Regulatory Swords That Slay Mad Cows: EU and U.K. Animal Feed Restrictions as Guides for the FDA

By Vera, Meredith Todd | Texas International Law Journal, Winter 2005 | Go to article overview

Regulatory Swords That Slay Mad Cows: EU and U.K. Animal Feed Restrictions as Guides for the FDA


Vera, Meredith Todd, Texas International Law Journal


I. INTRODUCTION

"We use everything but the squeal, the cluck, and the moo."1 This has been the agriculture industry's resourceful response to unmarketable animal parts. In the wake of the mad cow crisis, however, this statement reveals the Pandora's Box unwittingly opened by our quest for cheap food.2 We realized that we could waste less and produce more by recycling our deceased, and in this case diseased, animals and feeding them back to our cattle.3

By turning these traditional herbivores into carnivores and cannibals, we effectively removed the species barriers that had protected both animals and humans from one another's illnesses.4 In Great Britain, cattle that had eaten the recycled remains of diseased sheep began contracting those diseases themselves.5 Then, much to the horror of the scientific community, people who ingested the diseased cattle also fell ill as this "mad cow" epidemic began its terrifying sweep across Europe.6 Though there is little scientific certainty about the disease or its transmission,7 Great Britain and the European Community discovered the key to stopping the epidemic: protecting the cattle feed supply from infectious material.8 European regulatory agencies then began enacting animal feed restrictions designed to prevent amplification of the disease among cattle populations,9 and in 1997, America's Food and Drug Administration (FDA) did the same.10

As of December 2003, mad cow disease is no longer just a European threat; the disease is now present in the United States.11 The U.S. Department of Agriculture (USDA)'s own international panel of scientists warns that the disease is likely spreading in the United States and that our most crucial line of defense against a European-style epidemic, the PDA's ruminant feed restrictions, are not sufficient to protect our cattle feed supply.12 Indeed, an evaluation of U.S. regulation does reveal unacceptable loopholes that would result in a proliferation of the disease. Encouragingly, our European neighbors have, through their own painful battle with mad cow, developed a working regulatory model proven successful in containing the disease. Thus far, however, the FDA is repeating European mistakes rather than learning from their invaluable experience.

This paper demonstrates that in order to avert a U.S. mad cow epidemic, the FDA must begin wielding certain European regulatory tools and modifying them to address our country's unique mad cow risks.13 Part II outlines the brief history of mad cow disease and the use of feed restrictions to contain it. Part III first provides components of adequate feed restrictions generally, then examines the adequacy of both U.S. and European Union (EU) regulation, and finally describes how internalizing EU and U.K. regulatory responsiveness can help the FDA improve the adequacy of its feed restrictions. Part IV lays out criteria employed in effective regulatory enforcement schemes and examines the effectiveness of U.S. and EU feed-restriction enforcement on both practical and systematic levels; possible solutions for the PDA's enforcement shortcomings are then provided in light of the more effective regulatory models of the EU and United Kingdom. Part V concludes by offering recommendations to the FDA and consumers alike.

II. HISTORY OF BSE

Mad cow disease is the common term for bovine spongiform encephalopathy (BSE),14 a neurodegenerative disease belonging to the family of transmissible spongiform encephalopathies (TSEs).15 TSEs are a group of fatal, neurological diseases "characterized by spongy degeneration of the brain," and different forms of the disease exist in several animal species.16 In addition to BSE in cattle, scrapie is the common TSE occurring in sheep and goats, and both Creutzfeldt-Jakob Disease (CJD) and variant-Creutzfeldt-Jakob Disease (vCJD) are prototype human TSEs.17

While the nature of the BSE agent is still being debated,18 the prion theory is generally accepted by researchers. …

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