therapiewoche 1995; 15: 886-92 5) Pattison,I.H.; Millson,G.C. - Distribution of the scrapie agent in the Tissues of experimentally inoculated goats - Journal of Comparative Pathology and Therpeutics 1962; 72: 233-44 6) Schrieber,R.; Seybold,U. - Gelatine production, the six steps to maximum safety - Developments in Biological Standardization 1993; 80: 195-8 7) Tamai,Y.; Kojima,H.; Kitajima,R.; Taguchi,F.; Ohtani,Y.; Kawaguchi,T.; Miura,S.; Sato,M.; Ishihara,Y. - Demonstration of the transmissible agent in tissue from a pregnant woman with Creutzfeldt-Jakob disease [letter] - New England Journal of Medicine 1992 Aug 27; 327(9): 649 8) Taylor,D.M.; Fernie,K. - Exposure to autoclaving or sodium-hydroxide extends the dose- response curve of the 263k strain of scrapie agent in hamsters - Journal of General Virology 1996; 77(APR): 811-3 9) Taylor,D.M.; Fraser,H.; McConnell,I.; Brown,D.A.; Brown,K.L.; Lamza,K.A.; Smith,G.R.A. - Decontamination studies with the agents of bovine spongiform encephalopathy and scrapie - Archives of Virology 1994; 139(N3-4): 313-26
Copyright Roland Heynkes 14 October 1996
Rendering Update
Listserve commentary 10.10.96
The change in rendering started in 1974, but the decisive (to cause BSE outbreak) changes probably occurred in 1980. Changes below:
*1974 Start of a low temp/short time/vacuum system in the Midlands (Hearth sp?) Produced greaves which were sent to a Northern solvent extraction plant.
*1977 Start of a low temp/short time/vacuum system in the North (Duncaster sp?). Produced greaves which were sent to on-site solvent extraction plant.
*January 1980 (possibly late Dec 79') Northern solvent extraction plant shut down. Both plants above started to sell proteins without the fat extracted via solvents.
*July 15, 1980 Startup of a new low temp/short time/vacuum system in the South (Silverton?). NO solvent extraction. (This site appears to be around BSE's ground zero.)
What this shows is that from 1974 to 1980 3 facilities, which processed about 30% of the ruminant material in the UK, switched from older systems which acheived 2 log inactivation potential to newer energy efficient systems with NO apparent inactivation potential. Within an 8 month period in 1980 the third low temp system started up and the other two existing low temp systems discontinued to send their finished products through the solvent extraction step.
The solvent extraction process provided only a small amount of inactivation compared to the 2 log inactivation previously employed on the materials processed at these 3 sites. See Dr. Taylor's comments on solvent extraction from the May 13, 1996 symposium in Riverdale MD found within Mark Varner's BSE site at:
I agree with the *hypothesis*, stated by Ray Bradley and posted by Ralph Blanchfield, that the BSE outbreak was triggered when the discontinuance of solvent extraction occurred. But it was not the sole cause, the UK was bordering upon the infectious dose already. If such lengths are needed, is there any hope of reasonably economic methods of decontamination of TSE-infected material? Taylor claimed that 4/15 rendering processes produced MBM with detectable BSE infectivity, i.e. 11/15 seemed to decontaminate infected MBM, as assessed by "mouse bioassay".
------- Taylor,D.M., Woodgate,S.L. & Atkinson,M.J. (1995) Inactivation of the BSE Agent by Rendering Procedures. Vet Rec DEC 9;137(24):605-610
Check David Taylor's May 13, 1996 comments regarding inactivation at:
Bovine brain infected with the BSE agent was used to spike material processed in pilot scale facsimiles of rendering processes which are used within the European Union, and 3 which are not. The raw materials for experimental rendering represented those used in practice, and consisted of appropriate proportions of BSE-infected brain tissue, bovine or porcine intestine, and bovine bone, MBM, and tallow were produced from the rendered tissues. Suspensions of all the MBM samples were assayed in inbred mice for BSE infectivity, and 2 of the tallow fractions were tested similarly. 4/15 processes produced MBM with detectable BSE infectivity. Neither of the tallow samples had detectable infectivity.
The published rendering inactivation study cited by above (D.M. Taylor) demonstrated that conditions found in 11 of the 14 "systems" studied achieved a minimum of a 2 log inactivation of the BSE agent (100 fold). The companion research study on scrapie, yet unpublished, demonstrated that conditions found in 2 "systems", both using pressure, achieved a minimum 3 log inactivation (1000 fold). So the question becomes "Are these levels of inactivation sufficient enough to prevent the transmission of BSE to cattle if/when a single BSE animal is processed into an ingredient for use in cattle feed."
From 1940 to 1980 rendering equipment which fell into the minimum 2 log inactivation category were the only major type used in the UK for processing ruminant material. BTW, heavy meat and bone meal feeding to cattle started in the UK around 1940 due to war time reduction in supply of alternative feed ingredients. Nothing sinister here, they just needed to feed the population.
Around 1980 three of about 7 of the major rendering facilities in the UK were converted to "energy efficient" systems. Remember the oil crisis? These systems evaporated water under lower temperatures, had much shorter material retention times and operated under hypobaric conditions (vacuum). D.M. Taylor's inactivation research later demonstrated that no detectable level of reduction in infectivity occurred under the operating conditions normally found in these low temp/short time/vacuum systems.
The rest is history, BSE appeared around 1985. We need to ask ourselves why not in 1945, 1950, 1955, 1960, 1965, 1970, 1975 or 1980? Where prevention of the potential to spread BSE via cattle feed is the goal (vs. eradication of existing BSE) would not a mandate to use equipment which achieves a minimum 2 or 3 log inactivation coupled with removal of known high risk TSE sources be a consideration? (ie: North America)
Rendering Practises and the Origin of BSE
Listserve 10.13.96
Around 1980 three of about 7 of the major rendering facilities in the UK were converted to "energy efficient" systems. Remember the oil crisis? These systems evaporated water under lower temperatures, had much shorter material retention times and operated under hypobaric conditions (vacuum). D.M. Taylor's inactivation research later demonstrated that no detectable level of reduction in infectivity occurred under the operating conditions normally found in these low temp/short time/vacuum systems.
On BSE genesis in the UK: there was another reason for the use of these processes and that was to improve the feeding quality of the MBM. The lower temperatures resulted in much less denaturing of the proteins and thus a premium product of higher digestibility. One feed where it would pay to pay a premium is in calf weaner pellets. In many UK herds I know of the calf weaner pellets look to have been the source of the infection.
The rest is history, BSE appeared around 1985. We need to ask ourselves why not in 1945, 1950, 1955, 1960, 1965, 1970, 1975 or 1980? Where prevention of the potential to spread BSE via cattle feed is the goal (vs. eradication of existing BSE), would not a mandate to use equipment which achieves a minimum 2 or 3 log inactivation coupled with removal of known high risk TSE sources be a consideration? (ie: North America)
In the case of an outbreak in the process of brewing up, these reductions will not be enough to prevent the feed from being infective, as we know from the UK. They may well stop one from starting. Banning MBM as a feed should be avoided as it provides many conservational, ecological and economic advantages. However we are no longer in the position that the UK was in the mid 80's, when little was known of the disease. It might be prudent to take more measures than those that have been completely effective for the first 80 years of this century.
One measure would be to ban the use of MBM for feeds designed to be used by cattle under 1 year, and certainly in calf weaner pellets. It is usual in the UK to use a low cost ration after weaning that is entirely derived from vegetable feeds and by-products and the animal would not come across a premium feed until the final finishing (beef) or until it entered the dairy herd.
As a result beef animals would be completely safe even if the MBM had become slightly infectious by chance since finishing only occurs in the final six months or so which one can be certain will not cause any expression of BSE in the carcass. The resultant animals will be BSE-free, even if the feed has trace infection. (Actually even if the feed has high levels of infection). [This is highly speculative -- webmaster]
As far as the dairy herd is concerned any possible infection would only start when the animal enters the herd aged 2 to 3 years old. It has been suggested that adult animals are significantly more resistant to infection than young ones and the typical incubation period of 3-5 years would mean that most animals would leave the dairy herd before expressing the disease, or producing an infective carcass, even if coming across trace infection. Those smaller numbers staying up to 10 years would provide a useful marker for assaying any potential disease and are valuable for public confidence. Since the use of MBM in tonnage terms for this young cattle feed is a very small proportion of the total, you would lose very little in imposing these regulations. Also incinerate all skulls complete with brain in the US. This alone would probably give a negative growth rate for any infectivity.
I hope that the compensation that you would give to your farmers who have a case of BSE is VERY generous for whole herd slaughter. Picking up cases early is very important. Generous compensation to cover the real replacement cost of cattle (not their 'valuation') and loss of earnings whilst the herd is being re-established is essential. If having a case of BSE results in bankrupcy or severe financial loss, then expect many cases to be concealed. It is VASTLY cheaper to do this than have a problem later. ---- Change in rendering started in 1980-81? The story is usually related to a combined abandonment of the solvent extraction process to remove fat, and reduction in heating, around that time. This was in fact part of the rationale in the hasty "detective work" in early 1988 to try to ascertain the cause of BSE and the reason for it. The conclusion did suggest measures which, after a time lag, mainly due to incubation period, have proved effective in bringing about dramatic year-on-year reductions in new BSE cases, but the historical facts are wrong.
As an example of the "official" account of the story, the following is a verbatim account given by Ray Bradley, BSE Coordinator, MAFF Central Veterinary Laboratory, at a BSE seminar on 29 February 1996
"The precipitating factor causing BSE was a sudden cessation of hydrocarbon solvent extraction of tallow in the rendering system. Why did this occur? Well, this process probably inactivated the causal agent sufficiently to prevent disease and when that procedure was stopped independently by the rendering companies for commercial reasons, this permitted sufficient infectivity to pass into the feed and cause disease. It was then recycled and initiated the escalation in the epidemic from mid 1989 onwards. How had the solvent extraction of tallow prevented the disease? We think by the double heating process which this particular rendering utilised and in particular the use of a second wet heat stage using steam in a low fat environment. When did that happen? It happened in the late 1970s and early 1980s, especially in the period 1981/82 when cattle were first exposed to sufficient agent to cause disease which was first recognised five years or so later after the incubation period was complete".
The reality of what happened and why, is as follows: There are two separate industries involved in the production of animal feedstuffs based on meat and bonemeal. They are the rendering industry, making and milling the meat and bonemeal, and the feed compounding industry. The renderers do not normally sell their product direct to farmers but to the compounders.
After the main rendering process at high temperature, much of the fat (tallow) was removed by pressing, leaving behind the "greaves" containing 8-10% residual fat. Delving further into detailed history, with a now-retired technologist who was active in the rendering industry at that time, it transpires that, in practice, "many of the older batch cookers, although rated to work up to 130 deg C , were frequently operated at atmospheric pressure to give increased throughput and to improve drainage of free fat at the end of the cook".
Why was solvent extraction ever involved? It was because it was virtually impossible, in the small-scale batch processing plants that existed in the early 1960s and before, to mill the meat and bonemeal without first removing the residual fat, by solvent extraction. Up to the early 1960s, the renderers therefore carried out solvent extraction, and sold the milled product to compounders on a commercial specification of 50% protein, which anyway could only be achieved by removing all the fat residues by solvent extraction (the fat-in-solvent solution was then evaporated to leave the by-product, tallow). After extraction, the residual solvent then was removed from the product by "stripping" it with steam.
But tallow was increasingly being added as an ingredient during compounding, as an energy supplement. Realisation gradually dawned that it was ridiculous to go to all the trouble, expense, hazard and environmental pollution involved in removing residual tallow by solvent extraction, only for it to be added back in compounding. This coincided with a worldwide trend to move from a larger number of renderers operating small-scale batch processing to fewer large-scale continuous processing plants of modern design, on which, moreover, it was possible to mill the product containing residual fat. This led to the increasing adoption of a commercial specification of a 45% protein meal with 8-10% fat, which could, of course, be achieved without solvent extraction.
So solvent extraction became eliminated. And, of course, where there was no solvent extraction, there was also no need for a post-extraction steam-stripping to remove the solvent residues. It should be noted that this trend started with the largest renderers back in the early 1960s, not in 1981, as the mythology would have it. It should be also be noted that these changes were taking place world-wide, not just in the UK, and, moreover, that there was a substantial export of UK meat and bone meal cattle feed. The pace was accelerated by the oil crisis in the early 1970s and in the UK by the Flixborough disaster in 1974 resulting in drastic tightening up of safety procedures in UK industry.
So the combined effect of removing the two unnecessary processes, interlinked with the changes in technology that made it possible, the increase in operating scale and the concentration of the industry into fewer larger units, started in the early 1960s.If the ruminant feed hypothesis is correct, at least as a major factor (as appears to be confirmed by the dramatic reduction in new cases in the last few years), and if the change in rendering was the key factor, it will have started in the early 1960s rather than around 1981 (as the mythology states).
Finally, so far research to investigate procedures to inactivate BSE infectivity indicates that it is highly unlikely that the steam-stripping process to remove solvent residues could have been sufficient to inactivate it.

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