An Analysis of the Law Regulating Mad Cow Disease - Research Paper Example

An Analysis of the Law Regulating Mad Cow Disease By Table of Contents 2 Introduction 4 Scientific Studies 5 Legislation 8 Introduction Bovine spongiform encephalopathy (BSE) known as mad cow disease is a disease that attacks and degenerates the brain and spinal cord of cattle. BSE was first identified and defined in the UK in 1986. In the ensuing four years, mad cow disease emerged as a serious epidemic in the UK (Kimberlin & Wilesmith, 1994). Scientists discovered that mad cow disease was caused by meat and bone meal (MBM) feed used to feed livestock (Nathanson, Wilesmith, & Griot, 1997). Although initially determined to be a disease that could not be transmitted to human beings, the human form of BSE was discovered in 1996: Creutzfedt-Jakob (vCJD) (Harris, 2004). It was further determined that vCJD was caused when the individual was exposed to BSE (Collinge, 1997). Mad cow disease eventually resulted in significant financial loss to farmers as approximately 5 million cows were killed in Europe to prevent the spread of BSE. In the meantime, 150 deaths were linked to BSE (Robinson, 2005). Other measures taken were the ban on MBM feed although it was not uniformly enforced across Britain (Stevenson, Morris, Lawson, et al., 2005). It therefore appears that mad cow disease was inadequately regulated amidst significant uncertainties, risk to life and health and the financial losses to farmers. Prior to the emergence of information that human who had consumed contaminated meat had succumbed to vCJD, the government had been adamant that British beef was safe to consume (Millstone & Zwanenberg, 2002). The public was said to be left to self-regulate and in this meant assessing the risks for themselves (Jasanoff, 1997). The BSE scare exposed the weaknesses of national food safety laws which were primarily regulated on an ad hoc basis (Vos, 2000). In this regard, the EU implemented a framework for institutional reform for the regulation of food safety across the EU. National governments also reformed the way in which they gathered and publicized information about food safety (Millstone & Zwanenberg, 2002). The purpose of this research study is to identify how mad cow disease is and should be regulated. This research study therefore examines the national laws of countries effected by the mad cow disease during the scare and the emerging laws developed by various countries in response to the mad cow disease scare. In order to determine whether the laws as they are now, compared to how they were during the scare are adequate, it is necessary to establish the historical and clinical facts surrounding mad cow disease and the scare. If the law is intended to protect public health and promote public safety, lessons from the scare will aid in achieving these goals. Given the misinformation, the uncertainties, the loss of life and financial losses attributed to mad cow disease, this study is important for identifying the appropriate laws for preventing a reoccurrence of a similar threat to public safety and the livelihood of farmers. As Campbell (2006) explained, the killing of cattle for either destroying infected cows or preventing the spread of mad cow disease cost the UK government approximately 6 billion Euros in compensatory damages to farmers. This together with the fact that mad cow disease has been linked to human death obviates the need to consider all avenues for preventing mad cow disease (Campbell, 2006). Scientific Studies Matthews (1990) reported that based on histopathological studies and clinical trials conducted in laboratories, mad cow disease was determined to be a member of a category of diseases inclusive of scrapie, kuru, and vCJD. Mad cow disease is “scarpie in cattle” and as such is “almost certainly acquired from infected sheep products in feed” (Matthews, 1990, p. 412). Straines of spongiform encephalopathy were also found in deer, mink and mice indicating that BES can originate from various other sources that are difficult to contain. As Matthews (1990) explained, “the agents are extremely persistent and difficult to destroy” (p. 412). Moreover, the disease itself can only be identified through tests when the disease is progressing or there are “pathological changes in the brain” (Matthews, 1990, p. 412). Complicating matters the disease is often dormant for 18 months (Matthews, 1990). In other words, it is not possible to test cattle for mad cow disease prior to putting the beef on the market for consumption. The United States Department of Agricultural Animal and Plant Health Inspection Service (2002) reported however that mad cow disease can be dormant for 2 years. In addition, there are no available vaccinations for preventing the disease and the disease is only present in the infected cow’s brain, retina and spinal cord (United States Department of Agricultural Animal and Plant Inspection Service, 2002). Chachra, Narang and Narang (1999) emphatically reported that mad cow disease is linked to two grave diseases: scrapie in sheep and vCJD in human beings. More alarmingly, mad cow disease causes “fatality in humans eating infected beef” (Chachra, 1999, p. 42). In explaining the etiology of mad cow disease, Chachra (1999) noted that mad cow disease and its family of diseases such as scrapie are “caused by an unconventional proteinaceous infective agent called prion” (p. 42). The scrapie prion which is said to cause mad cow disease is virtually indestructible and as such it is not sensitive to boiling temperatures and can withstand boiling temperatures for up to half an hour. It can also withstand freezing temperatures, thawing and a wide number of chemicals and “20% formalin” (Chachra, 1999, p. 42). In addition, prions are resistant to antibodies and therefore, vaccinations against prions are impossible (Chachra, 1999). Chachra (1999) also reported that the disease can be dormant for several years as opposed to 2 years. According to Chachra (1999), mad cow disease was first transmitted between 1981 and 1982 when UK cattle feed was comprised of bone and meat meal. It is believed that this feed contained prions originating from infected sheep. Although exposed to the prions as early as 1981, the mad cow disease was not detected until 1985 (Chachra, 1999). Balter (2000) reported that a task force was assigned to study cases of vCJD which has been linked to consuming meat from cows infected by mad cow disease. The task force discovered that as of 2000, there were only 80 known cases of vCJD. Although possible case of vCJD are lower than estimated, case of vCJD are increasing (Balter, 2000). The increase in cases of vCJD may be a result of the fact that mad cow disease can be dormant for at least two years and certainly longer. Thus these cases may have been contracted prior to official and self-regulatory measures were implemented. More serious uncertainties surround the causes of mad cow disease. As Broxmeyer (2004), informs there is no scientific certainty that prions transmit mad cow disease to cattle. It is quite possible that bacteria or viruses contained in the prions are the transmitters. These viruses or bacterium may well be incapable of identification particularly since the prion is resistant to extreme temperatures for extended periods which would kill any virus or bacteria in the prion. Broxmeyer (2004) argues that prions are “misfolded proteins”, yet a great number of animals that die of transmissible spongiform enchephalopathies (TSE) did not “show evidence of misfolded protiens” (Broxmeyer, 2004, p. 731). Hooper (2003), suggests that there may be yet another cause of mad cow disease. According to Hooper (2003), proteasome causes misfolded and normal proteins to degrade. It is therefore possible that inhibited proteasome “might promote the neurotoxic properties of the prion and its conformational conversion to the infectious form” (Hooper, 2003, p. 144). Both Hooper (2003) and Broxmeyer’s (2004) studies reveal the scientific uncertainty associated with the cause of mad cow disease and indicate that scientist may never agree on the exact cause of mad cow disease. This scientific uncertainty runs parallel to the scientific certainty that mad cow disease is fatal to cows and human beings. Legislation Bibliography Balter, M. (1 September 2000). “Epidemiology: Tracking the Human Fallout from ‘Mad Cow Disease.’” Science, Vol. 289(5484): 1452-1454. Broxmeyer, L. (2004). “Is Mad Cow Disease Caused by a Bacteria?” Medical Hypotheses, Vol. 63(4): 731-739. Campbell, P. N. (2006). “Mad Cow Disease.” Acta Biologica Szegediensis, Vol. 50(3-4): 89-95. Chachra, A.; Narang, D. and Narang, R. (April 1999). “Mad Cow Disease: Bovine Spongiform Encephalopathy.” Resonance, Vol. 4(4): 42-44. Collinge, J. (1997). “Human Prion Diseases and Bovine Spongiform Encephalopathy (BSE).” Hum. Mol. Genet. Vol. 6(10): 1699-1705. Harris, D.A. (2004). Mad Cow Disease and Related Spongiform Encephalopathies, Vol. 284. Berlin: Springer. Hooper, N.M. (April 2003). “Could Inhibition of the Proteasome Cause Mad Cow Disease?” Trends in Biotechnology, Vol. 21(4): 144-145. Jasanoff, S. (July 1997). “Civilization and Madness: the Great BSE Scare of 1996.” Public Understanding of Science, Vol. 6(3): 221-232. Kimberlin, R.H. and Wilesmith, J.W. (May 1994). “Bovine Spongiform Encephalopathy.” Annals of the New York Academy of Sciences, Vol. 724: 210-220. Matthews, W.B. (17 February 1990). “Bovine Spongiform Encephalopathy: The Safety of Beef Has not yet been Tested and May not be Testable.” British Medical Journal, Vol. 300: 412-413. Millstone, E. and Zwanenberg, P.V. (December 2002). “The Evolution of Food Safety Policy-Making Institutions in the UK, EU, and Codex Alimentarius.” Social Policy & Administration, Vol. 36(6): 593-609. Nathanson, N.; Wilesmith, J. and Griot, C. (1997). “Bovine Spongiform Encephalopathy (BSE): Causes and Consequences of a Common Source Epidemic.” American Journal of Epidemiol. Vol. 145(11): 959-969. Robinson, R.A. (February 2005). “Mad Cow Disease.” United States Government Accountability Office, Report to Congressional Requesters, GAO-05-101: 1-79. Stevenson, M.A.; Morris, R.S.; Lawson, A.B.; Wilesmith, J.W.; Ryan, J.B.M. and Jackson, R. (June 2005). “Area-Level Risks for BSE in Britain Cattle Before and After the July 1988 Meat and Bone Meal Feed Ban.” Preventive Veterinary Medicine, Vol. 69(1-2): 129-144. United States Department of Agricultural Animal and Plant Inspection Service. (February 2002). “Bovine Spongiform Encephalopathy.” APHIS Veterinary Services, Factsheet, 1-3. Vos, E. (2000). “EU Food Safety Regulation in the Aftermath of the BSE Crisis.” Journal of Consumer Policy, Vol. 23(3): 227-255. Read More