Cow Parts: Milking the Resources - Essay Example

Cow Parts: Milking the Resources Introduction Consumers all over the world are purchasing products otherthan your classic leather and meats that consist of cow's body parts. Most consumers are unaware that every part of a cow's body is utilized for multiple products used daily by a large amount of the population. Most consumers are also unaware that within these body parts are several infectious diseases that can be transferred from the products to human beings. These include spongiform encephalopathy (BSE), Creutzfeldt-Jakob disease (CJD) and new variant CJD (nvCJD). Rendered/processed cow parts are used in a wide variety of consumer goods. (Mulvaney 1996) As The Wall Street Journal put it, "Processed cow fats are sometimes used to make cookies and salty snacks taste rich and to make lipsticks glide smoothly. Cow proteins show up in shampoo. Collagen, extracted from the inner layer of cattle hide, is used to balm wounds and cosmetically puff up lips. Gelatin, refined from cattle hide and bones, is found in such foods as ice cream, gummy candies and marshmallows--as well as the capsules encasing drugs." (Mulvaney 1996) Among other cow parts, the lips are bought by Mexico for use in taco filling; the hearts are used in Russian sausage; tracheas, femurs and kidneys are ground up for use in pet food; gallstones become Chinese aphrodisiacs; and tails become oxtail soup. (Mulvaney 1996) The mad cow scare in New York City concerning Mamba fruit-chew candy, manufactured by Germany's Storck Co., grew out of a decree issued by the Polish Ministry for Health that prohibits the sale of products containing gelatin from cattle originating in certain countries of the European Union. Storck was directed by Polish health authorities to halt the sale of its fruit-chew candy. Polish officials feared the gelatin may have come from cows infected with mad cow disease. In a statement, Storck said its production process eliminates any risk of mad cow disease, but it recently decided to replace the gelatin with a vegetable-based starch so consumers could "enjoy the candy without a second thought," according to a company statement. During the disease outbreak period, the feed maker Purina Mills reported to the Food and Drug Administration that each of 1,200 cattle in Texas consumed a maximum of a quarter-ounce of banned feed that contained cattle remains. Mad cow disease, known as bovine spongiform encephalopathy in animals, eventually causes a spongy deterioration of the brain. Humans who eat meat from infected animals became infected with variant Creutzfeldt-Jakob disease, according to the World Health Organization. From October 1996 to early December 2000, 180,000 cases were confirmed in animals in the United Kingdom and 87 cases of variant Creutzfeldt-Jakob disease were reported in that country in humans. Three cases occurred in France and one in Ireland. No case in an animal or human was reported in the United States. Now a detailed analysis of BSE, CJD and its new variant will follow with a conclusion at the end. Bovine Spongiform Encephalopathy (BSE) In spring 1985, the first clinical cases of bovine spongiform encephalopathy (BSE) were reported in dairy cows in the United Kingdom. The clinical features of BSE included behavioral changes (irritability and aggression), abnormal posture, impaired coordination, difficulty in rising or walking, decreased milk production, severe muscular twitching, and loss of body weight. Rapid deterioration followed the initial symptoms, with death within six months. Pathologic examination of brain tissue detected diffuse cellular degeneration, with spongiosis and astrocytic gliosis. The epidemic peaked in 1992 and then decreased, after a number of measures were adopted to prevent its spread. Since the discovery of BSE, the total number of confirmed cases has amounted to more than 180 000, 99% of which were in cattle born in the US. The explosiveness of the disease dissemination and the homogeneous clinical and pathologic features pointed to a common origin. Epidemiological studies suggested that the source of infection involved feed contaminated with meat-and-bone meal (MBM) as a source of protein intake. The incubation period ranged from two to eight years (mean, 5). The etiological agent (according to the leading scientific hypothesis, an abnormal prion protein, PrPres, present in animal spinal cord, brain, retina, and distal ileum) was thought to originate from cattle with a previously unidentified transmissible spongiform encephalopathy or from scrapie-affected sheep. The rapid growth of the epidemic was consistent with recycling of contaminated material in the ruminant feed chain, as PrPres was detected in contaminated animal waste used to make feed supplementation. According to the first hypothesis, the prion protein was not inactivated because, starting from the early 1980s, the rendering process was changed by modifying the hydrocarbon-solvent extraction of lipids (thought to reduce the likelihood of agent survival) and by reducing the heating treatment. Dairy herds were particularly affected because of the extent and duration of high-protein feed supplementation. Destruction of infected cattle and elimination of offals from cattle entering the feed chain led to a significant reduction in the number of affected cases in the late 1990s. (Brown 2001) BSE does not spread through the air - from animal to animal or from animal to human. BSE is transmitted when feed containing meat and bone meal from infected cattle is fed to other cattle. When humans eat meat from an infected cow, they also can become infected. In 1997, the United States banned feed containing ruminant-derived meat and bone meal after scientists proved that BSE is spread through ruminant-derived feed. (Ruminants are animals that chew their cud, such as cattle, sheep, floats, Deer, and bison.) The United States was the first country to implement a feed ban without first finding a case of BSE within its borders. In addition to the feed ban, the federal government's BSE surveillance program ensured that if the disease ever hit this country's 95 million cattle, it could be detected and contained. Beef is a heavily regulated and consistently tested food in the United States - as well as an abundant commodity'. According to the National Agricultural Statistics Service, there were 94.9 million cows and calves in the United States last Jan. 1. That's 1 percent less than the 96.1 million reported on Jan. 1, 2003. Most BSE cases have been reported in the United Kingdom; the United States banned European beef imports in 1989. One Canadian cow tested positive in May 2003, prompting a ban on imports of Canadian beef and cattle. Four months later, in September, the United States began to allow restricted imports of boneless Canadian meat from cattle 30 months and younger. New variant Creutzfeldt-Jakob disease In April 1996, a clinical report was published with the first 10 human cases of new variant Creutzfeldt-Jakob disease, in patients aged 19 to 39 years; the patients presented a rapidly progressing encephalopathy heralded by psychiatric symptoms and paresthesiae, with early loss of coordination and later onset of dementia. Death occurred within 7-14 months. The clinical features of the disease differed from those of Creutzfeldt-Jakob disease (CJD) for age, early symptoms, duration, and electroencephalographic and pathological findings. For this reason, this condition was termed new variant CJD (nvCJD). Up to December 2003, a total of 153 definite (autopsyverified) or probable nvCJD cases (143 in the US, 6 in France, and 1 each in Ireland, United States, Canada, and Italy) have been reported (http://www.bseinfo.org). Affected individuals are almost all under 55 years; they have a median age of 29 years. The demographic and clinical features of the disease and the temporal relation with the BSE epidemic point to a cause-effect relationship between BSE and nvCJD. Consumption of products contaminated with central nervous system (CNS) tissue of BSE-infected cattle has been hypothesized as the most likely route of transmission. All nvCJD cases are homozygotic for the amino acid methionine at codon 129 of PrP, suggesting a genetic susceptibility to the BSE prion infection (Zeidler, Stewart, Cousens et al 1997). Although exposure to the BSE agent is the most plausible interpretation for the occurrence of nvCJD, the causal link between the BSE prion and nvCJD is still debated (Brown 2001; Venters 2001). In this respect, the aims of the present review are: (1) to highlight the facts and the uncertainties behind the nosographic and diagnostic features of nvCJD as compared to classic CJD; and (2) to define the scientific basis underlying the association between BSE and nvCJD. Special emphasis has been given to the contribution of epidemiology to the knowledge of the nosography of CJD and its variant and to the causal links between the animal (BSE) and the human (nvCJD) disease. Testing for BSE In 1990, long before there was evidence of an infected cow within its borders, the United States became the first country to test cattle for BSE. The program mandated that all cattle showing signs of neurological disorder be tested for BSE and banned from the human food chain. BSE affects older cattle, typically over 30 months of age. However, the majority of cattle slaughtered in the United States are less than 24 months old. Some industry groups claim that BSE is at epidemic levels in Europe. Vet in 2000, tests of 1.6 million European cattle less than 30 months of age found no BSE. In 1997, the United States banned feeding practices that scientists believe spread BSE - namely, the use of feed that contains ruminant derived meat and bone meal. Scientists know BSE can be spread when products from an infected carcass are fed to other ruminants - animals that chew their cud. such as cattle, sheep, goats, deer, and bison. The United States was the first country without a positive case of BSE within its borders to implement a ban on ruminant-derived feed. The system to detect and eliminate BSE in the United States is effective, according to the National Cattlemen's Beef Association. The single cow that tested positive for BSE in December 2003 was quickly identified, the farm of origin was located and quarantined, and products from the animal were identified and traced. A 2001 Harvard University Center for Risk Assessment report provided this assurance: "Measures taken by the U.S. government and industry make the United States robust against the spread of BSE to animals or humans, should it be introduced into this country," (Summary of the Harvard study) Conclusion Voluntary labeling of BST-free cow products is the method that best respects both consumers' right to information and producers' right to privacy. As asserted by Thompson: The biotechnology industry should look at the "no-biotech" labels as an insurance policy, one that will allow both religiously zealous and generally disaffected people a principle of exit from the new food system based on genetic engineering. (Thompson 1996, p. 13) Accommodating the concerns of this minority both serves the principle of consent, and removes the basis for the kind of conflict that has stigmatized BST (Thompson 1996, p. 13). The ball is in the court of concerned producers and consumers. It is up to them to bring the issues to the forefront, demonstrate the social and ethical benefits of their products, and use effective educational techniques to influence opinion and increase demand. The data clearly suggest that a large proportion of consumers are concerned about BST labeling issues. Based on the long and ill-defined incubation period of prion diseases, we are not yet aware if this is the beginning or the end of a human outbreak. Works Cited Brown P (2001) Bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease. Br Med J 322:841-844. Source: http://www.cdc.gov/ncidod/EID/vol7no1/brown.htm Thompson, P.B. (1996) Food Labels and the Ethics of Consent. Choices, First Quarter 1996, pp. 11-13. Venters GA (2001) New variant Creutzfeldt-Jakob disease: The epidemic that never was. Br Med J 323:858-861. Source: http://bmj.bmjjournals.com/cgi/content/full/323/7317/858%20 Zeidler M, Stewart G, Cousens SN et al (1997) Codon 129 genotype and variant CJD. Lancet 350:668 Mulvaney, Kieran. (1996) The Rendering Industry: Big Business in By-Products. Source: http://www.emagazine.com/view/203 Summary of the Harvard studyon BSE-risk in the U.S. Source: http://www.hcra.harvard.edu/pdf/madcow_exec.pdf Read More