PeteFree.comMad Cows and Variant Creutzfeldt-Jakob Disease - The New Stature of the Precautionary Principle in European Law and Health Practice - Footnotes
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Mad Cows and Variant Creutzfeldt-Jakob Disease ─ The New Stature of the Precautionary Principle in European Law and Health Practice ─ Footnotes
[1] Ken Geiser, Establishing A General Duty of Precaution in Environmental Protection Policies in The United States, in PROTECTING PUBLIC HEALTH & THE ENVIRONMENT: IMPLEMENTING THE PRECAUTIONARY PRINCIPLE xxi, xxiii (Carolyn Raffensperger & Joel A. Tickner eds., 1999).
[2] See Frank B. Cross, Paradoxical Perils of the Precautionary Principle, 5 WASH. & LEE L. REV. 851, 851 (1996).
[3] Andrew Jordan & Timothy O'Riordan, The Precautionary Principle in Contemporary Environmental Policy and Politics, in PROTECTING PUBLIC HEALTH & THE ENVIRONMENT: IMPLEMENTING THE PRECAUTIONARY PRINCIPLE 15, 25 (Carolyn Raffensperger & Joel A. Tickner eds., 1999).
[5] See generally Joel A. Tickner, A Map Toward Precautionary Decision Making, in PROTECTING PUBLIC HEALTH & ENVIRONMENT: IMPLEMENTING THE PRECAUTIONARY PRINCIPLE 162, 164 (Carolyn Raffensperger & Joel A. Tickner eds., 1999) (listing predominantly similar elements, but with less specific wording).
[7] This would undoubtedly be the biggest hurdle in the United States.
[8] Andrew Jordan & Timothy O'Riordan, The Precautionary Principle in Contemporary Environmental Policy and Politics, in PROTECTING PUBLIC HEALTH AND THE ENVIRONMENT: IMPLEMENTING THE PRECAUTIONARY PRINCIPLE 15, 22 (Carolyn Raffensperger &Joel A. Tickner eds., 1999).
[9] Carl F. Cranor, Asymmetric Information, The Precautionary Principle, and Burdens of Proof, in PROTECTING PUBLIC HEALTH AND THE ENVIRONMENT: IMPLEMENTING THE PRECAUTIONARY PRINCIPLE 74, 83-4 (Carolyn Raffensperger &Joel A. Tickner eds., 1999).
[12] Historically, it clear that when no one has the power to take meaningful responsibility for what belongs to all, individuals will not be motivated or able to protect the resource against degradation.
[13] A prion is “a slow infectious particle that lacks nucleic acids; prions are the cause of Creutzfeldt-Jakob disease and scrapie.” DORLAND’S ILLUSTRATED MEDICAL DICTIONARY 1354 (27th ed. 1988).
[14] See Paul Brown et al., "Friendly Fire" in Medicine: Hormones, Homografts, and Creutzfeldt-Jakob Disease, 340 LANCET 24, 24, 27 (Jul. 4, 1992) (illustrating, among others, the problem of transmission via medical instruments); WHO Infection Control Guidelines for Transmissible Spongiform Encephalopathies. Report of a WHO Consultation, Geneva, Switzerland, 23-26 March 1999, Department of Communicable Disease Surveillance and Response, at 2-9, U.N. Doc. WHO/CDS/CSR/APH/2000.3 (visited Mar. 4, 2001) <http://www.who.int/emc-documents/tse/whocdscsraph2003c.html> (describing medical settings and recommended techniques for reducing the risk of iatrogenic transmission).
[15] Jane Holder & Sue Elworthy, The BSE Crisis: A Study of the Precautionary Principle and the Politics of Science in Law in 1 LAW AND SCIENCE: CURRENT LEGAL ISSUES 1998 129, 135 (Helen Reece ed. 1998). This policy was initiated after the food shortages of World War II. Id. at 135.
[16] Id. at 134-35. But see LORD PHILLIPS OF WORTH MATRAVERS ET AL., 1 THE BSE INQUIRY: FINDINGS AND CONCLUSIONS 25-27 (2000) (visited Feb. 8, 2001) <http://www.bseinquiry.gov.uk>. The Phillips report explains that the rendering changes were made as industry switched from batch to continuous systems. Solvent extraction was phased out in the 1970s due to high costs, risks of fire and explosion, and a desire for higher fat content in the meat and bone meal product. Id. at 26. The Inquiry disagrees with the idea that the modified rendering process was to blame for the BSE epidemic. "Neither the old nor the new processes would have inactivated the BSE agent. No rendering process has yet been devised which can guarantee to do so, though infectivity is reduced." Id. at 38.
[17] The ban was put in place on March 29, 1996. Ministry of Agriculture Fisheries and Food, MAFF BSE Information: Chronology of Events (30 June 2000) (visited Mar. 11, 2001) <http://www.maff.gov.uk/>.
[18] LORD PHILLIPS OF WORTH MATRAVERS ET AL., 1 THE BSE INQUIRY: FINDINGS AND CONCLUSIONS 27, 95 (2000) (visited Feb. 8, 2001) <http://www.bseinquiry.gov.uk>. The United States still permits mammalian-derived feed in pigs and poultry. Cross-contamination on a Ralston Purina feed manufacturing line led to the quarantine of 1,222 cattle in south Texas in Jan. 2001. Elizabeth Allen, S. Texas Cattle Quarantined, SAN ANTONIO EXPRESS-NEWS, Jan. 27, 2001, at 2d.
[19] S. Love et al., Methods for Detection of Haematogenous Dissemination of Brain Tissue after Stunning of Cattle with Captive Bolt Guns, 99 J. NEUROSCIENCE METHODS 53 (2000). The European Union banned use of the bolt method after October 1, 2000. European Commission, Decision 2000/418/EC (29 June 2000), 2000 O.J. (L 158) 76. The bolt in the captive bolt gun is used to pith (mash) the cattle brain after the animal is stunned. This prevents involuntary kicking. U.K. Food Standards Agency, Press Release: Consultation Begins on EU-Wide Ban on "Pithing" (Nov. 6, 2000) <http://www.foodstandards.gov.uk/press_releases.htm>. Absent pithing, dead cattle can kick and thrash for up to half an hour, according to one report. Consequently, the EU ban on bolt use has been protested by people who see pithing as a safety measure that should not be abandoned on the remote chance that infected brain tissue will get into the cattle blood stream. Some two-thirds (254) of British abattoirs were still using the technique when the EU decision was made. Christopher Booker, Meat Workers' Lives Put at Risk by Latest Brussels Diktat, Sunday Telegraph (London), November 19, 2000, at 18.
[20] The dorsal root ganglia connect the CNS with the peripheral nervous system. Evidence has shown that the ganglia are infected 32 to 40 months after a cow is infected with BSE. See LORD PHILLIPS OF WORTH MATRAVERS ET AL.,1 THE BSE INQUIRY: FINDINGS AND CONCLUSIONS 19, 118 (2000) (visited Feb. 8, 2001) <http://www.bseinquiry.gov.uk>.
[21] LORD PHILLIPS OF WORTH MATRAVERS ET AL., 1 THE BSE INQUIRY: FINDINGS AND CONCLUSIONS 137, 114 (2000) (visited Feb. 8, 2001) <http://www.bseinquiry.gov.uk> (finding prion infectivity in the distal ileum (part of the small intestine) of a calf, and noting governmental recognition that brain, spinal cord, tonsils, spleen, thymus and intestines were generally high-risk tissues).
[26] Id. at 115. Ministry of Agriculture Fisheries and Food officials initially believed that cleaning the intestines prior to use would remove infectivity. Research proved this to be mistaken, at least in the case of sausage casings. Id. at 115.
[27] Insulin and glucagon can be derived from beef pancreas. Aprotonin comes from bovine lungs and heparin from intestinal mucosa. Sutures have come from the intestine, and heart valves and pericardium patches have been taken from beef heart. Indirect uses of bovine materials include the use of serum or serum albumin for cell cultures in vaccine preparations. LORD PHILLIPS OF WORTH MATRAVERS ET AL., 1 THE BSE INQUIRY: FINDINGS AND CONCLUSIONS 28 (2000) (visited Feb. 8, 2001) <http://www.bseinquiry.gov.uk>
[31] This is the only place the Precautionary Principle is mentioned in the European Union's founding legislation. See Europa, Consumers: The Precautionary Principle (visited Mar. 29, 2001) <http://europa.eu.int/scadplus/leg/en/lvb/132042.htm>.
[32] Consolidated Version of the Treaty Establishing the European Community [i.e., The Treaty on European Union, Feb. 7, 1992, as amended by the Treaty of Amsterdam, Oct. 2, 1997], Oct. 2, 1997, title XIX, art. 174 (2), (visited Mar. 29, 2001) , <http://europa.eu.int/eur-lex/en/treaties/dat/ec_cons_treaty_en.pdf>.
[34] The European Commission is the executive body for the European Union.
[35] European Commission, Communication from The Commission on The Precautionary Principle (2 Feb. 2000) <http://europa.eu.int/comm/off/com/health_consumer/precaution.htm>.
[38] Id. at (3) (emphases deleted).
[48] Ministry of Agriculture Fisheries and Food, MAFF BSE Information: Chronology of Events (30 June 2000) (visited Mar. 11, 2001) <http://www.maff.gov.uk/>.
[49] Michael O'Brien, Have Lessons Been Learned from the UK Bovine Spongiform Encephalopathy (BSE) Epidemic?, 29 INTERNATIONAL JOURNAL OF EPIDEMIOLOGY 730 (2000).
[50] U.K. Ministry of Agriculture Fisheries and Food, MAFF BSE Information: Weekly Cumulative Statistics (23 Feb. 2001) (visited Mar. 10, 2001) http://www.maff.gov.uk/animalh/bse/bse-statistics/level-4-weekly-stats.html>.
[51] LORD PHILLIPS OF WORTH MATRAVERS ET AL., 1 THE BSE INQUIRY: FINDINGS AND CONCLUSIONS 2 (2000) (visited Feb. 8, 2001) <http://www.bseinquiry.gov.uk>. This is a 16 volume inquiry done at the request of the government of the United Kingdom. It is available in pdf form.
[52] U.K. Department of Health, Monthly Creutzfeldt-Jakob Disease Statistics (5 Mar. 2001) (visited Mar. 10, 2001) <http://www.doh.gov.uk/cjd/stats/mar01.htm>.
[53] Office International Des Epizooties, Number of Reported Cases of BSE Worldwide (excluding the United Kingdom) (6 Mar. 2001) (visited Mar. 10, 2001) <http://www.oie.int/eng/info/en_esbmonde.htm>. It is important to note that the discovery of BSE likely depends upon the rigor of the efforts to find it. Finding BSE has a negative impact on the international trade of beef products as the British learned.
[54] Agence France Presse, Scientists See Progress Towards New Mad Cow Test (Feb 28, 2001) <www.afp.fr.>.
[55] Report Flags Hazards of Risk Assessment, 290 SCIENCE 911 (3 Nov. 2000).
[56] Dorothy Bonn, Future Uncertain for Reliable vCJD Screening Tests, 356 LANCET 228 (July 15, 2000).
[57] See J. Gerald Collee & Ray Bradley, BSE: A Decade On-Part 1, 349 LANCET 636, 636 (1997) (estimating BSE incubation in cattle at 2.5 to 8 years).
[58] Paul Brown et al., Bovine Spongiform Encephalopathy and Variant Creutzfeldt-Jakob Disease: Background, Evolution, and Current Concerns, 7 EMERGING INFECTIOUS DISEASES 6, 11 (Jan.-Feb. 2001).
[59] Paul Brown et al., Bovine Spongiform Encephalopathy and Variant Creutzfeldt-Jakob Disease: Background, Evolution, and Current Concerns, 7 EMERGING INFECTIOUS DISEASES 6, 11 (Jan-Feb 2001).
[60] Azra C. Ghani et al., Predicted vCJD Mortality in Great Briatain, 406 NATURE 583 (Aug. 10, 2000).
[61] European Commission, Communication from The Commission on The Precautionary Principle (4) (2 Feb. 2000) <http://europa.eu.int/comm/off/com/health_consumer/precaution.htm>.
[62] This bias, however, does have the effect of bringing both scientists and political decision-makers into the realm of making value judgments in the face of uncertainty even when pretending to be scientific. When scientific data is lacking, scientists are increasingly expected to forecast the implications of data already obtained. This is particularly true in cases in which the potential environmental risk is high, but the data trend is uncertain or unprovable. Obvious examples include ozone depletion and global warning. It is arguably a fact of modern culture that scientists and policy makers come together to create "metanarratives." These are agreed-upon stories that simplify data and uncertainty to present issues in ways that favor or disfavor intervention. See Theresa Garvin & John Eyles, The Sun Safety Metanarrative Translating Science into Public Health Discourse, 30 POLICY SCIENCES 47, 48 (1997). Though this practice might seem unethical, it would be a poor scientist indeed who was unwilling to provide affected parties with interpretations of just what her data might mean at a practical level. In medicine, for example, prognostication is a vital part of practice, despite the fact that it is often wrong, due to the uncertainties inherent in most biological systems as currently understood. Patients expect prognostication so that they might know the future and plan accordingly. See NICHOLAS A. CHRISTAKIS, DEATH FORETOLD: PROPHECY AND PROGNOSIS IN MEDICAL CARE (1999).
[63] LORD PHILLIPS OF WORTH MATRAVERS ET AL., 1 THE BSE INQUIRY: FINDINGS AND CONCLUSIONS xx (2000) (visited Feb. 8, 2001) <http://www.bseinquiry.gov.uk>.
[65] Id. at xx, 99, 238. A CJD surveillance group was set up in May 1990. Id. at 99, 502.
[66] Scrapie was experimentally transmitted from sheep to goats in 1936. The prion diseases, kuru and Creutzfeldt-Jakob disease, were transmitted to primates in the 1960s. John Collinge, Variant Creutzfeldt-Jakob Disease, 354 LANCET 317, 318 (July 24, 1999). The 1966 chimpanzee-kuru report observed that the neuropathology of scrapie and kuru was very similar. D. C. Gajdusek et al., Experimental Transmission of a Kuru-Like Syndrome to Chimpanzees, 209 NATURE 794 (Feb. 19, 1966). William Hadlow had made the same observation in 1959. W. J. Hadlow, Scrapie and Kuru, 2 LANCET 289 (Jul.-Dec. 1959). One of the world's foremost prion researchers had published a book on prion disease in 1987. STANLEY B. PRUSINER & MICHAEL P. McKINLEY EDS., PRIONS: NOVEL INFECTIOUS PATHOGENS CAUSING SCRAPIE AND CREUTZFELDT-JAKOB DISEASE (1987).
[67] Bruna De Marchi & Jerome R. Ravetz, Risk Management and Governance: A Post-Normal Science Approach, 31 FUTURES 743, 749-50 (1999).
[69] "The increasing knowledge about BSE over the years, which threw doubt on the theory that it would behave like scrapie, was not concealed from the public. However, the public was not informed of any change in the perceived likelihood that BSE might be transmissible to humans...The public was repeatedly reassured that it was safe to ear beef...These statements conveyed the message not merely that beef was safe but that BSE was not transmissible." Id. at xxi.
[70] Great Britain alone passed about thirty statutory instruments regulating BSE between 1988 and 1995. LORD PHILLIPS OF WORTH MATRAVERS ET AL., 1 THE BSE INQUIRY: FINDINGS AND CONCLUSIONS 246 (2000) (visited Feb. 8, 2001) <http://www.bseinquiry.gov.uk>.
[71] See generally Michael O'Brien, Have Lessons Been Learned from the UK Bovine Spongiform Encephalopathy (BSE) Epidemic, 29 INTERNATIONAL J. EPIDEMIOLOGY 730 (2000).
[72] Id. at 730. O'Brien, Chairman of the Northumberland Health Authority, points to the 10 month gap between diagnosing a case of TSE in a cow to governmental acceptance of the TSE as a new disease. This resulted in a 7 month delay before Agricultural Ministers were advised, and an added 9 months before the Department of Health was notified. Although a meat and bone meal feed ban was imposed on cattle feed 7 months after epidemiological evidence implicated cattle feed in causation, it took 9 years for government to make the ban fully effective by extending it to feed for all farm animals. He notes that it took 2 years to set up a committee to advise on research, and therefore, it was 3 years after BSE was recognized before government sponsored research really got underway. He is critical of the fact that government took 10 years to fully integrate the work of all the agencies involved in BSE control. Id. at 730-31.
[73] For this and the following chronology, see Merle Jacob & Tomas Hellström, Policy Understanding of Science, Public Trust and the BSE-CJD Crisis, 78 J. HAZARDOUS MATERIALS 303, 304 (2000).
[75] The ruminant feed ban was ordered on June 14, 1988 but went into effect only on July 18. Ministry of Agriculture Fisheries and Food, MAFF BSE Information: Chronology of Events (30 June 2000) (visited Mar. 11, 2001) <http://www.maff.gov.uk/>. The delay was for the benefit of feed producers. It was reasoned that 380 weeks had passed since the discovery of BSE and another five weeks would not hurt. LORD PHILLIPS OF WORTH MATRAVERS ET AL., 1 THE BSE INQUIRY: FINDINGS AND CONCLUSIONS 39 (2000) (visited Feb. 8, 2001) <http://www.bseinquiry.gov.uk>. Given what was known at the time, the Inquiry Panel does not fault the government. Instead it finds evidence that the ban was ignored after July 18 by some feed producers. Id. at 40. Those critical of government efforts think that the five week delay between the ordering and implementation of the ruminant feed ban misled people into believing that the contaminated feed could not be that dangerous. Helen Gavaghan, U.K. Mad Cow Disease: Report Flags Hazards of Risk Assessment, 290 SCIENCE 911 (3 Nov. 2000).
[76] Born after ban cattle, called BABs, included 5,600 in 1990, 4,500 in 1991, 3,000 in 1992, 2,200 in 1993 and 1,000 in 1994. The Phillips Panel concluded that most of these cases resulted from cross-contamination of feed in mills preparing both cattle feed (subject to the meat and bone meal ban) and pig/poultry feed (not subject to the prohibition). LORD PHILLIPS OF WORTH MATRAVERS ET AL., 1 THE BSE INQUIRY: FINDINGS AND CONCLUSIONS 40-41 (2000) (visited Feb. 8, 2001) <http://www.bseinquiry.gov.uk>.
[80] European Commission, Decision 96/239/EC (27 March 1996), 1996 O.J. (L 78) 47.
[81] LORD PHILLIPS OF WORTH MATRAVERS ET AL., 1 THE BSE INQUIRY: FINDINGS AND CONCLUSIONS xvii (2000) (visited Feb. 8, 2001) <http://www.bseinquiry.gov.uk>.
[82] This was the date the government announced BSE might be transmissible to people. Helen Gavaghan, U.K. Mad Cow Disease: Report Flags Hazards of Risk Assessment, 290 SCIENCE 911 (3 Nov. 2000).
[83] "So far as other animals, and humans, were concerned...nobody knew whether BSE was a hazard or not. In such a situation the Government has to decide what precautionary measures to adopt against the possibility that risk exists...The aim is to reduce the possible risk so that it is As Low As Reasonably Practicable." Id. at 32.
[85] The tenor of the Inquiry's criticisms of government more closely harmonize with the Precautionary Principle as interpreted by the EU Commission than it does with its own definition of ALARP. This may be due to the fact that the Inquiry committee highly valued the preservation of health. Therefore, it tacitly considered the costs incurred in maintaining health to be proportionally undertaken, despite the fact that ALARP implies a more rigorous quantification of the differential costs between acting and not acting.
[86] European Commission, Communication from the Commission on the Precautionary Principle (2 Feb. 2000) <http://europa.eu.int/comm/off/com/health_consumer/precaution.htm>.
[87] LORD PHILLIPS OF WORTH MATRAVERS ET AL., 1 THE BSE INQUIRY: FINDINGS AND CONCLUSIONS 235-36 (2000) (visited Feb. 8, 2001) <http://www.bseinquiry.gov.uk>.
[88] "What went wrong was that no one foresaw the possibility of the entry into the animal feed cycle of a lethal agent far more virulent than the conventional viral and bacterial pathogens, and one which would be capable of infecting cattle despite passing through the rendering process." Id. at 227.
[91] Id. at 239. "Drafts were circulated and recirculated among a large number of officials, who might have input to contribute. Submissions were refined, polished and supplemented with minutes as they passed up the administrative hierarchy on their way to the Minister. The process could take a very long time." Id. at 244.
[94] Id. at 242. Zoonotic diseases are those that can be transmitted from animals to humans under natural conditions. DORLAND'S ILLUSTRATED MEDICAL DICTIONARY 1866 (27th ed. 1988).
[101] Id. at 19, 238, 241. Members of the SEAC went to see a slaughterhouse in the spring of 1990. They "were given a 'Rolls-Royce' demonstration of carcass-splitting and removal of spinal cord. Those who saw this concluded that spinal cord could be extracted from the carcass without difficulty." The Ministry of Agriculture Fisheries and Food (MAFF) knew better and had already written that contamination of spinal column with spinal cord was inevitable. The unfortunate result was that MAFF concluded the SEAC was not taking action to prohibit mechanical meat recovery, because the scientists judged that the inevitable contamination itself would not be a cause for concern. But the reality was that the SEAC thought "that clean removal of spinal cord was easy and thus something that could be achieved in practice. It was on the basis of that assumption that they advised that there was no need for any action." The Inquiry notes that the SEAC was overworked, and the question they addressed was the wrong one. Slaughterhouse practice was not their area of expertise; the potential consequences of ingesting bits of spinal cord were. Since MAFF was the expert on real world slaughterhouses, the question the SEAC should have been asked to answer was whether government should be concerned about the amount of contamination that MAFF knew to occur. Id. at 125.
[103] Id. at 141, 237. Oral doses of 0.5 gram were enough to transmit BSE to sheep and goats. One gram was sufficient to infect cattle. Id. at 40.
[104] The appearance of BSE in cattle born after the ban on ruminant-derived feed to ruminants indicated that infected feed was still getting into cattle food. The European Union's Scientific Steering Committee attributed this phenomenon in France, Switzerland, and the United Kingdom to cross-contamination of ruminant-free cattle feed with ruminant-derived feed for pigs and poultry on the same feed-manufacturing line. Scientific Steering Committee, Opinion of the Scientific Steering Committee: (1) On the Scientific Basis for Import Bans Proposed by 3 Member States with Regard to BSE Risks in France and the Republic of Ireland; (2) On the Scientific Basis for Several Measures Proposed by France with Regard to BSE Risks; (3) and on the Scientific Basis for Banning Animal Protein from the Feed for All Farmed Animals, Including Pig, Poultry, Fish and Pet Animals, 14 (Nov. 27-8, 2000) (in pdf format) (visited Apr. 4, 2001) <http://europa.eu.int/comm/food/fs/sc/ssc/outcome_en.html>.
[105] Disposal of BSE infected animals and "specified risk materials" became a significant EU concern. Specified risk materials are potentially infected tissues that must be removed from cattle, sheep and goats. As of March 2001, these included the cattle skull, brain, eye, tonsil, vertebral column, spinal cord, and dorsal root ganglia from animals over 12 months. Bovine intestine had to be removed from animals of all ages. Rules were stricter for the United Kingdom and Portugal. These states had to remove the entire head, excluding the tongue, including the brain, eyes, trigeminal ganglia, tonsils, thymus, spleen, and spinal cord from animals over 6 months. In regard to sheep and goats, all states had to remove brain, eyes, tonsils and spinal cord from animals over 12 months or from those that already had an erupting permanent incisor. The spleen had to be removed from sheep and goats of all ages. European Commission, Decision 2001/233/EC (14 March 2001) art. 1, 2001 O.J. (L 84) 59. The risk materials were to be stained with a dye and destroyed by incineration or pre-treatment prior to landfill disposal. Id. at annex I (3). Pre-treatment prior to landfill required reducing particle sizes to no more than 50mm. The material was then to be subjected to saturated steam treatment for 20 minutes at 133° C under 3 bars pressure. (A bar of pressure is roughly equivalent to 0.99 atmospheres.) European Commission, Decision 1999/534/EC (19 July 1999) art. 1(2), annex 1, 1999 O.J. (L 204) 37. The EU Scientific Steering Committee became concerned over the buildup of infectious material beyond member states' capacity to destroy it. It issued guidelines on storage and handling to protect the workforce, public, and environment. The guidelines were intended to minimize dermal contact, dust, access by animals and children, contamination of watercourses, microbial growth, and fire risk. European Commission: Food Safety, The Safe Handling, Transport and Temporary Storage of Meat-and-Bone Meal which May Be Contaminated with a BSE Agent or Other Pathogens—Notes Adopted by the Scientific Steering Committee at Its Meeting of 26-27 October 2000 (visited Apr. 4, 2001) <http://europa.eu.int/comm/food/fs/sc/ssc.html>. It may be that the U.K. has been overwhelmed by the mass of material to be treated and cannot comply with risk-reducing guidelines. Some allege that secret dumps exist and these are at least partially open to animals and atmosphere. The Hidden Fallout of Mad Cow Disease: Deadly Mountains of Toxic Meat, 16 EARTH ISLAND J. 17 (Spring 2001).
[115] Id. at 270. The guidelines were issued on March 10, 1989. Essentially they asked the industry to avoid using risk tissues or cell cultures of bovine materials; serum should be acellular. The cover letter called the guidance a "purely precautionary measure" that represented "a standard that is deemed to be best practice for the future, and steps should be taken to implement it. However, it is realised that this guidance may not be fully applicable in all circumstances." Id. at 177. This wording gives the impression that the risk to safety was remote even if the advice was not followed. Id. at 178. The overwhelming medical opinion at the time indicated that existing vaccine stocks should not be withdrawn. Id. at 179. The Inquiry concludes "Knowing what is now known, a harder line might have been taken to reduce the length of time both people and animals continued to be exposed to suspect products." Id. at 190. One company, for example, continued to make oral polio vaccine from bovine serum taken from British herds apparently well into 2000. The Department of Health then delayed release of this news to the public for two months. Karen Birmingham, Were Some CJD Victims Infected by Vaccines?, 408 NATURE 3 (2 Nov. 2000). The U.S. Food and Drug Administration had similar difficulty with voluntary guidelines. In December 1993, it recommended that US manufacturers of medicinal and biological products not use animal materials from BSE countries. The agency was concerned that BSE might cause Creutzfeldt-Jakob disease. When vCJD arrived in 1996, the FDA sent another letter to manufacturers, asking them to necessary steps to reduce the risk of BSE transmission. In March 2000, the FDA discovered that its "recommendation had not been universally followed." Some manufacturers were still using fetal calf serum from BSE countries in producing viral and bacterial vaccines. The problem of detecting non-compliance is heightened by the secrecy of proprietary information. Charles Marwick, FDA Calls Bovine-Based Vaccines Currently Safe, 284 JAMA 1231 (Sep. 13, 2000).
[117] Id. at 265. Credibility requires trust, and trust can only be generated by openness. Id. at 266.
[146] Case 180/96, United Kingdom v. Commission, 1998 ECJ Celex Lexis 5270 (May 5, 1998).
[147] European Commission, Decision 96/239/EC (27 March 1996), 1996 O.J. (L 78) 47. The ban prevented the United Kingdom from exporting to the European Union or third countries. The prohibition included bovine animals, semen, embryos, and mammalian derived meat and bone meal, as well as bovine-derived products likely to enter the feed or food chain or medicinal, cosmetic, or pharmaceutical products. Id. at art. 1. The Decision also required the United Kingdom to make biweekly reports on BSE control measures being taken. Id. at art. 3.
[148] Ministry of Agriculture Fisheries and Food, MAFF BSE Information: Chronology of Events (30 June 2000) (visited Mar. 11, 2001) <http://www.maff.gov.uk/>.
[149] Case 180/96, United Kingdom v. Commission, 1998 ECJ Celex Lexis 5270 (May 5, 1998), para. 31.
[150] Id. at para. 32. A 1990 directive had required member states to notify the European Commission of zoonoses and diseases likely to constitute a serious hazard to animal or human health. It authorized the imposition of interim protective measures by member states. Council Directive 90/425/EEC, art. 10 (1), O.J. (L 224) 29. The other directive ordered the Commission to review all such advisements and adopt and monitor necessary measures. Council Directive 89/662/EEC, art. 9 (4), 1989 O.J. (L 395) 13.
[167] Id. at 81. The British reasoned that few countries were authorized to export cattle and bovine products to the EU, and EU import requirements were strict.
[189] Id. at para. 120 (citing Case 68/86, United Kingdom v. Council, 1988 E.C.R. 855, para. 12).
[191] Id. at para. 122 (citing Article 39 (1) of the Treaty on European Union.)
[192] The United Kingdom's agricultural policy argument set the obvious negative impacts on trade and wealth against the Commission's amorphous appeal to the generalized, overriding health concerns expressed in the Treaty on European Union. The Court sided with the Commission and the Treaty.
[193] Case 477/98, Eurostock Meat Marketing Ltd v. Department of Agriculture for Northern Ireland (5 December 2000) (visited Apr. 16, 2001) <http://curia.eu.int/jurisp/cgi-bin/form.pl?lang=en>. European Union case law may be accessed at the Europa website, <http:europa.eu.int>, by following the links accessed through "official documents."
[194] Id. at para. 19, 20. These materials included the bovine head (excluding the tongue), spinal cord, spleen, thymus, tonsils and intestines of animals six months old or older. Although the European Commission had adopted legislation prohibiting the use of specified risk materials and requiring their destruction, implementation of the decision was successively postponed until December 1999. The United Kingdom enacted its own version of the regulation when the Commission's original implementation date (Dec. 29, 1997) was delayed. Id. at para. 21.
[195] Directives 89/662 and 97/534.
[200] Id. at para. 58. This would not be true if the Commission had postponed the measure, because no action was required. Id. at para. 60.
[201] Id. at para. 69. "It is sufficiently apparent from the recitals in the preamble to Decision 97/534 that the risk posed by specified risk material existed long before that decision was adopted, that several international scientific committees had previously recommended the removal of that material, that the Commission approved the measures already adopted by certain Member States and that it regarded Decision 97/534 as a minimum emergency measure the scope of which could be extended in the light of new scientific information."
[203] Id. at para. 77. The seizure of the heads was permissible, "since they contained material with very high infectivity and the slaughtering and transport methods used gave rise to a serious risk of contamination of healthy tissues, especially on account of leakage of cerebrospinal fluid onto cheek meat." Id. at para. 78.
[205] See European Commission: Health & Consumer Protection Directorate-General: Scientific Steering Committee, Opinion: Pre-Emptive Risk Assessment Should BSE in Small Ruminants Be Found under Domestic Conditions (8-9 Feb. 2001) <http://europa.eu.int/comm/food/fs/sc/ssc/out170_en.pdf>. See also European Commission: Health & Consumer Protection Directorate General, First Report on the Harmonisation of Risk Assessment Procedures: The Report of the Scientific Steering Committee's Working Group on Harmonisation of Risk Assessment Procedures in the Scientific Committees Advising the European Commission in the Area of Human and Environmental Health 26-27 October 2000 (published on the Internet 20 Dec. 2000) <http://europa.eu.int/comm/food/fs/sc/ssc/out82_en.html>.
[206] European Commission: Health and Consumer Protection Directorate-General, BSE: Scientists Publish Geographical Risk Assessment for Thirteen Third Countries (2 Apr. 2001) <http://europa.eu.int/comm/dgs/health_consumer/library/press/press123_en.html>. The countries named were Albania, Cyprus, Czech Republic, Estonia, Hungary, Lithuania, Poland, Slovak Republic, and Switzerland.
[207] United Kingdom: Food Standards Agency, BSE Control Breach-German Beef Seized (29 Jan. 2001); Beef Seized in Breaches of BSE Controls (2 Feb. 2001); BSE Breaches Detected in Imported Beef (1 Mar. 2001); Further BSE Breaches Detected in Imported German Beef (2 Mar. 2001); Further Breach of BSE Controls in Imported Dutch Beef (5 Mar. 2001); Licenses of Two German Abattoirs Suspended after Breaches of BSE Controls (6 Mar. 2001); and Breach of BSE Controls in Imported Spanish Beef (12 Mar. 2001) <http://www.foodstandards.gov.uk/press_releases/uk_press/2001/>.
[208] As an example of the difficulty of overcoming this hurdle, the United States Food and Drug Administration recommended in December 1993 that US manufacturers of medicinal and biological products not use materials from animals in BSE-affected countries. The FDA reissued the warning in 1996, after vCJD was reported in the United Kingdom. In March 2000, the agency learned that its advice had been ignored. The problem of non-compliant self-interest is compounded by laws protecting proprietary confidentiality. Charles Marwick, FDA Calls Bovine-Based Vaccines Currently Safe, 284 JAMA 1231 (Sep. 13, 2000).
[209] Vaccine risk is ordinarily quantifiable by combining data from clinical trials with that taken from subsequent medical practice. A portion of vaccine administrations cause severe adverse consequences or death in a small number of patients. Public health administrators are accustomed to pointing to the huge excess of lives saved by the use of vaccines over the few occasions of harm. In the case of BSE contamination, however, the risk cannot be quantified. Additionally, vCJD is an ugly way to die. The public could rationally decide that even small numbers of vaccine-induced vCJD deaths are an unacceptable price to pay for even large numbers of lives saved.
[210] Steven Kleinman, New Variant Creutzfeldt-Jakob Disease and White Cell Reduction: Risk Assessment and Decision Making in the Absence of Data, 39 TRANSFUSION 920 (Sep. 1999).
[211] Id. at 920. The action was taken in July 1998.
[216] Experimental evidence, as yet, has failed to clear up the blood safety uncertainty. One group, whose earlier work had been used in the British sponsored risk-assessment, concluded that the rodent model overestimates naturally occurring CJD infectivity present in human blood. Therefore, the actual transfusion risk to humans is close to zero. P. Brown et al., Further Studies of Blood Infectivity in an Experimental Model of Transmissible Spongiform Encephalopathy, with an Explanation of Why Blood Components Do Not Transmit Creutzfeldt-Jakob Disease in Humans, 39 TRANSFUSION 1169, 1175 (Nov./Dec. 1999). Another group reported the transmission of BSE by blood transfusion from one sheep to another. F. Houston et al., Transmission of BSE by Blood Transfusion in Sheep, 356 LANCET 999 (Sep. 16, 2000). This report, based on experience in only one animal, was criticized for being published before it had even had time to validate positive controls. Paul Brown, BSE and Transmission through Blood, 356 LANCET 955 (Sep. 16, 2000). Yet another report confirmed that infectivity could potentially still be present when leukocytes are removed. This experiment demonstrated that plasma and platelets are the main reservoirs for normal PrP in blood. Storage promotes release of soluble PrP protein. If PrPSc acts like PrP, then there may be some cause for concern. Hagop Bessos et al., The Release of Prion Protein from Platelets during Storage of Apheresis Platelets, 41 TRANSFUSION 61, 65 (Jan. 2001).
[217] Certainly BSE has given voice to critics of industrialized agriculture. The current epidemic of foot and mouth disease, again in the United Kingdom, is causing many to question the wisdom of an agricultural base that is heavily dependent on transportation and far-flung trade. In both cases, there can be no question that animal crowding and maximized mono-cultural production bears significant costs.
[218] DORLAND’S ILLUSTRATED MEDICAL DICTIONARY 566 (27th ed. 1988).
[219] See Michael T. Osterholm et. al., Epidemiologic Principles, in 1 MANDELL, DOUGLAS, AND BENNETT'S PRINCIPLES AND PRACTICE OF INFECTIOUS DISEASES 156-67 (Gerald L. Mandell et al., ed., 2000).
[220] "Encephalopathy" designates a degenerative disease of the brain. "Spongiform" refers to the pathologic result in the central nervous system of affected animals and people; the brain loses tissue and becomes sponge-like. See DORLAND’S ILLUSTRATED MEDICAL DICTIONARY 550, 1567 (27th ed. 1988)(definitions); S. J. Ryder et al., The Neuropathology of Experimental Bovine Spongiform Encephalopathy in the Pig, 122 J. COMPARATIVE PATHOLOGY 131 (2000) (pathology); and Torres Sweeney et al., Molecular Analysis of Irish Sheep Scrapie Cases, 81 J. GENERAL VIROLOGY 1621 (June 2000) (pathology and molecular basis). TSEs in animals include scrapie in sheep and goats, chronic wasting disease in deer and elk, transmissible mink encephalopathy, and BSE in cattle. BSE from meat and bone meal from cattle is probably responsible for TSEs in zoo ruminants, monkeys, and felines. Human TSEs include kuru, Gerstmann-Straussler-Scheinker syndrome, fatal familial insomnia, sporadic fatal insomnia, and Creutzfeldt-Jakob disease. The latter comes in three types: iatrogenic (from infection caused by medical intervention), sporadic (presumably from sudden mutation), familial (genetic), and variant Creutzfeldt-Jakob disease caused by BSE. Jon S. Abramson et al., Technical Report: Transmissible Spongiform Encephalopathies: A Review for Pediatricians, 106 PEDIATRICS 1160, 1160 (2000).
[221] Kenneth L. Tyler, Prions and Prion Diseases of the Central Nervous System (Transmissible Neurodegenerative Diseases), in 2 MANDELL, DOUGLAS, AND BENNETT'S PRINCIPLES AND PRACTICE OF INFECTIOUS DISEASES 1971, 1972 (Gerald L. Mandell et al., 2000).
[222] Stanley B. Prusiner & Michael R. Scott, Genetics of Prions, 31 ANNUAL REVIEW OF GENETICS 139, 143 (1997).
[223] Markus Glatzel & Adriano Aguzzi, Peripheral Pathogenesis of Prion Diseases, 2 MICROBES AND INFECTION 613, 613 (2000).
[225] WHO Infection Control Guidelines for Transmissible Spongiform Encephalopathies. Report of a WHO Consultation, Geneva, Switzerland, 23-26 March 1999, Department of Communicable Disease Surveillance and Response, at 1, U.N. Doc. WHO/CDS/CSR/APH/2000.3 (visited Mar. 4, 2001) <http://www.who.int/emc-documents/tse/whocdscsraph2003c.html>.
[226] Kenneth L. Tyler, Prions and Prion Diseases of the General Nervous System (Transmissible Neurodegenerative Diseases, in 2 MANDELL, DOUGLAS, AND BENNETT'S PRINCIPLES AND PRACTICE OF INFECTIOUS DISEASES 1971 (Gerald L. Mandell et. al., ed., 2000). Prions are small infectious pathogens made largely or entirely of protein. Id. at 1971. They are unusual in that they appear to lack the genetic nucleic acids in RNA or DNA that characterize bacteria and viruses. Id. at 1971. It is thought that the prion does its harm, not by replicating itself via nucleic acids (DNA and RNA) in the manner of bacteria and viruses, but by altering the manufacture of the host's own PrP protein so that the normal protein becomes like the infecting prion. Id. at 1972. See also Stanley B. Prusiner & Michael R. Scott, Genetics of Prions, 31 ANNUAL REVIEW OF GENETICS 139 (1997) (Prusiner won the Nobel Prize for his work on prions; it is virtually impossible to read anything in this area without seeing his name.).
[227] Adriano Aguzzi, Prion Diseases, Blood and the Immune System: Concerns and Reality, 85 HAEMATOLOGICA 3,5 (Jan. 2000).
[229] Kenneth L. Tyler, Prions and Prion Diseases of the General Nervous System (Transmissible Neurodegenerative Diseases, in 2 MANDELL, DOUGLAS, AND BENNETT'S PRINCIPLES AND PRACTICE OF INFECTIOUS DISEASES 1971, 1972-73 (Gerald L. Mandell et. al., ed., 2000).
[230] Adriano Aguzzi, Prion Diseases, Blood and the Immune System: Concerns and Reality, 85 HAEMATOLOGICA 3,5 (Jan. 2000).
[232] Kenneth L. Tyler, Prions and Prion Diseases of the General Nervous System (Transmissible Neurodegenerative Diseases, in 2 MANDELL, DOUGLAS, AND BENNETT'S PRINCIPLES AND PRACTICE OF INFECTIOUS DISEASES 1971, 1972-73 (Gerald L. Mandell et. al., ed., 2000). One hypothesis assumes that one PrPSc molecule joins with one PrP molecule to make a heterodimer (a molecule with different halves). The joined molecule is subsequently transformed into two PrPSc molecules. In other words, the infecting prion becomes a template that transforms normal protein into the abnormal form represented by the prion. Successive cycles of this mechanism create an exponential infection. Id. at 1973.
[233] Jon S. Abramson, Transmissible Spongiform Encephalopathies: A Review for Pediatricians, 106 PEDIATRICS 1160, 1160 (Nov. 2000).
[235] Humor refers to the fluid/semi-fluid materials in the body. DORLAND'S ILLUSTRATED MEDICAL DICTIONARY 779 (27th ed. 1988).
[236] John Collinge, Variant Creutzfeldt-Jakob Disease, 354 LANCET 317, 318 (July 24, 1999).
[238] Kenneth L. Tyler, Prions and Prion Diseases of the General Nervous System (Transmissible Neurodegenerative Diseases, in 2 MANDELL, DOUGLAS, AND BENNETT'S PRINCIPLES AND PRACTICE OF INFECTIOUS DISEASES 1971, 1973 (Gerald L. Mandell et. al., ed., 2000).
[239] Adriano Aguzzi, Prion Diseases, Blood and the Immune System: Concern and Reality, 85 HAEMATOLOGICA 3, 8 (Jan. 2000).
[240] Markus Glatzel & Adriano Aguzzi, Peripheral Pathogenesis of Prion Diseases, 2 MICROBES AND INFECTION 613, 614 (2000).
[242] Andrew F. Hill et al., Diagnosis of New Variant Creutzfeldt-Jakob Disease by Tonsil Biopsy, 349 LANCET 99 (Jan. 11, 1997).
[243] Stanley B. Prusiner & Michael R. Scott, Genetics of Prions, 31 ANNUAL REVIEW OF GENETICS 139 (1997). See also Kenneth L. Tyler, Prions and Prion Diseases of the Central Nervous System (Transmissible Neurodegenerative Diseases, in 2 MANDELL, DOUGLAS, AND BENNETT'S PRINCIPLES AND PRACTICE OF INFECTIOUS DISEASES 1971, 1974 (Gerald L. Mandell et al., ed., 2000) (a more detailed overview); and Jon S. Abramson et al., Technical Report: Transmissible Spongiform Encephalopathies: A Review for Pediatricians, 106 PEDIATRICS 1160 (Nov., 2000) (a well written review for clinicians).
[244] Id. Prusiner at 139, Tyler at 1973 (human disease only), Abramson at 1161.
[245] Herman K. Edskes & Reed B. Wickner, A Protein Required for Prion Generation: Induction Requires the Ras-regulated Mks 1 Protein, 97 PROCEEDINGS OF THE NAT. ACAD. OF SCIENCES U.S.A. 6625, 6625 (June 6, 2000). See also Kenneth L. Tyler, Prions and Prion Diseases of the Central Nervous System (Transmissible Neurodegenerative Diseases, in 2 MANDELL, DOUGLAS, AND BENNETT'S PRINCIPLES AND PRACTICE OF INFECTIOUS DISEASES 1971, 1974 (Gerald L. Mandell et al., ed., 2000) (noting that 85 to 95 percent of the cases of Creutzfeldt-Jakob Disease per year worldwide is sporadic.)
[246] This fact was not lost on Lord Phillip's committee in their preparation of THE BSE INQUIRY. Noting that sporadic mutation might lead to transmissible spongiform encephalopathies in other animals, they recommended that precautionary measures be applied to keep the risk of zoonosis low. (A zoonosis is a disease that can be transmitted from animals to people under natural conditions.) LORD PHILLIPS OF WORTH MATRAVERS ET AL., 1 THE BSE INQUIRY: FINDINGS AND CONCLUSIONS 250 (2000) (visited Feb. 8, 2001) <http://www.bseinquiry.gov.uk>.
[247] Michael R. Scott et al., Compelling Transgenetic Evidence for Transmission of Bovine Spongiform Encephalopathy Prions to Humans, 96 PROCEEDINGS OF THE NAT. ACAD. OF SCIENCES OF THE U.S.A. 15137, 15137, 15140-41 (Dec. 21, 1999).
[248] Jason C. Bartz et al., Adaptation and Selection of Prion Protein Strain Conformations following Interspecies Transmission of Transmissible Mink Encephalopathy, 74 J. VIROLOGY 5542, 5542 (Jun. 2000).
[252] Michael R. Scott et al., Compelling Transgenetic Evidence for Transmission of Bovine Spongiform Encephalopathy Prions to Humans, 96 PROCEEDINGS OF THE NAT. ACAD. OF SCIENCES U.S.A. 15137, 15139 (Dec. 21, 1999).
[254] Via the phenomenon illustrated by Jason C. Bartz et al., Adaptation and Selection of Prion Protein Strain Conformations following Interspecies Transmission of Transmissible Mink Encephalopathy, 74 J. VIROLOGY 5542 (June 2000). The scrapie prion remains capable of affecting transgenic mice that have the bovine prion gene; although the pathological changes it causes are different. See Michael R. Scott, Compelling Transgenetic Evidence for Transmission of Bovine Spongiform Encephalopathy Prions to Humans, 96 PROCEEDINGS OF THE NAT. ACAD. OF SCIENCES U.S.A. 15137, 15139, 15141 (Dec. 21, 1999). Similarly, scrapie from Suffolk sheep passaged in cattle produced a disease distinct from BSE, even after several passages. Id. at 1541. At the molecular level, the BSE and scrapie prions exhibit differing glycosylation (linkages with carbohydrate groups) and proteinase resistance (resistance to the cutting of the peptide bonds that hold protein molecules together) patterns. Torres Sweeney et al., Molecular Analysis of Irish Sheep Scrapie Cases, 81 J. GENERAL VIROLOGY 1621, 1625 (June 2000).
[255] Paul Brown et al., Bovine Spongiform Encephalopathy and Variant Creutzfeldt-Jakob Disease: Background, Evolution, and Current Concerns, 7 EMERGING INFECTIOUS DISEASES 6, 8 (Jan-Feb. 2001) (citing respectively: A.J. Fleetwood & C. W. Furley, Spongiform Encephalopathy in an Eland, 126 VETERINARY RECORD 408-09 (1990); J.K. Kirkwood et al., Spongiform Encephalopathy in an Arabian Oryx (Oryx leucoryx) and a Greater Kudu (Tragelaphus strepsiceros), 127 VETERINARY RECORD 431-34 (1990); K. Willoughby et al., Spongiform Encephalopathy in a Captive Puma (Felis concolor), 131 VETERINARY RECORD 431-34 (1992); and J.M. Wyatt, Spongiform Encephalopathy in a Cat, 126 VETERINARY RECORD 513 (1990).)
[256] S.J. Ryder et al., The Neuropathology of Experimental Bovine Spongiform Encephalopathy in the Pig, 122 J. COMPARATIVE PATHOLOGY 131, 132 (2000). This protocol inoculated the pigs with 0.5ml intracranially, 1-2 ml intravenously, and 8-9 ml intraperitoneally (inside the abdominal cavity) with homogenized BSE-infected beef brain stem. Id. at 132. These small doses are characteristic of BSE, and part of what makes disease control in the food chain so difficult. Disease incubation in the pigs ranged from 17 to 38 months. Id. at 133.
[257] J.D. Foster et al., Detection of BSE Infectivity in Brain and Spleen of Experimentally Infected Sheep, 138 VETERINARY RECORD 546 (1996). Infecting doses were small. The oral dose given was only 0.5 gram of pooled BSE-infected cattle brain homogenate. Incubation for the orally induced disease was 734 days. Intracerebral infection of other sheep resulted from only 0.5 ml of a 10 percent homogenate of the same pool. Incubation in these sheep varied from 440 to 2353 days. When nervous tissue from the infected sheep was introduced into mice, the resulting pathology closely paralleled that seen in mice following infection with BSE. Id. at 546-47.
[259] Michael Balter, Hunt for Mad Cow in Sheep Reassuring, 289 SCIENCE 849 (Aug. 11, 2000).
[260] Paul Brown et al., Bovine Spongiform Encephalopathy and Variant Creutzfeldt-Jakob Disease: Background, Evolution, and Current Concerns, 7 EMERGING INFECTIOUS DISEASES 6, 10 (Jan-Feb. 2001).
[261] Dorothy Bonn, Future Uncertain for Reliable vCJD Screening Tests, 356 LANCET 228 (July 15, 2000).
[262] M.E. Bruce et al., Transmissions to Mice Indicate that 'New Variant' CJD Is Caused by the BSE Agent, 389 NATURE 498 (2 Oct. 1997).
[263] Michael R. Scott et al., Compelling Transgenetic Evidence for Transmission of Bovine Spongiform Encephalopathy Prions to Humans, 96 PROCEEDINGS NAT. ACAD. OF SCIENCES U.S.A. 15137 (Dec. 21, 1999). Bovine PrP genes were inserted into mice. The hypothesis was that the inserted cattle gene would manufacture normal prion protein. The normal protein would likely be as vulnerable to BSE as the same protein in cattle. Therefore, if the transgenic mice were also vulnerable to vCJD prions, the likelihood that the two disease causative prions were the same or acted identically would be strengthened. This experiment demonstrated that the incubation time, pathology, and PrP isoforms for BSE and vCJD are indistinguishable. The researchers concluded that this transgenic mouse model provided compelling evidence that BSE cause vCJD in people. Id. at 15141.
[264] WHO Infection Control Guidelines for Transmissible Spongiform Encephalopathies. Report of a WHO Consultation, Geneva, Switzerland, 23-26 March 1999, Department of Communicable Disease Surveillance and Response, at 2, U.N. Doc. WHO/CDS/CSR/APH/2000.3 (visited Mar. 4, 2001) <http://www.who.int/emc-documents/tse/whocdscsraph2003c.html>.
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