Rethinking the BSE Crisis: A Study of Scientific Reasoning under Uncertainty

Rethinking the BSE Crisis

Louise Cummings

Rethinking the BSE Crisis A Study of Scientific Reasoning under Uncertainty

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Prof. Louise Cummings School of Arts and Humanities Nottingham Trent University Clifton Campus Clifton Lane NG11 8NS Nottingham United Kingdom [email protected]

ISBN 978-90-481-9503-9 e-ISBN 978-90-481-9504-6 DOI 10.1007/978-90-481-9504-6 Springer Dordrecht Heidelberg London New York Library of Congress Control Number: 2010932529 © Springer Science+Business Media, B.V. 2010 No part of this work may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, microfilming, recording or otherwise, without written permission from the Publisher, with the exception of any material supplied specifically for the purpose of being entered and executed on a computer system, for exclusive use by the purchaser of the work. Cover picture: Cow on a Bun © Corbis #12759508/Fotolia Printed on acid-free paper Springer is part of Springer Science+Business Media (www.springer.com)

In fond memory of my grandmother Ruby Stewart Who taught me to value learning

Preface

Uncertainty is a well trodden area of intellectual inquiry. Whether we are concerned with the philosophical dimensions of this concept or the psychological strategies that human agents use to cope with uncertainty, this is not a notion that investigators can readily ignore. This statement is even more apt in the case of scientific inquiry where sophisticated bodies of knowledge notwithstanding, uncertainty can appear as an insurmountable obstruction to further progress on a scientific issue or question. Uncertainty, and scientific responses to it, is the overriding theme of this book. Yet, the context is a more specific one than scientific inquiry in general. For the aim is to examine novel modes of reasoning that are only in evidence under conditions of extreme uncertainty and then only when combined with certain practical imperatives for action. To this end, I will examine the reasoning of scientists who are charged with understanding and containing a newly emerging infectious disease. The disease in question is bovine spongiform encephalopathy (BSE). Although I have selected BSE for this study, I could have chosen with equal legitimacy any one of a number of other infectious diseases that have challenged scientists in recent years. These diseases include HIV/AIDS, severe acute respiratory syndrome (SARS) and avian and swine influenzas. What all these diseases have in common is the pressing demand for effective containment in the absence of scientific knowledge of the pathogens involved and their routes of transmission. However, there is also a compelling reason to make BSE the focus of investigation. The UK’s BSE epidemic has been the subject of a public inquiry which was conducted over a three-year period between 1998 and 2000. The team in charge of this inquiry was headed by Lord Phillips of Worth Matravers. The Inquiry Report, which was published in October 2000 and examined all matters relating to BSE up to March 1996, represents the most extensive record of any human or animal health phenomenon in recent years. The report charts in minute detail every decision and action that was taken in relation to BSE. Importantly for this study, it provides an exhaustive account of the work of each of the scientific advisory committees that were established to provide advice to successive British governments on the handling of BSE. In short, this report is an invaluable resource for any investigator wanting to study the reasoning of scientists during what has been a significant episode in the public

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health of the UK. Certainly, no comparable document exists in relation to any of the aforementioned diseases. Although the issues that I will discuss relate to BSE, the lessons from this study move beyond this single infectious disease. At the heart of this investigation is the attempt to conceptualise certain traditional informal fallacies as reasoning strategies that can facilitate scientific inquiry under conditions of uncertainty. This book is thus a contribution to the theoretical study of the fallacies. Yet, this is a contribution with a distinctive twist. For while there is nothing new in the idea that fallacies can have non-fallacious variants in certain contexts of use, the novelty of the current approach rests in presenting the fallacies as forms of argument that are specially adapted to conditions of uncertainty. Quite apart from being fallacious, these arguments are a key component of a cognitive rationality that has evolved to deal with adverse epistemic conditions such as those that confront scientists in the early stages of scientific inquiry. In achieving a significant reconfiguration of the fallacies, I am also making a contribution to epidemiology, the branch of science that identifies and tracks newly emerging infectious diseases. One cannot go far in epidemiological literature, or at least in the more critical aspects of this literature, without realising that there are calls from within epidemiology for investigators to engage with new modes of reasoning in contexts of uncertainty. This book proposes to take these calls seriously but also to move beyond them in a significant way. For the model of reasoning that I will advance challenges the dominance of deductive and inductive frameworks in epidemic modelling. The emphasis in this book on new modes of reasoning that eschew deduction and induction as the only reasoning frameworks of relevance to epidemiology is the second enduring lesson of this study. Nottingham, UK

Louise Cummings

Acknowledgements

I wish to acknowledge with gratitude the assistance of the following people: Melania Ruiz of Springer for her receptive response to my proposal of this book; Judith Heaney for her careful preparation of the bibliography and diagrams; Louise Crane and Laura Pastorelli of the Wellcome Trust for their provision of photographs; Chris Mills, Art and Design, Nottingham Trent University for his work on images; Maurice Bardsley and Heather Hulse of the Veterinary Laboratories Agency, Weybridge, England for their help in locating images and staff at the Boots and Clifton libraries of Nottingham Trent University for their assistance in obtaining literature. The contribution of each of these individuals to this book has been invaluable. Several images and photographs appear in the following pages. They have been provided by the following individuals and agencies: D. Carleton Gajdusek/Wellcome Images; Professor Sebastian Brandner, Institute of Neurology, London; Veterinary Laboratories Agency, Weybridge, England; Controller of Her Majesty’s Stationery Office; Elsevier Science Publishers B.V.; Dr Jason C. Bartz, Creighton University, Nebraska; Wisconsin Department of Natural Resources; Dr Kurt VerCauteren, National Wildlife Research Center, Colorado; Veterinary Diagnostic Laboratory, Colorado State University; Kerry Mower, New Mexico Department of Game and Fish and the US Department of Agriculture, Animal and Plant Health Inspection Service (APHIS). I owe a huge debt of gratitude to each of these individuals and agencies. Finally, I have been supported in this endeavour by family members and friends who are too numerous to mention individually. I am grateful to them for their kind words of encouragement during my many months of writing.

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Contents

1 BSE – A Leap Into The Unknown . . . . . . . 1.1 Introduction . . . . . . . . . . . . . . . . . 1.2 Transmissible Spongiform Encephalopathies 1.2.1 Creutzfeldt-Jakob Disease . . . . . 1.2.2 Kuru . . . . . . . . . . . . . . . . . 1.2.3 Gerstmann-Sträussler Syndrome . . 1.2.4 Scrapie . . . . . . . . . . . . . . . . 1.2.5 Transmissible Mink Encepalopathy . 1.2.6 Chronic Wasting Disease . . . . . . 1.3 The BSE Knowledge Problem . . . . . . . 1.3.1 The Knowledge Problem Exposed . 1.3.2 The Knowledge Problem Bridged .

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2 The Scientific Challenge . . . . . . . . . . . . . . . . 2.1 Introduction . . . . . . . . . . . . . . . . . . . . 2.2 The Current Paradigm in Epidemiology . . . . . 2.2.1 Theoretical Development in Epidemiology 2.2.2 Epidemiology and Other Disciplines . . . 2.2.3 Reasoning and Epidemiology . . . . . . . 2.2.4 Spatiotemporal Factors and Epidemiology 2.3 Early Epidemiological Investigations . . . . . . .

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3 Arguing Through Uncertainty . . . . . . . . . . . . . . . . . . 3.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . 3.2 Presumption and Science . . . . . . . . . . . . . . . . . . . 3.2.1 Feature 1: Presumptions Display an Orientation to Action . . . . . . . . . . . . . . . . . . . . . . . . 3.2.2 Feature 2: Presumptions Exhibit Rational Justification 3.2.3 Feature 3: Presumptions are Inherently Defeasible . . 3.2.4 Feature 4: Presumptions Display Context Sensitivity . 3.2.5 Feature 5: Presumptions Have a Low-Grade Epistemic Status . . . . . . . . . . . . . . . . . . . . 3.3 Presumption and Uncertainty Management . . . . . . . . . . 3.4 Presumption, Reasoning and Fallacies . . . . . . . . . . . .

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4 Good Arguments During the BSE Inquiry 4.1 Introduction . . . . . . . . . . . . . . 4.2 The Early Years: 1986–1989 . . . . . 4.2.1 Argument from Analogy . . . 4.2.2 Argument from Ignorance . . . 4.2.3 Question-Begging Argument . 4.3 Summary . . . . . . . . . . . . . . .

Contents

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5 The Unravelling of an Argumentative Strategy . 5.1 Introduction . . . . . . . . . . . . . . . . . . 5.2 The Middle Years: 1989–1994 . . . . . . . . 5.2.1 Argument from Analogy . . . . . . . 5.2.2 Argument from Ignorance . . . . . . . 5.2.3 False Attribution of a Part to a Whole 5.3 Summary . . . . . . . . . . . . . . . . . . .

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6 An Unchallengeable Scientific Consensus . . 6.1 Introduction . . . . . . . . . . . . . . . . 6.2 The Final Years: 1994–1996 . . . . . . . 6.2.1 Argument from Analogy . . . . . 6.2.2 Argument from Ignorance . . . . . 6.2.3 Arguing to the Wrong Conclusion 6.3 Summary . . . . . . . . . . . . . . . . .

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7 Political and Commercial Interests in the BSE Inquiry . . . . 7.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . 7.2 Reasoning and Non-scientific Interests in the BSE Inquiry . 7.2.1 Argument from Authority . . . . . . . . . . . . . . 7.2.2 Argument Against the Person . . . . . . . . . . . . 7.2.3 Argument from Analogy . . . . . . . . . . . . . . 7.3 Summary . . . . . . . . . . . . . . . . . . . . . . . . . .

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8 Learning the Lessons of the BSE Crisis . . . . . . . . . 8.1 Introduction . . . . . . . . . . . . . . . . . . . . . . 8.2 A Model of Reasoning in Scientific Inquiry . . . . . 8.2.1 A Model of Reasoning in Early Inquiry . . . 8.2.2 A Model of Reasoning in Middle Inquiry . . . 8.2.3 A Model of Reasoning in Late Inquiry . . . . 8.3 The Model, Risk Analysis and Public Health Science 8.3.1 The Precautionary Principle . . . . . . . . . . 8.3.2 As Low As Reasonably Practicable . . . . . . 8.4 Summary . . . . . . . . . . . . . . . . . . . . . . .

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Bibliography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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List of Figures

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Kuru victims at Kuru Research Centre, Papua New Guinea, late 1950s . . . . . . . . . . . . . . . . . . . . . . . . . . . A boy from the Fore tribe, Papua New Guinea . . . . . . . . Victims of kuru, Papua New Guinea, c1950s . . . . . . . . . A young boy from the Fore tribe in Papua New Guinea . . . Deposition of abnormal prion protein . . . . . . . . . . . . A sheep with scrapie . . . . . . . . . . . . . . . . . . . . . Stellate prion protein deposits in sheep . . . . . . . . . . . . Mink affected with encephalopathy . . . . . . . . . . . . . A haematoxylin and eosin section of the thalamus of mink at the stage of clinical disease with TME . . . . . . . . . . A CWD positive whitetail deer . . . . . . . . . . . . . . . . A CWD positive elk . . . . . . . . . . . . . . . . . . . . . A section from the solitary tract of the brainstem . . . . . . Tonsillar biopsies . . . . . . . . . . . . . . . . . . . . . . . BSE positive cows . . . . . . . . . . . . . . . . . . . . . . BSE positive-neuropil vacuolation . . . . . . . . . . . . . . Scrapie-associated fibril . . . . . . . . . . . . . . . . . . .

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List of Diagrams

2.1 4.1 8.1

Reconstruction of the arguments linking BSE to scrapie . . . . . . . Circle in the reasoning of the Tyrrell Consultative Committee on research . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . A model of scientific reasoning under uncertainty . . . . . . . . . .

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Chapter 1

BSE – A Leap Into The Unknown

1.1 Introduction In 1986, the UK’s scientific community was confronted with the emergence of a new and invariably fatal brain disease in cattle. Diagnosed as bovine spongiform encephalopathy (BSE), this disease joined a group of pre-existing pathologies called the transmissible spongiform encephalopathies (TSEs). TSEs were known to affect a wide range of mammalian vertebrates, including humans. Yet, their study prior to 1986 had occupied something of a twilight zone between veterinary science and medicine. The only apparent implications of TSEs for human health were cases of Creutzfeldt-Jakob disease and the occurrence in the 1950s of a TSE called kuru in the remote Fore tribe of New Guinea. The emergence of BSE in the UK’s national herd thus served to refocus scientific attention on this devastating group of diseases. Although no TSE had previously been identified in cattle, spongiform encephalopathies were nonetheless familiar to farmers and veterinarians through the long-standing presence of scrapie in sheep populations in the UK and elsewhere. Scrapie was also one of the most extensively investigated TSEs with experimental studies of the disease initiated in earnest some decades earlier. Here, it seemed, was a template for how BSE would behave in cattle. In this chapter, I will examine what was known about human and animal TSEs when BSE first emerged in British cattle. This knowledge base had a profound influence on the reasoning of scientists whose task it was to understand and contain this new disease. Certainly, it provided scientists with working hypotheses that were to shape scientific advice to government ministers as well as health pronouncements to the public at all stages of the BSE epidemic. In examining this knowledge base, I will be concerned to establish if its full epistemic potential was exploited by scientists or if certain aspects of this knowledge were allowed to unduly influence scientific thinking about BSE. Of course, in addressing questions about BSE, scientists were compelled to employ reasoning strategies that took them beyond the comfortable confines of what was certain and known about TSEs. Coping with uncertainty was thus a major part of the challenge that BSE presented to scientists. Much will be said in subsequent chapters about the ways in which BSE scientists

L. Cummings, Rethinking the BSE Crisis, DOI 10.1007/978-90-481-9504-6_1,  C Springer Science+Business Media B.V. 2010

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addressed this uncertainty. For my purposes in this chapter, however, I will assess the extent to which the scientific knowledge base about TSEs contributed to that uncertainty.

1.2 Transmissible Spongiform Encephalopathies By 1986, several human and animal TSEs had been identified by scientific researchers. These diseases included the human TSEs Gerstmann-Sträussler syndrome, kuru and Creutzfeldt-Jakob disease.1 The animal TSEs that had been identified included scrapie in sheep and goats, chronic wasting disease in wild deer in North America and transmissible mink encephalopathy. Despite extensive investigation of at least some of these TSEs by 1986, there was still considerable scientific uncertainty about the type of pathogen that was responsible for these diseases. This uncertainty was clearly conveyed in a 1982 article about the scrapie agent by Stanley Prusiner. Prusiner coined the term ‘prion’ (pronounced pree-on) to refer to a proteinaceous infectious particle that he believed was the pathogen responsible for scrapie. Prusiner’s work was to earn him the 1997 Nobel Prize in Medicine. Yet, the chemical structure of this extraordinarily resistant particle2 was still not established in 1982. Specifically, the results of Prusiner’s study indicated that the scrapie agent lacked nucleic acid found in other types of pathogen.3 But, at the same time, postulating the existence of a protein that was devoid of nucleic acid was ‘clearly heretical’.4 Moreover, the absence of a nucleic acid in the scrapie agent suggested that some novel mechanism was needed to explain the replication of prions.5 By the time BSE emerged in British cattle, Prusiner’s prion hypothesis was beginning to gain acceptance. However, as is clear from scientific articles that were published in 1986 and later, investigators still subscribed to the view that a ‘slow’ or ‘unconventional’ virus was responsible for diseases such as scrapie.6 We will return to the issue of what scientists knew about the pathogen responsible for TSEs in later sections. In the meantime, we will consider the state of knowledge of TSEs that existed in 1986.

1.2.1 Creutzfeldt-Jakob Disease By 1986, Creutzfeldt-Jakob disease (CJD) had already been extensively discussed in the scientific literature. Epidemiological studies revealed that CJD had an estimated prevalence rate of approximately 1 per one million population (Tsuji and Kuroiwa 1983). Annual incidence for England and Wales for the periods 1964–1973 and 1970–1979 was 0.09 cases per million (Matthews 1975) and 0.3 cases per million (Will et al. 1986), respectively. Tsuji and Kuroiwa (1983) obtained an annual incidence in Japan of 0.19 per one million population. The disease was generally thought to affect males and females with approximately equal frequency (Brown et al. 1986; Baron et al. 1986; Cathala et al. 1980). However, one study did report an unexpected excess of female cases (Will et al. 1986). CJD typically affects

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individuals in the sixth and seventh decades of life. Brown et al. (1986) reported a mean age of 61.5 years in their study of 230 patients with the disease. The most frequent age at onset in 124 consecutive cases of CJD in France was 60–64 years (Brown et al. 1979a). The three subjects with CJD studied by Mitrová et al. (1978) had a mean age at onset of 52.3 years. Haltia et al. (1979) reported a lower mean age at onset (52 years) in a Finnish family with 9 cases of the disease in three generations. Masters et al. (1981a) found that the onset of disease in familial cases is significantly earlier than in sporadic cases. Cases of CJD have also been reported in adolescents (Brown et al. 1985; Monreal et al. 1981). There is some evidence that certain ethnic groups may be disproportionately affected by CJD. Baron et al. (1986) found that Mediterranean Jews accounted for one-third of cases of CJD in continental France between 1968 and 1982 with Tunisian Jews constituting two-thirds of this ethnic group (see also Cathala et al. 1985). Neugut et al. (1979) found statistically significant clustering of CJD within Libyan-born Israeli families. Space-time clustering of cases has been reported in some studies (Matthews 1975; Mayer et al. 1978) but is not substantiated by other studies (Will et al. 1986; Masters et al. 1979; Brown et al. 1979b). There are three types of CJD: sporadic, familial and iatrogenic CJD. (A new variant of CJD, that is related to exposure to BSE, was not identified until 1996.) Sporadic CJD is the most common form of the disease, with the familial form accounting for 4–8% (Brown et al. 1986), 11.5% (Baron et al. 1986), 15% (Masters et al. 1979) and 45% (Gálvez et al. 1983) of cases in epidemiological studies. In familial cases, the pattern of inheritance appears to be autosomal dominant (Baron et al. 1986; Gálvez et al. 1983; Masters et al. 1981b; Cathala et al. 1980; Haltia et al. 1979). The iatrogenic form of CJD describes cases of the disease that are caused by some form of medical intervention. This can occur through the use of contaminated electrodes during neurosurgery (Bernoulli et al. 1977), cadaveric dura mater grafts and cadaver pituitary-derived growth hormone (Powell-Jackson et al. 1985; Tintner et al. 1986; Rappaport 1987). Natural case-to-case transmission is advanced to explain the repeated finding of a positive correlation between frequency of CJD and population density (Brown et al. 1979b, 1983; Cathala et al. 1982). Experimental transmission of CJD to a range of species has been achieved, including goats, guinea pigs, mice, rats, marmosets and squirrel and patas monkeys (Dr˘ag˘anescu et al. 1984, 1985; Tateishi et al. 1980, 1981a, b; Cathala et al. 1981; Espana et al. 1975–1976; Peterson et al. 1978; Hadlow et al. 1980a). CJD has also been transmitted to hamsters and Mongolian gerbils through rats (Tateishi et al. 1980). Intracerebral inoculation is the most efficient route of transmission followed by other parenteral and oral routes (Tateishi et al. 1980, 1981a). The relationship of CJD to scrapie in sheep had been the subject of a number of epidemiological studies by 1986. Chatelain et al. (1981) found no evidence that regional lamb consumption was correlated with the frequency of CJD between 1968 and 1979 in France. Nor was the geographic distribution of scrapie-affected flocks related to the residential location of patients with CJD. Similarly, Brown et al. (1979b) found that potential exposure to scrapie was not associated with an increased risk of contracting CJD in 170 patients in France between 1968 and 1977

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BSE – A Leap Into The Unknown

(see also Cathala et al. 1979). Studies that suggested a link between CJD and scrapie were Lo Russo et al. (1980) in Italy and Chatelain et al. (1981) in France who found that lamb consumption in nationwide categories of increasing population density correlated with an increasing frequency of CJD (but see studies above that indicate a correlation between population density and frequency of CJD). Also, Dickinson (1976: 213) sounded a cautionary note when he stated that ‘[w]e should not assume, at this stage of our knowledge, that scrapie agents are never transmissible to man from infected meat, particularly as we know that some types of cooking would not inactivate the infectivity’. The clinical symptoms of CJD are numerous. Brown et al. (1979a) established 14 broad categories based on the symptoms they observed during the clinical course of 124 consecutive cases of CJD. Some symptoms were observed infrequently and included cranial nerve anomalies (2%), vegetative symptoms (3%), sensory disturbances (7%) and seizures (9%). Mental deterioration, predominantly dementia, was observed in all subjects. A movement disorder, mostly myoclonus, was observed in 90% of subjects, while 77% of subjects had an evocative electroencephalogram (EEG). Brown et al. (1986) found that the great majority of neurological symptoms in their consecutive series of 230 patients with CJD were of cerebellar or visual origin. In over 95% of these patients, involuntary movement or periodic EEG activity were observed. Ataxia, tremulousness and dementia were observed in two cases of sporadic CJD described by Leiderman et al. (1986). Haltia et al. (1979) described the following consistent clinical features in six subjects with familial CJD: progressive dementia, upper motor neuron signs, muscular rigidity, twitching and irregular tremors. By 1986, atypical cases of CJD had also been described in the literature. Tintner et al. (1986), for example, described the case of a 32-year-old man with iatrogenic CJD who displayed atypical symptoms. This man had predominantly cerebellar signs, little mental deterioration and no abnormal movements or periodic EEG activity. The duration of illness in patients was typically less than a year and often only a few months. In their study of 124 consecutive CJD cases, Brown et al. (1979a) reported that the most frequent duration was 2–3 months. In a later study of a consecutive series of 230 patients, Brown et al. (1986) recorded a median duration of illness of 4 months and a mean of 7.6 months. Of these patients, 90% were dead within a year of onset of the disease. There is some evidence that duration is longer in familial than sporadic CJD (although Baron et al. (1986) concede that this may be due to ascertainment bias). For example, Haltia et al. (1979) reported an average duration of illness in six familial CJD cases of 21 months (range 11–36 months). Brown et al. (1979a) reported much longer durations of illness in the familial CJD cases in their study. In one patient the duration of illness was 40 months, while in another the illness lasted for 120 months. Long incubation periods for CJD in humans and animals have been reported. Baron et al. (1986) found minimal incubation periods of up to 43 years in their study of 329 patients with CJD. Dr˘ag˘anescu et al. (1985) recorded a very long incubation period (over 360–420 days) in guinea pigs which were intracerebrally inoculated with cerebrospinal fluid and/or brain tissue suspensions from patients with CJD.

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By 1986, CJD was most reliably diagnosed by means of post-mortem histological examination. Diagnosis could be performed ante mortem using brain biopsy. However, Levy et al. (1986) argued that brain biopsy is unnecessary in making a diagnosis. These investigators considered that ‘[t]he presence of periodic sharp wave complexes [in EEG] in association with the appropriate clinical, biochemical, cerebrospinal fluid and neuroradiological findings is diagnostic of CJD’ (1986: 1). The histopathological features of CJD were well characterized by 1986. All three CJD patients studied by Mitrová et al. (1978) exhibited neuronal loss, intracytoplasmic vacuolation, spongiosis and astrocytosis. Cortical regions, basal ganglia and cerebella were severely affected. Yamanouchi et al. (1986) described spongiform change, neuronal loss and severe proliferation of astrocytes at autopsy in a 73-yearold woman with CJD. These pathological changes were unusual in this subject in that they only affected the left side of the brain. Amyloid plaques were also known to occur in the brains of some CJD patients (Kitamoto et al. 1986). By 1986, investigators were beginning to examine the role of genetics in CJD. Studies were revealing that genetic factors played a significant role in susceptibility to CJD and controlled the incubation period of the disease. Kuroda et al. (1986) found a highly significant increase of a human leukocyte antigen in 16 cases of CJD in Japan compared to normal subjects. These investigators claimed that this finding provided evidence for the genetic control of susceptibility to CJD in humans. In a study of inbred strains of mice which had been intracerebrally inoculated with the CJD agent, Kingsbury et al. (1983) identified previously unrecognized genes that controlled the length of the CJD incubation period.

1.2.2 Kuru This human TSE was first described in 1957 by Gajdusek and Zigas.7 Kuru was confined to several adjacent valleys in the mountainous interior of New Guinea, where it affected 160 villages with a total population of just over 35,000 people (Gajdusek 1977: 949). Over 80% of kuru cases occurred in the Fore cultural and linguistic group in New Guinea and it is from this group that the disease takes its name (‘kuru’ is the Fore word for shivering or trembling). Between 1957 and 1960, the prevalence of kuru in the South Fore was 20.1 cases per annum per 1,000 population, while in the North Fore prevalence was 10.1 cases (Gajdusek et al. 1961). Kuru mortality in the South Fore was twice that in the North Fore, 16 and 8 cases per annum per 1,000 population, respectively (Gajdusek et al. 1961). These deaths were not evenly distributed between the sexes or, indeed, between different age groups. In the 3-year period between 1957 and 1959, 60% of kuru deaths occurred in adult females. Only 2% of deaths were in adult males, while female and male children accounted for 19 and 12% of kuru deaths, respectively. Zigas and Gajdusek (1959) reported that 23.5% of the first 200 kuru cases studied occurred in pre-adolescent or early adolescent children under 15 years of age. Whatever causative factor(s) gave rise to kuru,8 it was clear they were affecting children and adult females to a much greater extent than adult males. A cultural practice in which women and

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children consumed the bodies of dead kinsmen has since been widely credited with explaining this distribution in kuru deaths. Conjunctival, nasal and skin contamination with highly infectious brain tissue was also thought to be a significant source of kuru infection during this ritual.9 Certainly, since cannibalism ceased in the late 1950s or early 1960s, there had been a steady decline in the number of kuru deaths.10 The first cases of kuru, it is believed, developed following cannibalism of a subject who died of CJD in about 1900 in the hamlet of Uwami (Scrimgeour et al. 1983) (Figs. 1.1, 1.2, 1.3, and 1.4). The clinical characteristics of kuru are numerous and vary with the course of the disease. Prusiner et al. (1982) described clinical features in 15 patients with kuru. Joint pains that preceded difficulty in walking occurred in all patients. Neurological dysfunction varied from mild truncal and limb ataxia to marked ataxia, rigidity, spasticity and dementia in terminal illness. All patients had an apprehensive, frightened facial expression and most had diminished or absent optokinetic nystagmus bilaterally. Apprehensive facies and an absent or diminished optokinetic nystagmus had not previously been described in kuru patients (but see below). Scrimgeour et al. (1983) described the features of kuru in a 42-year-old male from the Eastern Highlands Province of New Guinea. This subject first noticed the gradual onset of weakness in the legs with ataxia in October 1977. He attended a government hospital in April 1978 complaining of occipital headache, pain in the neck and legs and severe gait disturbance. On examination, various primitive reflexes were elicited. The subject presented with dysarthria and moderate ataxia of the upper limbs with intention tremor and dysdiadochokinesis. He was unable to stand without support due to mild truncal ataxia and severe ataxia of the legs. At rest and on movement, irregular, jerky, involuntary contractions of muscle groups in the neck, shoulders

Fig. 1.1 Kuru victims at Kuru Research Centre, Papua New Guinea, late 1950s. The pregnant patient on the left delivered a healthy infant 4 months before her death. Kuru is so advanced in these women that they require the use of one or two sticks for support. Photograph courtesy of D. Carleton Gajdusek/Wellcome Images

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Fig. 1.2 A boy from the Fore tribe, Papua New Guinea, with moderately advanced kuru. He has athetoid (involuntary, repetitive) movements of the arms and strabismus (squinting). Photograph courtesy of D. Carleton Gajdusek/ Wellcome Images

Fig. 1.3 Victims of kuru, Papua New Guinea, c1950s. One of the women has developed choreiform movements of the upper limbs. A number of the women are seen smiling. One of the characteristics of the disease is unmotivated laughter. Photograph courtesy of D. Carleton Gajdusek/Wellcome Images

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Fig. 1.4 A young boy from the Fore tribe in Papua New Guinea with advanced stages of kuru. He had muscular weakness preventing him sitting up without support. There was also strabismus present. Photograph courtesy of D. Carleton Gajdusek/Wellcome Images

and limbs were present. The clinical features of cerebellar dysfunction became progressively more severe. Dementia and dyspraxia were present. Sustained clonus of knee and ankle and hyperreflexia (both indicative of pyramidal tract dysfunction) developed latterly. Basal ganglia dysfunction appeared in the late stages of the disease. Like Prusiner’s subjects, this patient presented with an anguished expression. The patient died 7 months after admission. Scrimgeour et al. estimated that the incubation period in this patient was over 20 years, while the duration of the disease was approximately 12 months. After death, this patient’s brain was examined to establish its histopathological features. Sections were taken from the frontal cortex, cingulate, motor strip, temporal cortex, occipital cortex, hippocampus and caudate/putamen. Spongiform change was observed in all these areas and was particularly severe in the cingulate, motor

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strip and caudate/putamen. Moderate gliosis was present in all areas except temporal and occipital cortices. Mild amyloid plaques were observed in two regions, the motor strip and occipital cortex. Neuronal loss was mild in the frontal cortex, motor strip and hippocampus and moderate in the cingulate and caudate/putamen. Neuronal loss was not observed in the temporal and occipital cortices. Zigas and Gajdusek (1959) obtained complete post-mortem examinations on 25 of over 300 cases of kuru that were investigated during the first year of intense field study. The main pathological findings in the central nervous system were widespread neuronal degeneration, myelin degeneration, astroglia and microglia proliferation, presence of plaque-like bodies and occasional perivascular cuffings with mononuclear cells. Neuronal degeneration was most severe in the cerebellum and extra-pyramidal system, although there were also changes in the anterior horn cells, inferior olives, thalamus and pontine nuclei. Myelin degeneration most commonly involved pyramidal, spinocerebellar tracts, brachia conjunctiva and brachia pontis. Astroglial and microglial proliferation were usually very intense. The former was found in areas of neuronal degeneration, although astrocytic gliosis was also intense in areas of minimal neuronal loss. Microglia proliferation occurred in degenerative grey and white matter. Plaque-like bodies were found in the majority of kuru cases. They occured frequently in the cerebellum and were found occasionally in the basal ganglia and cerebral cortex. Perivascular cuffings were seen in some kuru cases and were usually found in the medulla, pons and basal ganglia. By 1986, it was known that kuru could be transmitted experimentally to a number of primates. They included rhesus monkeys (Gambarelli et al. 1981), spider monkeys (Beck et al. 1975, 1982; Gajdusek et al. 1968), pigtail macaques (Gambarelli and Vuillon-Cacciuttolo 1983), squirrel monkeys (Gibbs et al. 1980; Scrimgeour et al. 1983), gibbons (Masters et al. 1976a), capuchin monkeys (Scrimgeour et al. 1983), marmosets (Peterson et al. 1978), sooty mangabeys (Masters et al. 1976a) and chimpanzees (Lampert et al. 1975). Transmission was achieved through intracerebral inoculation (e.g. Gambarelli and Vuillon-Cacciuttolo 1983) and the oral route (Gibbs et al. 1980). Variable incubation periods were observed via these different routes of infection. The squirrel monkey which was orally exposed to kuru by Gibbs et al. (1980) had an incubation period of 36 months. The squirrel and capuchin monkeys intracerebrally inoculated by Scrimgeour et al. (1983) displayed incubation periods of 27.5, 37, 39 and 43 months. Histopathological features of experimental kuru include spongiosis of the neuropil, neuronal vacuolization, astrocytic hyperplasia and neuronal loss (Masters et al. 1976b; Gambarelli et al. 1981; Gambarelli and Vuillon-Cacciuttolo 1983). Beck et al. (1975) described the histopathological features of experimental kuru in spider monkeys which were incubating the disease but were free of neurological signs. Bi-nucleated neurones were found in the limbic cortex, striatum, hypothalamus and amongst Purkinje cells of the cerebellum at 4 weeks after inoculation. There was a loss of neurones and proliferation of fibrous astrocytes in the cerebral and cerebellar cortex in the later stages of incubation. Fibrous astrocytes also proliferated in the hypothalamus. Status spongiosis and generalized astrocytic proliferation and hypertrophy, both of which are characteristic of fully developed experimental kuru, were not

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observed. Ultrastructural abnormalities included membrane-bound intracytoplasmic vacuoles predominantly in dendrites and concentric laminar arrays derived from the endoplasmic reticulum.

1.2.3 Gerstmann-Sträussler Syndrome Gerstmann-Sträussler syndrome (GSS), also called Gerstmann-Sträussler-Scheinker syndrome, was certainly the least known and investigated human TSE in 1986. Since 1928, when Gerstmann recorded an unusual cerebellar disease in a female who was 25 years of age at onset, several cases of GSS have been described in the literature. What these cases had in common was the appearance of the disease in a number of family members over two or more generations. In this way, Hudson et al. (1983) described an Italian family in which two sisters and the son of one of the sisters were known to have GSS. This spongiform encephalopathy was known to differ from CJD in a number of respects. Firstly, GSS progresses more slowly than CJD. The duration of illness in the three subjects examined by Hudson et al. was 3.5, 6 and 8 years, respectively. Secondly, the age at death in GSS is lower than in CJD. In 17 cases examined by Masters et al. (1981b), the mean age at death was 48 years (range 29–62 years). Thirdly, amyloid plaques, which are only observed in some CJD patients, are found in all GSS subjects (Kitamoto et al. 1986). Fourthly, spongiform change is less severe in GSS than in CJD (although Vinters et al. (1986) reported a much greater degree of cortical spongy change in the subject in their study than was observed in the relatives of this subject, a finding which indicated phenotypic heterogeneity in the disorder). Other histopathological features of GSS include severe astrocytic gliosis in the grey and white matter, pronounced neurone loss (Vinters et al. 1986) and white matter loss or degeneration (Masters et al. 1981b) (Fig. 1.5). The clinical features of GSS vary with progression of the disease. In one of the three cases examined by Hudson et al. (1983), difficulty in walking was the first clinical sign. Within the first year of illness, the patient experienced an impairment of writing, slurred speech and had slight difficulty swallowing. At 2.5 years after onset, a slight nystagmus on upward gaze, pseudobulbar dysarthria, slow movement of all limbs, slight awkwardness in arms, frank weakness and ataxia of lower limbs, brisk deep tendon reflexes and bilateral Babinski’s signs were observed. At 3.5 years after onset, the patient was confined to a wheelchair. He had severe dysarthria, nystagmus on lateral and vertical directions of gaze, weakness of convergence of eyes, incoordination of all extremities, moderate weakness of lower extremities, absent deep tendon reflexes in upper and lower limbs and bilateral Babinski’s signs. At 1 year prior to death, he was unable to feed himself because of extreme incoordination and weakness of arms. He was incontinent of urine, his speech was difficult to interpret and his swallowing was poor. At this time, he appeared intellectually normal, although his mental state subsequently deteriorated. At 1 month prior to his death, he was severely dysarthric but could say ‘yes’ and ‘no’. He appeared alert

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Fig. 1.5 Deposition of abnormal prion protein (PrP) in different types of prion diseases. (a) In many cases of sporadic CJD, there is a synaptic (diffuse granular) deposition of PrP. (b) Variant CJD often shows plaques, which are sometimes surrounded by small vacuoles. In addition, there are also synaptic deposits seen. (c) Kuru often shows deposition of prion protein in the form of dense core plaques, but many areas may also show deposition of synaptic PrP. (d) Deposition of plaques of variable size in inherited prion disease with P102L mutation (Gerstmann-SträusslerScheinker syndrome). In addition to the plaques, this form of prion diseases may also show synaptic deposition. Scale bar: (a), (c) 50 µm; (b), (d) 100 µm (Courtesy of Professor Sebastian Brandner, Chair of Neuropathology, Division of Neuropathology and Department of Neurodegenerative Disease, Institute of Neurology, London)

and cooperative, but could only respond to simple commands. He exhibited bilateral limitation of lateral and upward gaze, nystagmus to both right and left lateral gaze, spastic muscle tone, flexed posture in upper limbs, extension of lower limbs and neck stiffness. Motor power was slightly decreased in his upper limbs and there was weakness in the lower extremities. There was marked wasting of muscle in the lower extremities, particularly below the knees. The lower limbs were immobile and upper limb movements were slow, ataxic and at times athetoid like. Deep tendon reflexes were present in the arms but absent in the lower extremities. Plantar responses were bilaterally extensor. Sensory testing was not possible. By 1986, GSS had been experimentally transmitted via intracerebral inoculation to marmosets (Baker et al. 1985) and mice (Tateishi et al. 1984). The marmosets inoculated by Baker et al. using brain tissue from a patient with CJD and a second patient with GSS displayed similar histopathological changes. Specifically, this included spongiform change which was most pronounced in the basal ganglia and thalamus. In neither case was amyloid deposition detected. Similar histopathological patterns were observed by Tateishi et al. in mice that had been inoculated with GSS and CJD. These patterns involved spongiform change and astroglial proliferation in the cerebral cortex, especially in the parietal lobe and hippocampus, thalamus and basal ganglia. Changes in the cerebral white matter, brainstem and cerebellum were less prominent in mice inoculated with GSS than in those inoculated with CJD. No amyloid plaques were observed in the mice receiving GSS inoculum. Baker et al. reported that the average survival time for marmosets inoculated with brain tissue from a GSS patient (29.5 months) was longer than that for animals inoculated with tissue from a CJD patient (21.4 months). Tateishi et al. recorded the appearance of

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clinical symptoms at 255 and 244 days after inoculation in the first passage mice which were inoculated with GSS in their study. This incubation period dropped to 144 and 153 days in second passage mice. The incubation periods in the first passage GSS mice were considerably shorter than those seen in mice inoculated with CJD.

1.2.4 Scrapie By 1986, scrapie11 was by far the best known animal TSE. Although the first published article on scrapie appeared in 1913 in the Journal of Comparative Pathology (Stockman 1913), the disease had first been recorded in England nearly 200 years earlier in 1732. Extensive research of this spongiform encephalopathy had been underway in Great Britain since the 1940s. This research was undertaken at three institutions, the Moredun Research Institute in Edinburgh, the Agricultural Research Council (ARC) Field Station at Compton in Berkshire and the ARC Animal Breeding Research Organisation in Edinburgh.12 An American veterinary neuropathologist, William Hadlow, worked at Compton in the 1950s. Hadlow’s work was to have a profound influence on our understanding of scrapie, a disease that had consistently confounded scientific researchers.13 In this way, Palmer (1957: 1318) remarked that ‘[t]here is a mystery about scrapie that makes it an unpopular subject for research; its study can be a chastening experience. The condition has defied solution so persistently that perhaps it should be classified as a disease extraordinary’. As importantly, however, Hadlow was also the first scientist to propose a link between scrapie in sheep and kuru in the Fore people of New Guinea.14 On the basis of his experience of the experimental induction of scrapie in sheep, Hadlow recommended that efforts be made to experimentally induce kuru in a laboratory primate.15 This recommendation prompted Carleton Gajdusek to reconsider his view of the aetiology of kuru,16 a view that had been gravitating towards a genetic basis for the disorder.17 Although Hadlow’s work didn’t receive the recognition at the time that many believed it warranted,18 his contribution to our understanding of TSEs was to be felt again nearly three decades later when BSE emerged in British cattle. By 1986, a number of epidemiological studies of scrapie had been undertaken. Dickinson (1976) reported that a 10% incidence of scrapie in certain breeds and flocks is not uncommon and it is occasionally much higher. In France, Chatelain et al. (1986) examined the incidence of scrapie in a flock of Ile de France sheep between 1978 and 1983. Incidence varied from year to year. The average incidence for the 5 year period of the study was 8.3%. The onset of scrapie occurred most frequently between the ages of 2 and 4 years with 25 of 45 (55% of) affected sheep developing the disease in this age group. In the later years of the study, the onset of the disease occurred in younger age groups suggesting the presence of genetic anticipation in this flock. In an earlier study of the frequency of scrapie in different breeds of sheep in France between 1968 and 1979, Chatelain et al. (1983) recorded 1.8 outbreaks of scrapie per 100,000 Ile de France sheep. Scrapie was most

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commonly found in Hampshire and Suffolk sheep in this study, with 60.0 and 40.0 outbreaks occurring per 100,000 sheep, respectively. Mortality rates due to scrapie have been found to vary considerably. Pálsson (1979) reported mortality rates due to rida (scrapie) in some Icelandic flocks of 3–5% annually among breeding ewes. In other Icelandic flocks, Pálsson noted a mortality rate among adults of more that 30% annually. The transmissible nature of scrapie had been apparent to scientists for many years prior to the emergence of BSE. The first sign that scrapie was transmissible was obtained inadvertently. In 1946, William Gordon reported that scrapie had been transmitted to sheep using a louping-ill vaccine. The vaccine had been prepared using a 10% saline suspension of brain, spinal cord and spleen tissues taken from sheep 5 days after infection with louping-ill virus. Some 18,000 doses from an infected batch of vaccine prepared in 1935 were administered to sheep. The incidence of scrapie in these sheep ranged from 1 to 35% with an average of about 5% (Gordon 1946). Natural transmission among sheep and between sheep and goats has since been demonstrated in a number of experiments.19 Hadlow et al. (1980b) found that three dairy goats became infected with scrapie while living with naturally infected Suffolk sheep. Brotherston et al. (1968) reported that 10 of 17 goats which were kept for long periods in the same pen as sheep infected with natural scrapie subsequently developed the disease. Transmission to goats did not occur when sheep with experimental scrapie were used. Blackface sheep which were kept in continuous contact with naturally infected sheep of various breeds from the time of birth for periods of 3 years 9 months to 4 years 4 months also developed scrapie. Dickinson et al. (1974) reported the occurrence of lateral transmission of scrapie under normal field conditions in 28% of purebred Scottish Blackface sheep which had been in lifetime contact with Suffolk × Blackface crosses (Suffolk sheep, unlike Scottish Blackface sheep, develop natural scrapie). This study also demonstrated a dominant role for maternal transmission of the scrapie agent. Animal-to-animal transmission has also been demonstrated in other species. Zlotnik (1968) found that uninoculated mice developed scrapie after a period of cohabitation of 15–16 months with mice which had been inoculated with the disease. The transmission studies examined above all relate to transmission under natural (i.e. non-experimental) conditions. However, as with other spongiform encephalopathies, scrapie has also been experimentally transmitted to a number of species. Hanson et al. (1971) reported the transmission of a spongiform encephalopathy to mink following intracerebral inoculation using a brain suspension from Suffolk sheep with naturally acquired scrapie. The resulting disease was indistinguishable in terms of both clinical signs and pathological lesions from transmissible mink encephalopathy. Hadlow and Race (1986) transmitted scrapie via intracerebral inoculation to four African pygmy goats. Pattison (1965) transmitted scrapie to goats and mice that had been inoculated intracerebrally with scrapie goat brain and scrapie mouse brain, respectively. Zlotnik and Rennie (1965) succeeded in experimentally transmitting mouse passaged scrapie to goats, sheep, rats and hamsters. Transmission was achieved through intracerebral inoculation (goats, rats, hamsters) and subcutaneous inoculation (sheep).

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Although scrapie can be experimentally transmitted via a number of routes, some have been shown to be more efficient than others. Kimberlin and Walker (1978) found that the intracerebral route was the most efficient, followed by intravenous, intraperitoneal and subcutaneous routes. Kimberlin et al. (1971) reported an increased incubation period in mice which were inoculated with scrapie via the intraperitoneal route. The incubation period was 3–4 weeks longer in the mice in this study than that which is routinely observed in BSVS (bacteria susceptible, virus susceptible) mice which are inoculated intracerebrally with the Chandler strain of scrapie agent. Kimberlin et al. attribute this increased incubation period to the delay that occurs after intraperitoneal inoculation before the agent reaches the brain.20 There was also evidence of qualitative differences in the distribution of lesions in these intraperitoneally inoculated mice compared to mice which had been inoculated intracerebrally. The mice in this study exhibited an absence of astrocyte reaction and of certain enzyme activity from the corpus callosum and there was a low incidence of vacuolation in the hippocampus. These differences in the distribution of lesions were attributed to different sites of entry of the scrapie agent into the central nervous system (CNS) in intraperitoneal and intracerebral inoculation.21 Pathogenesis studies of scrapie conducted by 1986 had consistently revealed early infectivity of tissues in the lymphoreticular system.22 Hadlow et al. (1982) found scrapie virus first in the lymphatic tissues and intestines of clinically normal lambs of 10–14 months of age. The first sign of scrapie virus in the CNS was in a clinically normal sheep of 25 months of age. These investigators stated that ‘[t]he early appearance of virus in tonsil, retropharyngeal and mesenteric-portal lymph nodes, and intestine suggests that primary infection occurs by way of the alimentary tract, either prenatally from virus in amniotic fluid or postnatally from virus in a contaminated environment’ (1982: 657). The important role of the spleen in the extraneural replication of the scrapie agent was demonstrated in a study by Fraser and Dickinson (1978). These investigators found that splenectomy in mice reduced the host’s capacity to replicate the ME7 scrapie agent. Splenectomy increased the incubation period of scrapie in mice following intraperitoneal infection by 10–30%. The replicative capacity that was lost following splenectomy remained for at least 60 days following the procedure. The replicative loss was less pronounced in newborn mice – the incubation period was prolonged in splenectomized newborn mice by over 9%. Experiments involving thymectomy failed to show any role for the thymus and its dependent lymphoid system in the pathogenesis and replication of scrapie in mice. Hadlow et al. (1980b) reported that scrapie virus was widespread in non-neural sites, particularly lymphatic tissues and intestines, in dairy goats that had become infected with scrapie while living with naturally infected Suffolk sheep. When scrapie agent progresses to the CNS, infectivity titres exceed those found in the lymphoreticular system and significant histological changes can also be observed.23 Hadlow et al. (1980b) found scrapie virus in much higher titres (5.1–5.8 log10 mouse intracerebral LD 50/30 mg of tissue) in nervous tissue in dairy goats than in non-neural sites (titres ranged from 3.0 to 3.5 log10 in these sites). The most severe histological changes were observed in the diencephalon, midbrain, medulla oblongata, and cerebellar cortex, all of which had the highest mean titres. Bruce

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(1981) used mice which had been intracerebrally inoculated with scrapie agent to examine the number of amyloid plaques and the severity of vacuolar lesions that developed during the incubation period. The first histological lesions, which appeared at 60 days after injection, were amyloid plaques (these plaques are now known to contain protease-resistant prion protein). The appearance of plaques long before vacuolation or other changes occurred suggested that they were not simply secondary to degenerative vacuolar lesions. The first plaques to appear were found close to the lateral ventricles and were probably related to the localization of inoculum soon after injection. In the later part of the incubation period, when vacuolation was also present, plaques were detected in areas distant from the ventricles. The histopathological pattern in the brain is influenced by the type of scrapie agent used in inoculation. Hadlow and Race (1986) found widespread spongiform degeneration of the cerebral cortex in four African pygmy goats that had been intracerebrally inoculated with scrapie agent from Suffolk sheep brain. This pattern is typical of that found in goats that are inoculated with transmissible mink encephalopathy. The scrapie agent that was used in this study had been passed three times in ranch mink. Fraser and Dickinson (1973) found that any of five different types of scrapie agent could be reliably distinguished from the others based on a lesion profile that involved damage in nine brain regions in two inbred mouse strains. The lesion profiles in the mice were not affected by the dose of scrapie agent used (Figs 1.6 and 1.7). By 1986, scientists knew that genes regulated the pathogenesis of scrapie in a host. Dickinson and Fraser (1969) investigated titres of scrapie agent in the spleen of mice with two different alleles of the sinc gene24 up to 29 days after inoculation. Some mice were homozygous for the s7 allele (short incubation period), while

Fig. 1.6 A sheep with scrapie. An intense itching sensation (pruritus) is one of the symptoms of the disease. This causes the animal to engage in rubbing, scraping or chewing behaviour with resulting deterioration of the fleece. © Crown copyright 2011. Published with the permission of the Controller of Her Majesty’s Stationery Office. The views expressed are those of the author and do not necessarily reflect those of Her Majesty’s Stationery Office or the Veterinary Laboratories Agency or any other government department

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Fig. 1.7 Stellate prion protein deposits in sheep. Radiating, branching deposits often centred on glial nuclei of diverse morphologies and occasionally around neurones. Can be found throughout the grey matter of most brain areas, including the cerebral and cerebellar cortices. © Crown copyright 2011. Published with the permission of the Controller of Her Majesty’s Stationery Office. The views expressed are those of the author and do not necessarily reflect those of Her Majesty’s Stationery Office or the Veterinary Laboratories Agency or any other government department

others were homozygous for the p7 allele (long incubation period). Mice with the long incubation period allele experienced a delay of 4 weeks in the initiation of an increase of scrapie agent in the spleen. Mice with the allele for a short incubation period experienced an almost immediate increase in the concentration of scrapie agent in the spleen. Dickinson et al. (1969) examined mice with the same alleles of the sinc gene for the period subsequent to 60 days after inoculation. At this later stage of disease progression, the titre of scrapie agent in the spleen of these mice did not differ. Where mice with these two alleles did differ was in the titre of scrapie agent in the brain. Mice with the p7 alleles exhibited a long initial delay in the increase of titre in the brain. However, mice with both types of alleles were similar in the subsequent rate of increase and in terminal scrapie titre. The two alleles (s7 and p7) of the sinc gene in mice show no dominance (Dickinson et al. 1968a). The same is not true, however, of genes that control the incubation period of scrapie in sheep. Dickinson et al. (1968b) found evidence of a gene in Cheviot sheep that controlled susceptibility to clinical scrapie. The dominant allele of this gene conferred susceptibility on the host – clinical signs appeared 197±7 days following intracerebral inoculation or 313±9 days when inoculation was performed subcutaneously. Sheep that appeared to be homozygous for the recessive resistant allele of the gene only developed scrapie after a very long interval of 917±90 days following intracerebral inoculation (see also Nussbaum et al. 1975). Breeding experiments were already underway by 1986 to develop flocks of sheep that displayed reduced susceptibility to experimental scrapie (Davies and Kimberlin 1985).

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1.2.5 Transmissible Mink Encepalopathy Although transmissible mink encephalopathy (TME) had not been studied to the same extent as scrapie, much was still known about this spongiform encephalopathy in 1986. The disease was first described in 1965 by Hartsough and Burger in Wisconsin. Hadlow (1965) described the same disease in Idaho ranch mink. Hadlow and Karstad (1968) reported the occurrence of the disease in Ontario, Canada. All three outbreaks occurred during the summer of 1963 (Hadlow and Karstad 1968). Only adult breeder animals over 1 year of age are affected by the disease (Barlow 1972). Hadlow and Karstad (1968) explain the age of affected animals by the ‘unusually long’ incubation period of 6.5 months or more. Dukur et al. (1986) found that the incubation period in the experimentally induced mink in their study varied from 7 to 9 months with different routes of inoculation. Marsh and Hanson (1979) reported that intradermal inoculation was an efficient means of exposure to the TME agent in the mink in their study. Barlow (1972) found little or no evidence of horizontal (lateral) or vertical transmission in naturally occurring TME (but see Dukur et al. (1986) who reported lateral and maternal transmission and Marsh and Hanson (1979) who described how bite wounds inflicted by littermates could spread the infectious agent between mink). By 1986, TME had been experimentally transmitted to other species including Chinese hamsters (Kimberlin et al. 1986) and squirrel monkeys (Eckroade et al. 1970). However, TME appeared to be biologically inactive in mice with experimental studies failing to achieve transmission of the disease (Taylor et al. 1986).25 The TME agent was known to possess the same extraordinary resistance to chemical and other challenge that had been witnessed in scrapie. In this way, Burger and Gorham (1977) reported that the TME virus retained biological activity after prolonged storage in formalin of approximately 3.5 years and in paraffin tissue blocks that are used for histological preparations (the latter for approximately 6.5 years). Marsh and Hanson (1969) found that the TME agent was resistant to ultraviolet irradiation and relatively resistant to 10% formalin.26 The TME agent was not an infectious nucleic acid (Marsh et al. 1974). As with other TSEs, no inflammatory response was observed in TME27 (Figs 1.8 and 1.9). The clinical signs of TME include locomotor disturbances and excitability. Over a few weeks, this progresses to ataxia which is characterized by stiff, jerky movements. There are increasing periods of somnolence (Barlow 1972). Marsh and Kimberlin (1975) reported that ataxia was not prominent in TME-affected hamsters. Rather, these animals tended to become more and more lethargic as the disease progressed. Hadlow and Karstad (1968) described histopathological changes that occurred in the brains of mink which had developed TME in the Ontario outbreak. These changes included a loosened or porous appearance of grey matter which varied from scattered patches of holes to diffuse sponginess of neural tissue. Some neurones were shrunken and deeply basophilic, while others had disappeared. The cytoplasm of some neurones was vacuolated. The size and number of astrocyte nuclei had increased. The cerebral cortex was affected,

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Fig. 1.8 Mink affected with encephalopathy may appear somnolent and grasp an object for extended time periods. Photograph taken from Virus Infections of Carnivores, M.J. Appel (ed), Elsevier Science Publishers B.V., 1987. The permission of Elsevier to reproduce this photograph is gratefully acknowledged

Fig. 1.9 A haematoxylin and eosin section of the thalamus of mink at the stage of clinical disease with TME. The diseased mink was experimentally inoculated with TME by the oral route. Like spongiform encephalopathies in other species, there is extensive vacuolation. Courtesy of Dr Jason C. Bartz, Medical Microbiology and Immunology, School of Medicine, Creighton University, Nebraska, USA

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sometimes to a large extent. Gyri along the midline in the more rostral parts of the cerebrum were often most severely affected. Sometimes the hippocampal formation was involved. The diencephalon and corpus striatum were regularly affected. The same histopathological changes of astrocytic hypertrophy, microvacuolation of the neuropil and neuronal degeneration have also been observed in TME-affected hamsters (Marsh and Kimberlin 1975). Different strains of the TME agent have been found to produce characteristic profiles of vacuolation in hamsters (Kimberlin et al. 1986). Studies of tissue infectivity in hamsters have revealed that the TME agent multiplies rapidly in the brain prior to the onset of clinical signs and that titres in the spleen were 4–6 logs lower than titres in the brain during the asymptomatic or clinical course of the disease (Marsh and Kimberlin 1975). In hamsters dying of TME, the corneal epithelium has been found to be infectious (Marsh and Hanson 1975). Marsh et al. (1973) failed to find infectivity in lymphocytes of mink with TME.

1.2.6 Chronic Wasting Disease In 1986, chronic wasting disease (CWD) was the least investigated TSE in animals. This disease was known to affect Rocky Mountain elk (Williams and Young 1982), mule deer and black-tailed deer (Williams and Young 1980). All affected animals were held in captivity in several wildlife facilities in Colorado and Wyoming. In mule deer and elk, clinical signs occurred after captivity lasting 2.5–4 years, and 3–5 years, respectively. The disease affected males, females and castrates. The duration of illness was 1–6 months in elk and 2 weeks to 8 months in mule deer (Williams and Young 1980; Williams and Young 1982). Behavioural changes were observed in all animals and included nervousness or hyperexcitability, alterations in personality and changes of behaviour towards handlers. Progressive weight loss led to emaciation. No motor or sensory neurological signs were observed. The course of the disease was usually interrupted by complications (e.g. pneumonia) or euthanasia. Histopathological changes, which were limited to the CNS, included the now familiar triad of widespread spongiform transformation of the neuropil, single or multiple intracytoplasmic vacuoles in neuronal perikaryons (cell bodies) and intense astrocytic hypertrophy and hyperplasia (Williams and Young 1980). Bahmanyar et al. (1985) found amyloid plaques in CNS tissues in 13 of 21 (62%) adult captive mule deer with CWD. In 1986, little was known about how CWD was transmitted. The elk studied by Williams and Young (1982) had sporadic fence-line contact with clinically normal and affected deer. They were also occasionally kept in pens in which CWD-affected deer had been previously held. This led Williams and Young to consider the role of horizontal transmission in the movement of this disease between species28 (Figs 1.10, 1.11, 1.12, and 1.13).

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Fig. 1.10 A CWD positive whitetail deer. There is extensive wasting of the neck, flank and hindquarters (Courtesy of the Wisconsin Department of Natural Resources)

Fig. 1.11 A CWD positive elk. This elk displayed an extraordinary rate of decline. Within just 6 days, it went from having normal appearance, to displaying obvious signs and then lying down, at which point it was euthanized. (Courtesy of Dr Kurt VerCauteren, Research Wildlife Biologist, CWD Project Leader, National Wildlife Research Center, USDA/APHIS/Wildlife Services, 4101 Laporte Ave, Fort Collins, Colorado 80521)

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21

Fig. 1.12 A section from the solitary tract of the brainstem at the level of the obex from a CWD positive elk that originated from Canada. It displays the vacuoles that are characteristic of CWD as well as cell nuclei (dark dots). It has been produced using haematoxylin and eosin (H&E) staining (Courtesy of Histopathology, Department of Pathology, Veterinary Laboratories Agency, Weybridge, England)

Fig. 1.13 Tonsillar biopsies can be used to diagnose CWD in animals suspected of having the disease. The stained circular areas in this image of tonsillar tissue are positive lymphoid follicles (Prepared by the Veterinary Diagnostic Laboratory of Colorado State University and supplied by Kerry Mower of the New Mexico Department of Game and Fish)

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BSE – A Leap Into The Unknown

1.3 The BSE Knowledge Problem The review in Section 1.2 of what was known about TSEs in 1986 is certainly not intended to be exhaustive. Yet, it nonetheless conveys something of the extent of the scientific knowledge base that existed at the time. That knowledge base, and the reasoning skills that scientists employed when assessing its contents, were the basis of the scientific response to the emergence of a new brain disease in cattle. In this section, we examine the different types of knowledge that scientists were able to bring to bear upon questions relating to the nature and behaviour of BSE. The BSE problem presented a uniquely difficult challenge to scientists. Never before had scientists had to assess the risk posed to human health by a spongiform encephalopthy that would have to jump species to infect man and that would most likely pass to man through the oral route, although parenteral transmission was also a possibility.29 Certainly, the cases of kuru and CJD showed that oral and parenteral transmission of a spongiform encephalopathy to man was possible. But the infectious agents in kuru and CJD were already adapted to a human host and did not have to cross a species barrier. Similarly, spongiform encephalopathies had been shown to transmit between species. But such transmission was achieved through experimental means (e.g. intracerebral inoculation) and the host was typically primates and lower mammals which would not necessarily have the same response as man to the infectious agent in TSEs. Whatever way investigators turned, pre-existing knowledge of TSEs in 1986 only permitted scientists to address questions about BSE indirectly. The challenge for scientists was to assess this background knowledge and decide which aspects of it would provide a rational basis for addressing issues relating to BSE. The species barrier that BSE would have to cross in order to infect man and the oral route through which this disease would most likely be transmitted to humans conferred a special seductiveness on another animal TSE. The disease in question was scrapie in sheep. Here was a spongiform encephalopathy that appeared to address two significant gaps in our scientific knowledge about BSE. Firstly, scrapie would have to overcome the same species barrier to transmission that was a source of considerable uncertainty in BSE. Secondly, if scrapie were to cross the species barrier to humans, the oral route was likely to be its most important route of transmission. In terms of both species barrier and route of transmission, scrapie seemed to assume special significance above all other animal and human TSEs for scientists considering the problem of BSE. Even more importantly, extensive veterinary experience with scrapie had failed to link any case of human disease to this animal TSE. The TSE that appeared closest to BSE in terms of its potential to cause disease in humans thus provided scientists with some degree of reassurance that BSE might have few, if any, implications for human health. As well as considering the knowledge gaps that confronted scientists in their deliberations about BSE, this section will examine those aspects of our knowledge of TSEs in 1986 that had epistemic salience for scientists who were attempting to close those gaps. The issue of whether that salience was warranted will be examined in subsequent chapters. For the purposes of this chapter, however, it will suffice to

1.3

The BSE Knowledge Problem

23

identify the gaps in knowledge of TSEs that were of relevance to scientists who were charged with responding to BSE in 1986 and to establish how scientists envisaged those gaps might be most effectively addressed.

1.3.1 The Knowledge Problem Exposed Scientists who were charged with responding to the emergence of BSE were in no doubt that theirs was a particularly daunting epistemic challenge. In private communications to each other and in evidence submitted to Lord Phillips and his team, scientists were candid about the lack of knowledge and uncertainty that confronted every aspect of their deliberations. In a letter dated 9 August 1988 to Dr E. Poole of the Radcliffe Infirmary in Oxford, Sir Richard Southwood30 stated that ‘[m]y colleagues and I have made various recommendations based, I have to admit, largely on guesswork and drawing parallels from the existing knowledge of scrapie and CJD’ (BSE Inquiry Report, Volume 1: 55). In oral evidence to Lord Phillips and his team, Sir Richard remarked: . . .the science was so uncertain here we often had to leave – what was distasteful for us as scientists – a really secure base and make a judgement. They are difficult judgements that people have to make from time to time. Good and wise men and women may reach different sorts of conclusions. We were actually all unanimous, but it would have been quite possible for us to have a minority report on some aspects of it because there were so many uncertainties (BSE Inquiry Report, Volume 4: 67).

Indeed, the science was uncertain. By 1986, Stanley Prusiner’s proposal that the causative agent in TSEs was an infectious protein was only beginning to gain ground, and was still contested in many scientific quarters. So even if it could be demonstrated that BSE was a TSE, this fact in itself did little to shed light on the type of pathogen that scientists were confronting or on how containment of this pathogen could be achieved. Mr Cruickshank of the Animal Health Group in the UK’s Ministry of Agriculture, Fisheries and Food (MAFF) succinctly captured the uncertainty and lack of knowledge that characterized the early days of this new disease when he remarked that ‘[w]e do not know where this disease came from, we do not know how it is spread and we do not know whether it can be passed to humans’ (BSE Inquiry Report, Volume 1: 44). When BSE first came to the attention of scientists, the knowledge problem for investigators was thus all pervasive. Although an extensive knowledge base existed for other TSEs, scientists lacked the knowledge that was required to link this new brain disease in cattle to that base. Specifically, the histopathological examinations and transmission experiments31 that would eventually lead to the identification of this new disease as a bovine TSE had yet to be undertaken and would not result in a definitive classification of the disease as a TSE until September 1988.32 The first knowledge gap to confront scientists therefore concerned the classification of the disease as a type of TSE.

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BSE – A Leap Into The Unknown

Knowledge Gap 1: The classification or nature of this new bovine brain disease The integration of this new bovine disease within the TSE knowledge base was actively pursued by investigators, as it secured a number of early gains for scientists. Firstly, this body of knowledge provided a highly structured framework in which scientists could proceed to generate predictions about this bovine TSE. Every aspect of these diseases from routes of transmission to pathogenesis, length of incubation period and clinical course had been previously examined in the context of other TSEs. Such examination might reasonably be expected to offer a rational basis upon which predictions about BSE could be generated and subsequently tested in a rigorous programme of research. Secondly, a practical demand for disease containment measures to be implemented could be satisfied by integrating BSE within the TSE knowledge base (although previous attempts to contain TSE diseases (e.g. outbreaks of scrapie in Iceland) had largely demonstrated the ineffectiveness of most containment efforts). Thirdly, an assessment of the risk posed by BSE to public health was also made possible through the integration of this new bovine disease with other TSEs. This assessment would inevitably draw upon pre-existing veterinary knowledge of the sheep TSE scrapie, the only TSE to afflict a farmed animal that was a significant part of the human food chain.33 And while there were obvious implications for BSE from scientists’ experience with scrapie, there was also the danger that any analogy between scrapie and a new TSE in cattle would be pushed too far. In subsequent chapters, we will consider if this danger was realized in the case of BSE. In the meantime, we consider further gaps that existed in the knowledge of scientists in the early days of the BSE crisis. When BSE first emerged in British cattle, considerable epidemiological effort was expended in establishing the source of this new disease. In May 1987, this task was assigned to Mr John Wilesmith of the Central Veterinary Laboratory’s Epidemiology Department. He concluded that the disease was caused by contaminated meat and bone meal which had been incorporated into cattle feed. The meat and bone meal contained offal from scrapie-infected sheep and had become infectious, he contended, due to changes in rendering practices.34 These early epidemiological conclusions were significant in at least two respects. Firstly, they led to the widely held view that BSE was bovine scrapie and, as such, this disease could be expected to behave like scrapie. This ‘bovine scrapie’ thesis was to have a profound influence on scientific assessments of the risk to humans posed by this new disease and on health pronouncements made by successive British Government ministers. Secondly, these conclusions were the basis for the first measure that was introduced to contain the spread of BSE, a ban on the inclusion of ruminant protein in ruminant feed that came into effect on 18 July 1988. Although this ban was intended to prevent scrapie-infected sheep tissues from entering animal feed (the tissues which scientists believed were responsible for BSE), it had the effect of also removing those tissues that were actually transmitting infection (i.e. BSE-infected cattle tissues). We will see in later chapters that these epidemiological conclusions were erroneous. Nevertheless, they formed the mainstay of the early scientific response to BSE and were to have a profound influence on the nature of subsequent

1.3

The BSE Knowledge Problem

25

inquiry into this disease. The investigations of epidemiologists were thus intended to address the following gap in scientific knowledge of this new brain disease in cattle. Knowledge Gap 2: The origin or source of this new bovine brain disease Early epidemiological investigation did more than suggest an ovine origin for this new disease in cattle. For it provided, in effect, an account of the mechanism by means of which the disease was being transmitted among cattle. Mr Wilesmith did not believe that an effective mechanism of cattle-to-cattle transmission existed. He argued that by far the most significant route of infection was a contaminated feed source in the form of meat and bone meal. Each affected animal, Mr Wilesmith contended, was an index case that had developed disease as a result of consumption of scrapie-infected feed.35 We now know that cattle were being infected through the consumption of feed that contained BSE-infected tissue and not scrapie-infected tissue. Moreover, we also know that no rendering process was probably ever capable of inactivating the scrapie agent. Indeed, given what was known about the extraordinary resistance of the scrapie agent prior to 1986 (see note 2), it could be argued that the scientists who were responsible for these early epidemiological conclusions about the transmission of BSE should also have known that no current or former rendering process could have inactivated this agent. Notwithstanding the erroneous nature of these conclusions, their generation was intended to bridge another important gap in scientists’ knowledge of BSE. Knowledge Gap 3: The transmission properties of this new bovine brain disease If the issue of how BSE was being transmitted among cattle was a knowledge gap for scientists, an even more grave uncertainty surrounded the question of whether this new bovine disease would transmit to humans. Here was a question that troubled scientists more than any other. If this question could not be addressed, or was addressed incorrectly, the consequences for human health could potentially be very serious indeed.36 The issue of BSE transmission within cattle at least provided scientists with certain ‘facts of transmission’ to work on – epidemiological investigation had revealed, for example, the age of cattle that were succumbing to disease, the geographical distribution of those cattle, amongst other things. Transmission among cattle had already occurred and was proceeding at an alarming pace.37 In considering the question of BSE transmissibility to humans, scientists lacked even these basic facts. On this question, the certainty of a prior transmission event (some disease agent had already transmitted to cattle to cause BSE) was replaced by the uncertainty of a future transmission event (the transmissibility of BSE to humans). If transmission to humans was occurring, epidemiologists in human disease had no evidence that such was the case. Yet, scientists knew enough about the long incubation period of TSEs, which would be lengthened still further by the species barrier that an infective agent would have to cross, to know that an absence of evidence of transmission to humans was not a guarantee that BSE posed no risk to human health. Government ministers sought early advice on the extent of this risk from

26

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expert scientific committees. Their deliberations and assessments of risk will be considered in detail in later chapters. In the meantime, it is clear that a particularly significant gap in early scientific knowledge of BSE was the following. Knowledge Gap 4: The transmissibility to humans of this new bovine brain disease These four knowledge gaps relating to the nature, origin, transmission and transmissibility to humans of this new brain disease in cattle capture the major sources of uncertainty that confronted scientists in the early days of the BSE epidemic. In subsequent chapters, these uncertainty sources will be examined in more detail with focus upon their philosophical and other features. For the moment, it suffices to emphasize that these knowledge gaps overlap each other to greater or lesser extents. For example, in order to address the question of BSE transmissibility to humans, one must first know something about the origin of this disease. We will see that the erroneous belief that BSE had an ovine origin was the basis of the mistaken scientific assessment that it was highly unlikely that BSE would transmit to humans. Also, each of these knowledge gaps also subsumes a number of more specific questions and areas in which scientists lacked knowledge. For example, knowledge of the nature of BSE subsumes questions about the histopathology, pathogenesis, prognosis and clinical course of this disease. The progressive, degenerative nature of the disease (clinical course), its invariably fatal outcome (prognosis), the widespread vacuolation in the brains of affected animals (histopathology) and the presence of peripheral infectivity before infectivity of the CNS (pathogenesis) are the very hallmarks of a TSE and were all vital elements in the identification of this new bovine brain disease. The pervasive nature of these knowledge gaps meant that scientists struggled to gain an early epistemic foothold on this emerging disease. It is little wonder, therefore, that urgent efforts were made to establish a robust framework of reasoning that could sustain scientists in their decision-making at a time of extreme uncertainty. It is to a preliminary examination of this framework that I now turn.

1.3.2 The Knowledge Problem Bridged It may seem self-evident that reasoning should be the central component of any scientific response to uncertainty. After all, our cognitive resources, and reasoning in particular, must be our first and last resort when an issue demands resolution, especially one as serious as the containment of a newly emerging infectious disease. The application of reason to the problems that confront us is not just our only, but is also our most powerful, response to a whole range of scientific and other challenges. The self-evidence of these statements notwithstanding, epidemiologists and public health scientists have displayed a somewhat uneasy relationship with the concept of reasoning. Seldom, if ever, is reasoning the focus of epidemiological discussion.38 More often than not, such discussion is preoccupied with technical

1.3

The BSE Knowledge Problem

27

questions that leave little room for the type of conceptual and theoretical inquiry that holds the best prospect of generating new modes of reasoning adapted to conditions of uncertainty.39 Moreover, reasoning in public health science and epidemiology is usually unduly constrained through its identification with deduction and induction. Philosophy has also been guilty of such identification. For most of the long history of logic, deduction and, to a lesser extent induction, has effectively dominated the logical terrain.40 It is only in more recent years that presumptive frameworks have begun to receive serious philosophical attention. These frameworks will be integral to the analysis of scientific reasoning that will be undertaken in the following pages. In this section, we begin that analysis by outlining the type of reasoning strategies that scientists used to bridge the knowledge gaps that confronted them when BSE first emerged in cattle. The analysis of scientific reasoning pursued in this book has at its heart two philosophical claims. The first claim is that deduction and induction have a rather negligible role to play in the reasoning of scientists who are engaged in a scientific inquiry that is in its formative stage. This is the stage of inquiry when knowledge gaps are at their most pronounced and scientists must conduct their deliberations in conditions of extreme uncertainty. Traditional philosophical accounts of scientific reasoning,41 in which investigators move from certain and known theses by means of deduction to other certain and known theses, bear little or no resemblance to the view of scientific reasoning that is being proposed here. In fact, it is questionable if such accounts have ever borne any resemblance to the actual process of scientific reasoning or if they have merely existed as some type of ideal abstraction from that process in the minds of philosophers. In any event, the relevance of these accounts to scientific reasoning is directly challenged in this study. The second claim of this book is that a group of so-called informal fallacies, which have been maligned throughout most of the long history of logic, are a scientist’s best friend in the early stages of an inquiry. Quite apart from being fallacious, these arguments, I will contend, are entirely acceptable strategies or modes of reasoning when the epistemic context is one of uncertainty. We will see in subsequent chapters that the gains that these arguments bestow on inquiry are really quite substantial – an economic ordering of the questions to be addressed in inquiry, the generation of specific lines of inquiry, and the progression of inquiry on an exploratory basis are just a few of them. Certainly, the view of these ‘fallacies’ that emerges is one in which these forms of reasoning are an integral part of cognitive rationality, the part that subserves our cognitive deliberations in the most straitened of epistemic circumstances. To appreciate the main thrust of this approach, consider the predicament in which scientists found themselves when BSE was first recognized in British cattle in 1986. As we saw in Section 1.3.1, all aspects of this new disease were essentially unknown to scientists – key questions about the nature, origin, transmission and transmissibility to humans of this bovine disease lacked readily available answers. Moreover, the evidence that could address these questions was still some way off – in the case of the transmissibility of BSE to humans, it could take many years for such evidence to emerge. In such circumstances, scientists’ epistemic choices were threefold: (1)

28

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to suspend all judgement until such time as appropriate evidence becomes available, (2) to continue in inquiry employing the same standards of rational acceptability that are employed when appropriate evidence is available or (3) to continue in inquiry employing a different standard of what is to qualify as rationally acceptable in full recognition of the fact that the epistemic context is one of uncertainty. Clearly, the suspension of judgement in (1) is not a viable cognitive policy for scientists to pursue. Scientists are not in the position of a cognitive sceptic who declines any and all commitment to theses. They are ultimately rooted in the practical sphere from where they must achieve a rational basis for action. In the case of an emerging infectious disease like BSE, decisions must be made in advance of the availability of evidence in order that effective disease containment measures may be instituted. Nor can scientists afford to proceed in inquiry in contexts of uncertainty with the same standards of rational acceptability that are operative when evidence is available. For by these standards, scientists’ decisions and judgements would invariably be found rationally wanting. This particular cognitive policy does not capture the fact that even when compelled to form judgements under the most difficult epistemic circumstances, scientists would affirm that those judgements are rationally motivated to the very best extent possible. The only cognitive policy that satisfies the demands of the practical sphere on the one hand and a commitment to attainable rationality on the other hand is option (3). Different standards of rational acceptability must be assumed to operate in the formative stage of an inquiry. These standards do not fall short of some ideal of cognitive rationality. Indeed, to view them as doing so is to experience perpetual dissatisfaction with our own cognitive resources.42 Rather, these standards are part of a highly evolved cognitive rationality that is adapted to cope with diverse epistemic conditions. These conditions must include the absence of knowledge as well as the presence of knowledge. Cognitive rationality that can only guide decisionmaking and judgement formation in favourable epistemic circumstances and that abandons us in adverse conditions is not only an ill-adapted resource but a positively dangerous one. No such rationality, I contend, is at issue in the scientific case (or in more mundane forms of thinking and reasoning, although I will not directly argue in support of this point). The cognitive rationality that sustains scientists in the early stage of an inquiry is an uncertainty-gravitating resource that seeks to bridge knowledge gaps through specially adapted heuristics of reasoning. These heuristics, I contend, are the argument forms that have traditionally been identified as informal fallacies. Whether we are arguing from an absence of knowledge or from a premise that is as uncertain as the conclusion we are attempting to prove, there is a fallacy that embodies the particular logical pattern in question (in this case, the argument from ignorance and question-begging argument, respectively). The aim of this book will be to demonstrate how these argument forms served to bridge the significant knowledge gaps that confronted scientists in the early stages of inquiry into BSE.

Notes

29

Notes 1. A further human TSE, fatal familial insomnia, had not been classified as a TSE in 1986, as there was no evidence at that time that the disease was transmissible (BSE Inquiry Report, Volume 2: 28–29). Medori et al. first characterized fatal familial insomnia as a prion disease in 1992. These investigators discovered a mutation in codon 178 of the prion protein gene in two members of a family who presented clinically with progressive insomnia, dysautonomia (disorder of autonomic nervous system function) and motor signs. 2. In his 1982 article, Prusiner remarked upon the ‘extraordinary resistance’ of the scrapie agent to formalin. This resistance was nowhere more clearly demonstrated than in a study by Pattison (1965) who found that scrapie occurred in 8 of 9 goats that had been intracerebrally inoculated with scrapie goat brain that had been stored at room temperature in 10 or 12% formalin for periods ranging from 6 to 28 months. Pattison (1965: 163) stated that ‘[i]n the light of these and other unusual findings regarding the properties of the scrapie agent, that has not yet been identified, the opinion is expressed that if the agent is a living virus it is likely to be a virus of a kind as yet unrecognised’. Other studies appeared to confirm the uniquely resistant properties of the scrapie agent to inactivation. For example, Gibbs et al. (1978) reported the survival of the kuru, CJD and scrapie viruses to unusually high doses of ionizing radiation. However, Rohwer (1984) reported the findings of kinetic studies which demonstrated that the resistance of the scrapie agent is limited to small populations of the total infectivity and that the majority population is highly sensitive to inactivation. 3. ‘The foregoing summary of experimental data indicates that the molecular properties of the scrapie agent differ from those of viruses, viroids, and plasmids. Its resistance to procedures that attack nucleic acids, its resistance to inactivation by heat, and its apparent small size all suggest that the scrapie agent is a novel infectious entity’ (Prusiner 1982: 141). 4. ‘Our data and that of other investigators suggest two possible models for the scrapie agent: (i) a small nucleic acid surrounded by a tightly packed protein coat or (ii) a protein devoid of nucleic acid, that is, an infectious protein. While the first model might seem the most plausible, there is no evidence for a nucleic acid within the agent. The second model is consistent with the experimental data but is clearly heretical’ (Prusiner 1982: 141–142). 5. ‘If prions do not contain a nucleic acid genome which codes for its protein (or proteins), alternative mechanisms of replication and information transfer must then be entertained’ (Prusiner 1982: 143). 6. For example, Strain et al. (1986) described scrapie as a ‘CNS slow virus infection’, Kascsak et al. (1986) and Kimberlin and Walker (1986) as an ‘unconventional slow virus’ and Davanipour et al. (1986) as a ‘slow viral encephalopathy’. Even to the present day, scientists subscribe to the view that a slow virus is responsible for TSEs, BSE specifically included. In this way, Manuelidis (2007: 897) remarks that ‘[t]he transmissible spongiform encephalopathies (TSEs) such as endemic sheep scrapie, sporadic human Creutzfeldt-Jakob disease (CJD), and epidemic bovine spongiform encephalopathy (BSE) may all be caused by a unique class of “slow” viruses. This concept remains the most parsimonious explanation of the evidence to date, and correctly predicted the spread of the BSE agent to vastly divergent species. With the popularization of the prion (infectious protein) hypothesis, substantial data pointing to a TSE virus have been largely ignored. Yet no form of prion protein (PrP) fulfills Koch’s postulates for infection’. 7. Vincent Zigas was an Estonian-born physician who was the district medical officer. He first learned of kuru in 1956 from an Australian district police officer. Carleton Gajdusek was an American paediatrician and virologist who heard about kuru while visiting Australia (Poser 2002a). Along with Baruch S. Blumberg, Gajdusek was the co-recipient of the 1976 Nobel Prize in Physiology or Medicine for his work on kuru. 8. While recognising that the agent that caused kuru was novel in certain respects, Gajdusek (1977) nevertheless subscribed to the view that this agent was a virus: ‘Kuru has led us. . .to

30

9.

10.

11.

12.

13.

14.

15.

16.

17.

1

BSE – A Leap Into The Unknown

a more exciting frontier in microbiology than only the demonstration of a new mechanism of pathogenesis of infectious disease, namely the recognition of a new group of viruses possessing unconventional physical and chemical properties and biological behavior far different from those of any other group of microorganisms. However, these viruses still demonstrate sufficiently classical behavior of other infectious microbial agents for us to retain, perhaps with misgivings, the title of “viruses”’ (Gajdusek 1977: 943). In his early published work on kuru, Gajdusek subscribed to the view that the disease had a genetic, rather than an infectious, basis (see note 17). The oral route was not the only, or even the most significant, route of transmission of the kuru agent, a point that is frequently overlooked in accounts of cannibalism in the Fore people. Gajdusek himself was aware of the significance of parenteral routes of transmission in kuru when he stated that ‘[i]nfection with the kuru virus was most probably through the cuts and abrasions of the skin, or from nose picking, eye rubbing, or mucosal injury’ (1977: 956). Alpers and Gajdusek (1965) examined the change in mortality of kuru between 2- and 3-year periods, 1957–1959 and 1961–1963. There was a 23% reduction in the total number of kuru deaths between the first and second of these periods. From 7.64 deaths per thousand population per annum between 1957 and 1959, kuru mortality rates had decreased to 5.58 deaths per thousand population per annum, a reduction that was statistically significant. Figures reported by Hornabrook and Moir (1970) show that kuru deaths continued to decrease after 1964, although not as rapidly as in the early 1960s. The term ‘scrapie’ derives from the scraping action that is habitually performed by affected sheep. Palmer (1957: 1318) states that ‘[a]lthough not necessarily the earliest sign of scrapie one of the most important is the apparent irritation that induces the animal to rub itself relentlessly, nibble the skin and tear out wool: the areas denuded of fleece are usually bilaterally symmetrical’. In 1981, the Agricultural Research Council and the Medical Research Council established a joint institution, the Neuropathogenesis Unit (NPU), which combined the scrapie research programmes and facilities of all three of these institutions (BSE Inquiry Report, Volume 2: 22). Although Hadlow’s work on scrapie is frequently remarked upon, it should not be overlooked that he also investigated transmissible mink encephalopathy. See Section 1.2.5 for discussion of some of Hadlow’s work on this spongiform encephalopathy. As Poser (2002a) recounts, a fortuitous set of circumstances was to lead Hadlow to suggest an analogy between scrapie and kuru. On 28 June 1959, Hadlow was visited at Compton by a colleague, William Jellison, who worked as a parasitologist at the Rocky Mountain Laboratory in Hamilton, Montana. Jellison happened to mention to Hadlow an exhibit on kuru that he had seen at the Wellcome Medical Museum in London. Five days later, Hadlow visited the exhibit. He was struck by the photomicrographs of the neurohistological changes that occurred in kuru and the similarity of these changes to those that he had witnessed in scrapie. On 18 July 1959, Hadlow wrote to the editor of The Lancet to express his thoughts about the similarities between these diseases. This letter appeared on 5 September 1959 entitled ‘Scrapie and Kuru’. ‘. . .it might be profitable, in view of veterinary experience with scrapie, to examine the possibility of the experimental induction of kuru in a laboratory primate, for one might surmise that the pathogenetic mechanisms involved in scrapie – however unusual they may be – are unlikely to be unique in the province of animal pathology’ (Hadlow 1959: 290). Fearing a printer’s strike, Hadlow sent a copy of his letter, soon to be published in The Lancet, to Gajdusek. In his book Deadly Feasts, Richard Rhodes commented that Gajdusek told him that Hadlow’s letter ‘had forced [him] to reconsider the problem’ (1997: 64). This view of the genetic basis of kuru was expressed in Gajdusek’s first published article on the disease and in subsequent articles. In this way, Gajdusek and Zigas (1957: 974) stated that ‘[t]hese clinical observations, along with further epidemiologic study, suggest a possible

Notes

18.

19.

20.

21.

22.

23.

24.

31

genetic etiology or, at least, hereditary predisposition for this unusual condition’. In a later paper, Alpers and Gajdusek (1965: 852) stated that ‘in view of the absolute ethnic limitation of the disease overriding all boundaries of custom and environment, some genetic mechanism must form the basis for it’. As investigators began to link kuru to the practice of cannibalism, the view that kuru had a genetic basis was increasingly challenged. In this way, Hornabrook and Moir (1970: 1178) stated that ‘the epidemiological data suggest that a special genetic constitution may not be a prerequisite for contracting kuru. Instead, the presence of the kuru agent in a limited geographical area, combined with a mode of transmission dependent on a primitive custom, is sufficient to explain the restriction of the disease to the Fore people and their neighbours’. Poser (2002a: 9) states that ‘[i]t is to William Hadlow’s enormous credit that he was the first to make the crucial connection between animal and human disease, paving the way for one of the most significant scientific developments of the twentieth century and making it possible for both Gajdusek and Prusiner to win the Nobel Prize, but not sharing in that recognition’. Although Hadlow’s realization that scrapie and kuru exhibited histological similarities was a key development on the road to Prusiner proposing his protein-only prion theory, other contributions also helped shape this theory. For discussion of these contributions, the reader is referred to Poser (2002b). In all these experiments, infected and disease-free animals were in direct contact with each other. Scrapie has also been shown to infect sheep under field conditions when infected and disease-free animals have used the same land separated by a period of years. Pálsson (1979) describes how Icelandic lambs developed rida (scrapie) when they were introduced to land that had been free from scrapie infected sheep for a period of 3 years. Pálsson (1979: 362) states that ‘[t]his experience indicates an indirect spread of the disease and at the same time a long term persistence of the agent causing rida’. This is also borne out by a later study in which Kimberlin and Walker (1979) examined intracerebral, intraperitoneal, intravenous and subcutaneous routes of scrapie infection in Compton white mice. In peripheral routes of infection, replication of the scrapie agent occurred early in the spleen and reached a plateau concentration of agent before replication occurred in the spinal cord, the latter after 25–42% of the incubation period (a roughly comparable percentage of the incubation period – 24–34% – had elapsed before replication occurred in the spinal cord in intracerebral inoculation). In peripheral routes, 41–55% of the incubation period had elapsed before replication of the agent occurred in the brain. This is much later than in intracerebral inoculation where replication of the agent in the brain was detected after just 13–19% of the incubation period had elapsed. Kimberlin and Walker claim that this pattern of replication suggests the spread of the scrapie agent from the spleen to the spinal cord and then to the brain in peripheral routes of infection. That route of inoculation has an effect on degree of vacuolation was confirmed in a study by Outram et al. (1973). These investigators inoculated two inbred strains of mice with the ME7 scrapie agent. Inoculation was performed intracerebrally and intraperitoneally. The route of injection had the largest effect on the degree of vacuolation, assessed in terms of the intensity of grey matter vacuolation in nine areas of the brain. Although the genotype of the donor and recipient also had a highly significant effect on the shape of the lesion profile, this effect was of a smaller magnitude than that due to route. The lymphoreticular system (LRS) contains bone marrow, tonsils, spleen, thymus and lymph nodes. Additionally, in ruminants, there is an additional primary lymphoid tissue in the gut called the ileal Peyer’s patch. In addition to histological changes, a number of gross changes of the brain can also be observed. Kimberlin and Millson (1967) reported a slow, progressive decrease in brain weight in scrapie affected mice that started at around 40–50 days after inoculation. This process greatly accelerated just before the first clinical signs of scrapie appeared. Dickinson et al. (1968a) proposed the term ‘sinc’ for this gene to denote scrapie incubation period.

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BSE – A Leap Into The Unknown

25. In 2005, Windl et al. succeeded in transmitting TME to transgenic mice which expressed the mink prion protein gene. 26. Marsh and Hanson also found that the agent was sensitive to ether and susceptible to proteolytic digestion with pronase. The combination of these features led these investigators to state that ‘[i]t appears that the TME agent cannot be easily differentiated from the scrapie agent on the basis of their biochemical properties’ (1969: 179). 27. Marsh et al. (1970) failed to demonstrate specific serum antibody or immune complexes in the brains of mink with TME. 28. It was some years later before oral transmission of CWD was demonstrated. Sigurdson et al. (1999) orally inoculated mule deer fawns with a brain homogenate that was derived from mule deer with naturally occurring CWD. PrPres, an abnormal prion protein isoform, was detected in alimentary-tract-associated lymphoid tissues as early as 42 days following inoculation and in all fawns at 53–80 days after inoculation. Sigurdson et al. (1999: 2757) state that ‘[t]he rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature’. 29. It will be seen in subsequent chapters that bovine tissues were used in the manufacture of human medicinal and surgical products including surgical catgut and vaccinations. These products thus presented a risk of parenteral transmission of BSE to humans. 30. Sir Richard Southwood was the Chairman of the Southwood Working Party, which was established on the recommendation of Sir Donald Acheson (Chief Medical Officer, 1983–1991) ‘to advise on the implications of Bovine Spongiform Encephalopathy and matters relating thereto’ (BSE Inquiry Report, Volume 4: 2). The Working Party consisted of a professor of zoology (Sir Richard Southwood), a professor of virology (Anthony Epstein), a clinical neurologist (Sir John Walton) and a veterinarian (Dr William B. Martin). 31. Of course, it could be argued that in performing transmission experiments to establish that this new disease was a bovine TSE, scientists were already assuming that such was the case (for if this were not the case, why would scientists perform transmission experiments as opposed to a myriad of other possible experiments?). Implicit in this contention is the claim that scientists were engaging in a cyclical process of argumentation whereby they had assumed that the new bovine disease was a TSE in order to be able to demonstrate that it was a TSE. I will argue in Chapter 4 that such cyclical patterns of argumentation are inherent in scientific inquiry and that these patterns are non-fallacious in nature. 32. The identification of BSE as a transmissible spongiform encephalopathy proceeded initially on the basis of histopathological examination of the brains of affected animals at the Central Veterinary Laboratory in Weybridge, Surrey. Hope et al. (1988) identified BSE fibrils which were similar to scrapie-associated fibrils (SAFs) in electron microscopic studies of brain homogenates. These fibrils contained the bovine homologue of a protease-resistant form of PrP which was a molecular marker of SAFs. Attempts at the CVL to transmit BSE to hamsters in February 1987 and then again in January 1988 were unsuccessful. The transmissible nature of BSE was finally confirmed in September 1988 when inoculations of mice, which had been undertaken in November 1987, were found to induce disease (BSE Inquiry Report, Volume 2: 68). 33. Some indication of just how significant sheep were in terms of human meat consumption can be gleaned from MAFF figures for meat production between 1986 and 1995. During this period, sheepmeat production in the UK experienced steady growth before flattening out. Production increased by 30% from 301,000 tonnes in 1986 to 400,000 tonnes in 1995, with a peak of 418,000 tonnes in 1991 (BSE Inquiry Report, Volume 10: 26). 34. In rendering, the raw material from slaughterhouses was crushed and heated. Moisture in the material was evaporated which enabled the fat (called ‘tallow’) to be separated from the highprotein solids (known as ‘greaves’). In order to remove further tallow, the greaves underwent more processing by pressing, centrifuging and solvent extraction. The protein-rich material that resulted from these further processes was then ground into meat and bone meal (BSE Inquiry Report, Volume 1: 25–26).

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35. ‘The form of the epidemic was typical of an extended common source in which all affected animals were index cases. . .The findings were consistent with exposure of cattle to a scrapielike agent, via cattle feedstuffs containing ruminant-derived protein’ (Wilesmith et al. 1988: 638). 36. Although the Southwood Working Party concluded that it was most unlikely that BSE would have any implications for human health, the general conclusions section of their report ended with this warning: ‘Nevertheless, if our assessment of these likelihoods is incorrect, the implications would be extremely serious’ (BSE Inquiry Report, Volume 1: 55). 37. At the time of the Southwood Report (submitted to government on 9 February 1989), suspected BSE cases were being reported at the rate of about 400 a month (BSE Inquiry Report, Volume 1: 17). 38. It is regrettable that the very scientific disciplines that need to examine how scientists engage in reasoning often devote little or no effort to this important reflective exercise. Journals in epidemiology routinely do not publish the type of critical and philosophical discussions that this reflection requires. Indeed, the dearth of such discussions has prompted the development of a new, online journal. In this way, Phillips et al. (2004) state that ‘the desire for new information means that the health science literature is overwhelmingly devoted to reporting new findings, leaving little opportunity to improve the quality of the science. Epidemiologic Perspectives & Innovations was created to provide a forum for efforts to improve the quality of health science research and its applications’. Humanities and social scientific disciplines, including philosophy, sociology and politics, are very often the only fields in which scientific reasoning and decision-making come under any scrutiny. 39. Christakos et al. (2005) adopt a critical stance towards the current state of epidemiology. They believe that the discipline’s preoccupation with technical practice has led to an impoverishment of the type of theoretical developments that will lead to the generation of new models of reasoning adapted to conditions of uncertainty. We will have cause to return to the views of these investigators in subsequent chapters. 40. And they are maybe still doing so. Walton (2002: 112) remarks that ‘logic textbooks are still dominated by deductive and inductive reasoning, many of them implying by their treatment of the subject matter that these two types of inference are all that are important to know about in logic’. 41. The deductive model of scientific reasoning in these accounts has its historical precedents in Aristotle and, latterly, logical positivism, as Bechtel (1988: 22) remarks in his discussion of the positivists’ deductive-nomological model of scientific explanation: ‘Following a tradition that does back at least to Aristotle, the Positivists maintained that explaining an event consisted of deriving a statement describing that event from statements of scientific laws and statements describing antecedently known empirical facts (initial conditions). Thus, deduction plays a central role in their account of explanation. . .’. 42. The dissatisfaction described here has its roots in a very old epistemological problem concerning the relationship of mind to the world. Philosophers have variously assumed that it is possible to step outside of our minds and assume a metaphysical standpoint (a God’s eye point of view) from which we can describe the world as it actually is or that it is not possible to make this leap, in which case we are confined to our mental procedures and resources which are unable to reflect how things actually are (hence, the dissatisfaction mentioned in the main text). Also, there are other philosophers (Hilary Putnam is a case in point) who challenge the very idea of an interface between mind and world that must be transcended and the notion that a metaphysical standpoint even makes any sense. For the reader who is interested in pursuing this debate, Putnam (1990, 1992, 1994) provides a good starting point. The same metaphysical standpoint, I have argued, has been lurking in discussions of argument and fallacy (see Cummings 2002a, 2003, 2004a).

Chapter 2

The Scientific Challenge

2.1 Introduction In the last chapter, I described how a number of argument forms that had traditionally been characterized by philosophers as weak or fallacious modes of reasoning could be shown to facilitate scientific inquiry into BSE when little was known about this new brain disease in cattle. The point was made that these argument forms have relevance to the epidemiologists and public health scientists whose task it was to identify and respond to this emerging infectious disease. However, this point requires some explanatory work if it is to have more than a very general application to the work of these public health professionals. For these professionals might ask with some justification why they should treat seriously argument forms that have been deemed to be logically inadequate by generations of philosophers. They might also wonder if philosophical discussion of reasoning has anything but the most abstract lessons for scientists who are charged with containing infectious diseases. In this chapter, I undertake this explanatory work by arguing that philosophical contributions on reasoning and argument are not only relevant to epidemiology, but that they also represent the very best prospect for investigators of addressing some of the criticisms of epidemiology that have been raised in recent years. These criticisms have been expressed most clearly by Christakos et al. (2005), although other theorists have also added their voices to the exchange. I believe, and will subsequently argue, that it is only when epidemiology and philosophy come together on questions relating to reasoning that true progress will be made on devising models of reasoning that are adapted to conditions of uncertainty. Certainly, this belief is the principal motivation for the model of reasoning that will be defended throughout this book. If the model of scientific reasoning that I am proposing is to have epidemiological value, it must be able to demonstrate its worth to the early investigations of epidemiologists in the BSE crisis. Accordingly, this chapter will also be used to extend the examination of those investigations which was commenced in Chapter 1. The aim will be to show how this model is very directly motivated by the deliberations that were undertaken as part of those investigations. Specifically, the conclusions of those early epidemiological studies set in motion an argumentative strategy that was

L. Cummings, Rethinking the BSE Crisis, DOI 10.1007/978-90-481-9504-6_2,  C Springer Science+Business Media B.V. 2010

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to shape all subsequent inquiry into BSE. That strategy was a form of analogical reasoning, the central premise of which sought to relate BSE in cattle to scrapie in sheep. The warrant that attended that premise is of critical significance in assessing the rational merits of this argument form and of the many decisions and risk assessments that were based upon analogical reasoning throughout the BSE crisis. In order to assess the strength of that warrant, we must first know something about the epidemiological context in which it was developed. A thoroughgoing examination of that context will be the second main task of this chapter.

2.2 The Current Paradigm in Epidemiology In a recent book, Christakos et al. (2005) undertake a much needed critical examination of the modern science of epidemiology. These authors present a strong case for their claim that the current paradigm in epidemiology is fundamentally flawed. Although I do not wish to rehearse the full details of their argument, its essence can be captured by the following points: (1) the focus of epidemiology is on technical practices rather than on theoretical developments1 ; (2) there has been little recognition in epidemiology of the essentially interdisciplinary nature of much public health research2 ; (3) the current paradigm has neglected to give any emphasis to epistemic cognition notions such as reasoning3 ; (4) there has been little or no attention given to the spatiotemporal characteristics of epidemics under conditions of uncertainty.4 To respond to these weaknesses of the current paradigm, Christakos et al. (2005: 5) propose the development of a synthetic epidemic paradigm (SEP) that will be able to account for the points listed above ‘in a mathematically tractable and epidemiologically thoughtful fashion’. The extent to which SEP succeeds in addressing the shortcomings of the current paradigm is the topic of another discussion. In the present context, I want to consider how the model of scientific reasoning that will be presented throughout this book can respond to these features and how a much greater role for philosophy within epidemiology is envisioned as a result.

2.2.1 Theoretical Development in Epidemiology A chief concern of Christakos et al. is the lack of theoretical development within epidemiology. This theoretical void has been filled by a proliferation of studies whose main concern is the use of techniques.5 Kaplan (2004: 127) states that: [T]here has been considerable lament regarding the ascendancy of technique over theory in epidemiology and its separation from basic foci of public health. Indeed, development of epidemiologic theory per se, separate from techniques for analyzing causal effects and partitioning sources of noise in data may be required.

In the absence of theoretical development, epidemiology has become preoccupied with conducting studies of associations. Many of these associations are weak and never replicated. Their combined effect has been to bring about an erosion of

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The Current Paradigm in Epidemiology

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public trust in the state of the science (Taubes 1995). Certainly, the findings of these various studies get us nowhere in the absence of an underlying theory that is able to offer some explanation of these associations. In relation to his own field of social epidemiology,6 Kaplan (2004: 128) remarks that: [T]he spatial scope over which determinants of specific outcomes such as all-cause mortality, infant mortality, or cardiovascular disease, or other outcomes, operate is less clear. Without some theory to suggest the ways in which the determinants of these outcomes are spatially embedded, one is left with a plethora of analyses of “area” effects that seem more often driven by the level of spatial data available, or other arbitrary factors, than by reasoned etiologic considerations.

The paucity of theoretical labour in epidemiology has adverse implications for the knowledge base of the discipline. When that knowledge base is impoverished, our ability to engage in scientific explanations and predictions is considerably diminished. Yet, these are the very activities that scientists must undertake in order to mount an effective response to a newly emerging infectious disease. To predict the behaviour of an epidemic across space-time, for example, scientists must draw upon theoretical frameworks in a range of disciplines, including mathematics, systems engineering, molecular biology, toxicology, climate change and demography (Christakos et al. 2005). Where these frameworks are lacking or are otherwise poorly developed, the epidemiologist must approach the task of prediction with the burden of uncertainty. It is this burden that the epidemiologist aims to minimize through the development of ever more powerful models of reasoning.7 The model of scientific reasoning that I will be proposing in this book is simultaneously realistic and optimistic about the place of uncertainty in inquiry. On the one hand, it recognizes that uncertainty is an unavoidable feature of scientific inquiry.8 On the other hand, it believes that uncertainty can be brought within manageable limits. Each of the argument forms that will be demonstrated throughout this book serves to contain uncertainty by bridging specific gaps in our knowledge. These gaps may ultimately come to be ‘filled in’ as results from experimental studies begin to emerge. Until such time as these results are forthcoming, however, reasoning strategies that include circular arguments, arguments based on analogy and arguments from ignorance perform a useful facilitative function, that of advancing inquiry on a tentative basis. To appreciate how this is possible in the case of one of these arguments, the argument from ignorance, one need only consider one of the many ways in which this argument was used during scientific inquiry into BSE. The lack of evidence that scrapie had transmitted to humans in the 250 years it had been present in British sheep populations was taken to support the proposition that scrapie was not transmissible to humans. This proposition was something very much worth knowing, as it was used in subsequent assessments by scientists of the risk that BSE posed to human health. A renewed emphasis on theoretical developments within epidemiology is essential if the knowledge base of this scientific discipline is to be expanded. But an equally important part of this emphasis must be the development of innovative ways of reasoning from the incomplete knowledge bases of epidemiology and related disciplines.

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2.2.2 Epidemiology and Other Disciplines As the above example of epidemic prediction demonstrates, the theoretical frameworks that inform the scientific activities of explanation and prediction come from a range of disciplines. Interdisciplinarity is at the heart of the SEP that Christakos et al. wish to see replace the current paradigm in epidemiology.9 According to these authors, ‘important sources of knowledge available in the physical and life disciplines are ignored at the cost of profoundly inadequate epidemic and human exposure studies’ (2005: 4). One discipline above all others that influences how Christakos et al. approach epidemiology is philosophy. These authors reflect very deeply on questions that are essentially epistemological in nature. They argue, for example, that ‘regardless of how technical or formal [public health scientists’] research may be, they will always need to gain intellectual access to issues such as the nature and reliability of knowledge, the conception of reality, the reasoning mode, and the underlying methodological assumptions’ (2005: 66). To this extent, public health scientists may find themselves operating as ‘applied philosophers’. Nor are Christakos et al. alone in envisioning a role for philosophy in epidemiology. While epidemiological studies have little difficulty demonstrating associations between risk factors and disease, only some of these associations are genuinely causal relationships. The strong tendency of epidemiologists to interpret even weak associations as causal relationships suggests that something may be wrong with the way these scientists conceive of the notion of causality.10 Rothman (2002: 15–16) states that how this notion is applied within science in general, and epidemiology in particular, is a question of interest to philosophers of science: [H]ow do we go about determining whether a given relation is causal? Some scientists refer to checklists for causal inference, and others focus on complicated statistical approaches, but the answer to this question is not to be found either in checklists or in statistical methods. The question itself is tantamount to asking how we apply the scientific method to epidemiologic research. This question leads directly to the philosophy of science.

Philosophy has a further intellectual contribution to make to discussion within epidemiology. As the critical discipline par excellence, philosophy has a key role to play in addressing scientists’ concerns that epidemiology has for many years experienced a grievous lack of critical analysis. For example, Phillips (2008: 62) remarks that ‘epidemiology is characterized by the cranking out of thousands of new research reports per month, with little attempt at critical analysis’.11 In an earlier article, Phillips et al. (2004: 2) state that: It is troubling that we plow ahead with billions of dollars worth of research every year while making minimal effort to answer fundamental questions about what the research is really telling us. Epidemiology is far too important to our society to be treated as an exercise in uncritically following existing formulae.

Clearly, epidemiologists must engage in a critical way with the very standards and methods that are integral to their own discipline. If critical analysis can reverse the largely uncritical bent of epidemiology to date, then philosophy is the obvious

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The Current Paradigm in Epidemiology

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place to seek out such analysis. Trainee epidemiologists would do well, for example, to engage with the critical thinking courses of philosophy students. For it is in such courses that significant questions concerning types of arguments and standards of evidence are routinely examined and debated.12 Christakos et al. (2005: 64) appear to concur with this emphasis on critical thinking when they state that ‘critical thinking systems based on the close interaction between concepts and experimental fact may be more valuable in public health research and development than belief-based systems’. It emerges that philosophy has much to offer the study of epidemiology. From epistemology to philosophy of science and critical thinking, philosophy undoubtedly has a strong contribution to make to this scientific discipline. Christakos and others are to be congratulated for recognizing the significance of that contribution. In the chapters to follow, however, I want to go much further than these investigators by extending philosophy’s contribution to epidemiology to that sub-discipline of logic that is concerned with the study of informal fallacies. In navigating the logical terrain between rationally acceptable and fallacious forms of argument, informal logicians are uniquely placed to address issues of uncertainty in reasoning. Some consideration of the task of argument evaluation reveals why this is the case (we will return to argument evaluation in later chapters). A central tenet of the presumptive and pragmatic frameworks that are at the heart of the model of reasoning presented in this book is that the boundary between rational acceptability and fallaciousness in the study of argument is not pre-ordained and absolute but is subject to variation on the basis of features of context. Uncertainty is a significant feature of epistemic context and, as such, must enter into the task of argument evaluation for the informal logician. To the extent that epidemiologists must also address issues of uncertainty, most notably during scientific inquiry, there is much that these scientists can glean, I will argue, from the critical insights of informal logic. Certainly, this particular parallel between the disciplines of informal logic on the one hand and epidemiology on the other hand will be very much in evidence in the arguments presented in this book.

2.2.3 Reasoning and Epidemiology Beyond challenging the dearth of theoretical research and lack of genuine interdisciplinarity in epidemiology, Christakos et al. mount another revealing attack on the current paradigm. This paradigm, they argue, effectively neglects the contribution of epistemic cognition notions to the study of epidemiology: The solution of mathematical models of epidemics has been viewed as a purely ontologic affair that focuses on abstract and dry formulas, whereas crucial factors – such as modes of perception and reasoning, and their integration – are neglected. Thus, what the current perspective is missing is that these models are imperfect constructs of the human mind, often they do not account for essential site-specific knowledge, and they constitute an uncertain representation of reality (2005: 4; italics in original).

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The emphasis given to our cognitive procedures in Christakos et al.’s epistemic cognition framework13 is at once refreshing and instructive. It is refreshing because for too long epidemiology has viewed our cognitive procedures with more than a little distrust. This is evident in the proliferation of formal and statistical techniques which, it is argued, deliver nature to us objectively – something that the current paradigm in epidemiology appears to have assumed our own cognitive resources are powerless to do.14 It is interesting to note that the epidemiologist is acting on the same impulse as the knowledge sceptic, who positively urges us not to accept what our cognitive procedures (e.g. perception) tell us about the world. That impulse leads both the epidemiologist and the knowledge sceptic to view our cognitive procedures as being irretrievably flawed for no other reason than they are prone to error. And a cognitive procedure that commits errors (so the argument goes) is a cognitive procedure that cannot be trusted to deliver knowledge to us. However, to dispense with our cognitive procedures on the ground that they are prone to error is to overlook the facts that these procedures can and do serve us well and that they are the basis of our many epistemic successes.15 The emphasis on cognitive procedures within Christakos et al.’s epistemic cognition framework is also instructive. For whatever epidemic models and solutions we set about developing, they are ultimately judged to be acceptable and plausible by standards that are implicit in our cognitive procedures: [T]he solution of [an epidemic] system should follow certain rules of reasoning. But these rules are, in the final analysis, propositions about one’s epistemic cognition process. The reasoning rules leading to a solution in uncertain space-time domains do not constitute an independent ontologic entity, but they are rather implicit in the epistemic cognition process that enforces them (Christakos et al. 2005: 22).

As well as urging the epidemiologist to relocate the focus of study on the cognitive procedures that generate mathematical solutions to epidemics, Christakos et al. believe those solutions should be judged by cognitively attainable standards. A similar cognitive reorientation is envisaged in the model of reasoning based on informal fallacies that will be advanced in this book. The philosophical study of fallacies has displayed the same neglect of the cognitive domain that Christakos et al. believe characterizes the current paradigm in epidemiology.16 This neglect has had rather unfortunate consequences. Despite fallacies being committed by arguers and detected (or not, as the case may be) by other arguers, the presence of a thinking agent has been largely subordinated to other issues in discussion of the fallacies. Moreover, fallacies have been evaluated according to standards that are set apart from our cognitive procedures.17 In aiming to locate fallacies firmly within a wider cognitive framework, I propose to take seriously a claim by John Woods (2004: xxvi) that ‘an account of fallacies needs to be set in a more general theory of cognitive agency’. When recast in cognitive terms, many informal fallacies lose the appearance of fallaciousness that has engendered so many centuries of philosophical rejection.18 Quite apart from being ‘improprieties of rational performance’ or ‘failures of one or another of our basic rational survival skills’ (Woods 2004: 10–11), the fallacies can be shown to have positive survival value for the cognitive

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The Current Paradigm in Epidemiology

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agents who possess them. Of course, these arguments can still misfire and cause agents to pursue unproductive and (occasionally) catastrophic courses of action. Nevertheless, they confer sufficient epistemic advantage on any agent that possesses them to warrant their continued inclusion in what Woods calls our ‘rational survival kit’.

2.2.4 Spatiotemporal Factors and Epidemiology Spatial and temporal factors play a significant role in the spread of any infectious disease. The widespread geographical distribution (space) of early BSE cases and the distribution of cases by month and year of onset (time) led epidemiologists to conclude that the epidemic had an extended common source (i.e. contaminated meat and bone meal). Spatial factors were of vital importance in the SARS outbreak of 2003. We now know that the outbreak in many locations began with ill travellers coming from SARS-affected areas and that healthcare settings played an important role in amplifying outbreaks (Lingappa et al. 2004). With the ongoing threat to human health from avian and swine influenzas,19 spatial and temporal considerations are integral to the epidemiological models that scientists are using to predict the behaviour of pandemic human influenza. These models predict, for example, that for effective control of this disease to be achieved, antiviral prophylaxis would have to be started within approximately 3 weeks of the first human-to-human transmissions and within two days of the onset of a new case once an outbreak is underway. This control strategy, Smith (2006) argues, would be extremely difficult to achieve in rural Southeast Asia. Beyond models of infectious diseases, spatial and temporal factors are equally important to disease modelling in other branches of epidemiology. Christakos et al. (2005: 7) state that ‘in the case of environmental epidemiology, the adequate description of the geographical and temporal distribution of the exposures (toxic chemicals, radioactive materials, etc.) to which the population has been subjected is a crucial component of any modelling study’. Krieger (2001: 694) places similar emphasis on spatiotemporal factors in social epidemiology when she states that ‘[a]dequate epidemiological explanations . . . must account for both persisting and changing distributions of disease, including social inequalities in health, across time and space’. Notwithstanding the centrality of spatiotemporal factors to the study of disease processes, it is clear that epidemiological investigations have not always acknowledged these factors. Christakos et al. (2005: 4) believe that the neglect of spatial and temporal factors represents one of the ‘significant limitations of the current epidemic paradigm’: Mathematically rigorous and epidemically meaningful stochastic tools (e.g., spatiotemporal random field theory) have been ignored in favor of deterministic methods and classical statistics techniques that neglect vital cross-correlations and laws of change on space-time manifolds.

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Kaplan (2004: 126) is equally critical of diagrammatic models in social epidemiology in which ‘[i]nformation is seldom available at the multitude of levels portrayed in such models and, where available, is often measured cross-sectionally, making the temporal influences that we consider so important in the assessment of causality opaque’ (italics added). Similarly, Holmes (1997: 111) bemoans the neglect of spatial considerations in epidemiological theory when she states that: [M]ost classical epidemiological theory glosses over the spatial dimension of disease transmission and instead assumes that every individual is equally likely to contact every other. A key question is to what extent do we lose insight or are quantitatively misled by modelling the intrinsically spatial process of disease spread with nonspatial theory.

Krieger (2003: 384) attempts to explain the loss of ‘place’ in epidemiology and proposes a possible remedy in the form of geographic information system technology: [D]espite epidemiology’s longstanding concern with “time, place, and person” (or, perhaps more accurately, “time, place, and population”), “place” had receded into the background by the mid-20th century, conceptually unmoored from increasingly influential etiologic frameworks based on characteristics of the individual. Fortunately, geographic information system technology has contributed in recent years to a reviving awareness that any epidemiologic explanation worth its salt must encompass geographic – and temporal – variations in population health.

The model of reasoning that will be presented in this book attempts to address this neglect of spatiotemporal factors by directly integrating these factors within the rational evaluation of the argument forms that were used by scientists during the BSE inquiry. The temporal dimension is particularly significant to such evaluation. It is to be expected, for example, that the epistemic context in which scientists conducted inquiry changed over time as more became known about BSE and as the results of experimental studies began to emerge. This context was thus dynamic and evolving rather than static and immutable as the epidemic raged on in the years during the late 1980s and early 1990s. Accordingly, the reasoning strategies that served scientists well at one time point in inquiry might be expected to become redundant at a later time point. To address this essential temporal dimension of the BSE problem, a chronological approach will be adopted when examining the reasoning of scientists. It is of interest to this study, for example, that a particular argumentative strategy was used intensively by scientists in the early weeks and months of the BSE epidemic when little was known about this new brain disease in cattle. But it is equally interesting to establish if this strategy persisted across the time course of the epidemic and, if not, how it was revised or discharged. The temporal dimension is integral to epidemic modelling in epidemiology and public health science. It will become evident to the reader that temporal considerations had an equally significant role to play in the reasoning of scientists during the BSE epidemic.

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Early Epidemiological Investigations

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2.3 Early Epidemiological Investigations It was described above how reasoning based on an analogy between BSE in cattle and scrapie in sheep was an integral part of the argumentative strategy that shaped scientific inquiry into BSE. This analogy had its origin in the early epidemiological investigations that were conducted into BSE and specifically a study that was undertaken by Wilesmith et al. (1988). This study sought to relate this new brain disease in cattle to scrapie in sheep and it is to it that we must turn in order to establish the strength or otherwise of this emergent analogy. Our task will be the reconstruction of the different arguments that these investigators used to support the claim that BSE and scrapie were essentially related diseases. These arguments are interlinked in revealing and complex ways (see Diagram 2.1). One of these arguments has the status of a main or primary argument. The conclusion of this argument is the analogical thesis that motivated much subsequent reasoning during the BSE crisis. Other arguments are subarguments in that their conclusions serve as premises within the main or primary argument. These subarguments developed a number of independent lines of evidence that converged on the same primary argument. Having reconstructed these arguments, our next task will be their rational evaluation.20 We cannot proceed to assess the rational merits of the different analogical arguments that were in evidence during the BSE inquiry if we don’t first establish the rational standing of the analogical thesis that is the main premise of these arguments. This latter, evaluative task will reveal the tentative, presumptive nature of the early reasoning of BSE scientists.

MOLECULAR ARGUMENT P1: BSE fibrils contain a bovine homologue of PrP, a molecular marker of SAFs (Hope et al. 1988)

C: There are molecular similarities between BSE and scrapie, in that both diseases contain aberrant forms of the PrP protein

HISTOPATHOLOGICAL ARGUMENT

PRIMARY ARGUMENT Molecular premise: BSE fibrils contain an aberrant protein that is similar to PrP in scrapie-associated fibrils

Histopathological premise: BSE produces similar histopathological changes in brain tissues as other TSEs, including scrapie

Epidemiological premise: Incidence and distribution of BSE cases is consistent with food-borne transmission of scrapie to cattle

P1: Vacuolation is present in neurones of grey matter in BSE cases (Wells et al. 1987)

EPIDEMIOLOGICAL ARGUMENT P1: All BSE cases were fed commercial concentrates (Wilesmith et al. 1988) P2: BSE incidence is greatest in dairy herds (Wilesmith et al. 1988) P3: Exposure of cattle to BSE is coincident with increased exposure to scrapie agent (Wilesmith et al. 1988) P4: Distribution of BSE cases is consistent with distribution of MBM (Wilesmith et al. 1988) P5: Food-borne transmission of scrapie has been suggested as a probable cause of TME (Marsh and Hanson 1979; Hartsough and Burger 1965) P6: Scrapie-like diseases found in nyala and gemsbok (Anon 1986; Jeffrey and Wells 1988). Investigation revealed that both animals had been fed concentrate ration containing MBM (Wilesmith et al. 1988)

P2: Fibrils that are morphologically similar to SAFs are found in BSE cases (Wells et al. 1987)

C: BSE produces similar histopathological changes in brain tissue as other TSEs, including scrapie

Aetiological conclusion: BSE is similar to (is aetiologically related to) scrapie in sheep (Wilesmith et al. 1988)

Diagram 2.1 Reconstruction of the arguments linking BSE to scrapie

C: Epidemiological evidence is consistent with food-borne transmission of scrapie to cattle

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The epidemiological study conducted by Wilesmith et al. (1988) was initiated in June 1987. This study undertook to obtain descriptive epidemiological, including genetic information, about early BSE cases; to monitor the incidence of BSE within herds and nationally; to collect data on the duration of the disease and the frequency of clinical signs, and to develop hypotheses about the aetiology of the disease. It is this last aspect of the study that is of particular significance to us as we seek to reconstruct the reasoning that led John Wilesmith and his colleagues to conclude that there were ‘aetiological similarities’ between BSE and scrapie in sheep. It is important to be clear from the outset about what this claim of aetiological similarity meant to these investigators. Wilesmith et al. were not merely stating that BSE was similar to scrapie in the sense that both diseases belonged to the group of TSEs (although this statement is clearly a corollary of their claim of aetiological similarity). Rather, these investigators were making the more specific claim that the infectious agent that causes scrapie in sheep had transmitted via a feed source to cattle and was now causing BSE. This specific claim of aetiological similarity, I will argue subsequently, was ‘strengthened’ during the BSE crisis to become a claim of aetiological identity (BSE is scrapie in cattle). This ‘bovine scrapie’ thesis and its weaker ‘similarity’ counterpart (BSE is similar to scrapie in sheep) assumed the status of explicit and implicit premises21 in the reasoning of BSE scientists. Certainly, these theses formed the cornerstone of much analogical reasoning during the BSE inquiry. In 1988, when Wilesmith et al. were advancing their claim of aetiological similarity, it could not be directly validated. Specifically, strain-typing studies, which were to reveal that the BSE ‘signature’ was distinct not only from scrapie but also from other naturally occurring TSEs, had yet to be completed.22 Consequently, Wilesmith et al. were forced to fall back on a number of less direct sources of evidence. One such source was histopathological evidence presented in a paper by Wells et al. (1987).23 This evidence consisted of two findings based on the investigation of

Fig. 2.1 BSE positive cows. The vacant stare, low head carriage and a wide-based hind limb stance are typical of the disease. Behavioural changes in temperament (e.g. nervousness or aggression), abnormal posture, incoordination and difficulty in rising, decreased milk production, and/or loss of weight despite continued appetite are followed by death in cattle affected by BSE (Published with the permission of the Controller of Her Majesty’s Stationery Office and the US Department of Agriculture, Animal and Plant Health Inspection Service (APHIS), respectively)

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pathological material obtained from four herds with BSE cases: (1) the presence in the grey matter of neuronal degeneration that most often involved intracytoplasmic vacuoles and (2) the electron microscopic identification of fibrils that morphologically closely resembled scrapie-associated fibrils (SAFs).24 (Figs. 2.2 and 2.3). It is clear that Wells et al. took these histopathological features to suggest a ‘similarity’ or ‘resemblances’ between BSE and encephalopathies caused by unconventional infectious agents in other species: There are strong resemblances between this disorder of cattle and the unconventional viral agent encephalopathies recorded in several species (1987: 420; italics added). [T]he authors regard this sporadic, slowly progressive, neurological disorder of adult cattle, characterised by grey matter vacuolation and scrapie associated fibrils, as compelling provisional evidence of similarity with diseases caused by unconventional infectious agents (1987: 420; italics added).

Yet, there are at least two significant ways in which these ‘similarity’ claims differ from those that were later advanced by Wilesmith et al. (1988). Firstly, Wells et al. did not attempt to draw any aetiological connection with scrapie in particular – the similarity in question was with TSEs in general. Secondly, although these resemblances were described as ‘strong’ and evidence of similarity was ‘compelling’, Wells et al. were also keen to stress the largely tentative nature of these early conclusions about the aetiology of BSE. Their caution is signalled through the emphasis of the ‘provisional’ nature of the evidence. Also, they remarked that ‘[a]dditional evidence is required. . .to establish the true nature of this entity’ (Wells et al. 1987: 420). Finally, these investigators stated that ‘[i]t should be emphasised that at present the aetiological basis of bovine spongiform encephalopathy remains

Fig. 2.2 BSE positive-neuropil vacuolation in the nucleus of the solitary tract (bovine brainstem at the level of the obex). © Crown copyright 2011. Published with the permission of the Controller of Her Majesty’s Stationery Office. The views expressed are those of the author and do not necessarily reflect those of Her Majesty’s Stationery Office or the Veterinary Laboratories Agency or any other government department

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Fig. 2.3 Scrapie-associated fibril, magnification X 39,000. © Crown copyright 2011. Published with the permission of the Controller of Her Majesty’s Stationery Office. The views expressed are those of the author and do not necessarily reflect those of Her Majesty’s Stationery Office or the Veterinary Laboratories Agency or any other government department

unknown and no connection with encephalopathies in other species has been established’ (1987: 420). The tentativeness and generality of Wells et al.’s ‘similarity’ claims are indicative of their rather low epistemic standing. Certainly, these claims had an altogether lower epistemic standing than the ‘similarity’ claims that were subsequently endorsed by Wilesmith and his colleagues. Histopathological evidence provided Wilesmith et al. with a rational basis upon which to begin developing an analogy between this new brain disease in cattle and scrapie in sheep. Yet, this evidence was still some way off establishing the more specific aetiological link with scrapie that emerged from Wilesmith et al.’s early epidemiological investigation. Additional evidence was needed in order to move from Wells et al.’s claim of similarity of BSE with TSEs in general to Wilesmith et al.’s claim of similarity with scrapie in particular. Such evidence was to emerge from a number of other sources. One of these was a molecular study conducted by Hope et al. (1988). These investigators demonstrated that the fibrils, which had appeared morphologically similar to SAFs in Wells et al.’s study, did indeed contain a protein that is the bovine homologue of PrP, a molecular marker of SAFs.25 This finding helped to strengthen the developing aetiological connection of BSE to scrapie: ‘Our protein data. . .confirm the homology of this novel cattle disorder and scrapie’ (Hope et al. 1988: 392). Further confirmatory evidence was obtained from Wilesmith et al.’s own epidemiological study. In order to establish the claim of aetiological similarity between BSE and scrapie, Wilesmith et al. needed to make a case for the claim that scrapie had transmitted to cattle. If scrapie had transmitted to cattle to cause BSE, then there were only two main routes by means of which transmission could have occurred. They included (1) direct or

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indirect contact between scrapie-affected sheep and cattle and (2) the consumption of scrapie-affected sheep tissues by cattle. Research into TSEs prior to 1986 had demonstrated that these diseases could be spread through direct and indirect contact between diseased and healthy animals both within and across species. In this way, scrapie could be transmitted between sheep through contaminated pastures and enclosures (see Section 1.2.4). Also, elk had been found to develop chronic wasting disease following sporadic fence-line contact with clinically affected deer and the use of pens in which such deer were kept (see Section 1.2.6). Yet, to the extent that 20% of farms with BSE did not have sheep (Wilesmith et al. 1988), route (1) appeared an unlikely means of transmission and was rejected by these investigators. A food-borne route of transmission did, however, receive support from several findings. Firstly, all BSE cases for which accurate records existed were at some time fed commercial concentrates, either as protein supplements used in home mixed rations or as finished rations such as pelleted calf feed and dairy cow cake. Secondly, Wilesmith et al. found a greater incidence of BSE cases in dairy herds (311 of 44,767) compared to beef suckler herds (11 of 54,166). The animals in the former herds received more commercial concentrates than the animals in the latter herds. Thirdly, a computer-based simulation model indicated that the exposure of cattle began in the winter of 1981/1982. This date is coincident with a number of developments which increased the exposure of cattle to the scrapie agent via feedstuffs.26 Fourthly, the widespread geographical distribution of BSE cases is consistent with the distribution of meat and bone meal in commercial feedstuffs. The geographical variation in BSE incidence was not, however, consistent with the distribution and use of tallow in these feedstuffs. Scrapie-like agents were known to be associated with cell membranes and were expected during the rendering process to partition with the cellular residues of the meat and bone meal fraction rather than the lipids of tallow. Each of these findings served to increase the plausibility of the food-borne hypothesis of the transmission of scrapie to cattle. Additional supportive warrant for this hypothesis was provided by the appearance many years earlier of a spongiform encephalopathy in ranch reared mink. Hartsough and Burger (1965) described several outbreaks of the disease between 1947 and 1963. They remarked that ‘[w]e feel that in the 1961 and 1963 episodes there is reasonable evidence of a food-borne exposure. . .we may even assume that tissues of bovine or perhaps ovine origin are possible sources for the as yet hypothetical contagion’ (Hartsough and Burger 1965: 392). Later, Marsh and Hanson (1979: 460) confirmed that TME had resulted from the oral transmission of scrapie to mink: ‘[T]here appear to be no major obstacles remaining to the probable fact that TME originates from feeding mink scrapie-infected tissues’. The development of a spongiform encephalopathy in mink provided Wilesmith et al. with an important precedent for the food-borne transmission of the scrapie agent. Certainly, this finding constituted a further, plausibility-raising thesis in support of the claim that scrapie had transmitted to cattle via a food source. The same could be said of the discovery in a wildlife park in England of a scrapie-like disease in a nyala and a gemsbok (MAFF/ADAS 1986; Jeffrey and Wells 1988), both of which had been fed

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a concentrate ration containing meat and bone meal (Wilesmith et al. 1988). Like the finding before it, Wilesmith et al. could contend that if scrapie had transmitted via a food source to infect these species,27 it could do so again to cause BSE in cattle. These additional findings complete the task of the reconstruction of the argumentation that was used by Wilesmith and his colleagues to support their claim of aetiological similarity between BSE in cattle and scrapie in sheep. As can be seen from Diagram 2.1, this claim relied on multiple sources of evidence from studies that separately examined the histopathology, molecular biology and epidemiology of this new disease. Individually, these sources carried little probative weight. Collectively, I will argue that they conferred sufficient rational warrant on Wilesmith et al.’s aetiological claim to give that claim legitimacy as a presumptive truth in subsequent scientific inquiry into BSE. This latter of our two tasks is an evaluative one. Its outcome will determine the rational credentials of the analogical thesis that was integral to much scientific reasoning about BSE. Not every source of evidence brought forward by Wilesmith et al. to support their claim of aetiological similarity conferred the same degree of warrant on this claim. We have already seen how Wells et al.’s histopathological findings only went as far as supporting a claim of similarity to TSEs in general, rather than scrapie in particular. By themselves, these findings could not support the more specific aetiological connection of BSE to scrapie that Wilesmith et al. were attempting to draw in their early epidemiological study. Accordingly, these investigators had to bring forward other forms of evidence that would raise the plausibility of their aetiological claim by suggesting a specific aetiological link between BSE and scrapie in sheep. This other evidence included the results of a molecular study by Hope et al. as well as Wilesmith et al.’s own epidemiological findings. These latter findings included the following four claims: (1) All BSE cases were fed commercial concentrates. (2) BSE incidence is greatest in dairy herds. (3) Exposure of cattle to BSE is coincident with increased exposure to the scrapie agent. (4) Distribution of BSE cases is consistent with distribution of meat and bone meal. Of these claims, only the first two could be established with any certainty. Claim (3) was based upon a number of factors which Wilesmith et al. (1988: 643) described as being ‘undoubtedly significant in the occurrence of this epidemiological phenomenon’. Yet, upon close examination, the significance of at least two of these factors may have been somewhat overstated. The two factors in question were (i) the introduction of continuous rendering processes during the 1970s and 1980s (the effect of which was to reduce the temperature and length of time at which animal material was rendered) and (ii) the decline in the practice of using hydrocarbon solvents and terminal heat treatment for fat extraction since the mid 1970s. Both factors relate to the rendering of animal material for commercial products, including cattle feedstuffs. However, it is clear from what was known about rendering

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practices on the one hand and the extraordinary resistance of the scrapie agent on the other hand that no rendering process was probably ever capable of inactivating TSE agents. During the BSE Inquiry, Lord Phillips and his team established that up until the 1970s, temperatures during rendering were not recorded or monitored systematically, that they could be very variable and that the absence of proper managerial control meant it was possible to discharge material before it was completely cooked (BSE Inquiry Report, Volume 13: 90). These various lapses in practice almost certainly resulted in a failure to deactivate the scrapie agent. Also, considerable evidence existed by 1988 to show that the scrapie agent failed to be deactivated by temperatures of 100◦ C or greater (Brown et al. 1982; Kimberlin et al. 1983; Rohwer 1984). Both considerations served to weaken Wilesmith et al.’s claim that changes in rendering practice played a significant role in increasing the exposure of cattle to the scrapie agent.28 Claim (3), it emerges, was not as strongly warranted as it first appeared. Claim (4) was also largely tentative in nature. When Wilesmith et al. were advancing their aetiological hypothesis, little was known about the exposure of cattle to meat and bone meal, the ingredient in commercial concentrates that was believed to be the source of infection. In April 1988, in response to a request from Mr Meldrum (Director of the Veterinary Field Service) to produce a report on BSE, Mr Wilesmith responded: ‘In brief we have no conclusions to explain why BSE should have occurred from the findings of the various investigations on the feedstuffs industry thus far’ (BSE Inquiry Report, Volume 3: 70). Even at the point of publication of their epidemiological findings in December 1988, Wilesmith et al. (1988: 643) indicated that their investigations of the feed industry, and the production and use of MBM in commercial feedstuffs in particular, were still some way off completion. These investigators stated that ‘[s]tudies are in progress to determine more precisely the exposure of affected and unaffected animals to meat and bone meal in commercial concentrates’. It is a presupposition of this statement that the exposure of animals to meat and bone meal had not been precisely determined by the stage at which these investigators were advancing their claim of aetiological similarity between BSE and scrapie. Lord Phillips and his inquiry team identified some reluctance on the part of investigators to make an early approach to the feed industry to enquire about its practices in general and MBM in particular. Such an approach, it was argued, could lead to a concealment of information.29 For this reason, confidential enquiries were made on an informal basis to individuals with industry experience, not all of it recent.30 These ‘off the record’ meetings meant that Wilesmith and his colleagues were unable to confirm their food-borne hypothesis for some months after this hypothesis began to be seriously entertained by investigators.31 Claim (4), it can be seen, was still subject to empirical validation even as it was being advanced by Wilesmith et al. in support of their aetiological link between BSE and scrapie. As well as epidemiological findings, Wilesmith et al. used the results of Hope et al.’s molecular study of bovine fibrils to support their claim of aetiological similarity between BSE and scrapie. Certainly, this study reveals similarities between the major protein of BSE fibrils and the PrP protein that is a molecular marker of

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scrapie-associated fibrils. In this way, BSE fibril proteins were similar in protease sensitivity and size to PrP in SAFs that were purified from the brain of a Cheviot sheep with natural scrapie. Also, the N-terminal 12 amino acids in bovine PrP were identical to those found in sheep SAF protein and differed by one amino acid from mouse, hamster and human PrP. The aetiological significance of these molecular similarities is somewhat doubtful, however. By 1988, studies demonstrating molecular similarities between the proteins in different transmissible spongiform encephalopathies were commonplace. In this way, Bendheim et al. (1985) found that CJD proteins had molecular weights similar to those observed for scrapie prion proteins. These investigators also remarked that ‘[p]urification of the two infectious pathogens by virtually identical procedures provided further evidence for similarities in their molecular structures’ (1985: 997). Kitamoto et al. (1986) found that antisera raised against hamster scrapie PrP stained amyloid plaques in the brains of humans and rodents with CJD and a human subject with Gerstmann-Sträussler syndrome. Bockman et al. (1985) reported a similar reaction to antibodies raised against the scrapie prion protein in proteins from the brains of two patients with CJD. These investigators stated ‘[o]ur findings suggest that the amyloid plaques found in the brains of patients with Creutzfeldt-Jakob disease may be composed of paracrystalline arrays of prions similar to those in prion diseases in laboratory animals’ (1985: 73).32 Molecular similarities between scrapie prions and prions in CJD and GSS certainly provide sufficient warrant for the claim that these diseases all belong to the group of transmissible spongiform encephalopathies caused by unconventional agents: ‘We conclude that the molecular and biologic properties of the CJD agent are sufficiently similar to those of the scrapie prion protein that CJD should be classified as a prion disease’ (Bendheim et al. 1985: 997). But this nosological relationship between these prion diseases is something quite different from the aetiological relationship between BSE and scrapie that Wilesmith et al. are seeking to support through Hope et al.’s molecular findings. The latter relationship does not merely seek to relate one prion disease (BSE) to another prion disease (scrapie). Rather, it goes one step further in asserting that the agent that causes scrapie in sheep is also causing BSE in cattle. It is this more specific aetiological relationship that is not supported by findings of molecular similarities between the prion proteins that cause BSE and scrapie. To see this, one need only consider studies such as that of Bendheim et al. which established molecular similarities between prion proteins in CJD and scrapie prions. These molecular similarities did not lead these various investigators to suggest that the scrapie agent had transmitted to humans to cause CJD. Indeed, by 1988 there was a developing scientific consensus that scrapie had not transmitted to humans to cause CJD despite extensive opportunity for it to do so.33 In this case, molecular similarities between CJD prion proteins and scrapie prions led to the (warranted) conclusion that these diseases were nosologically related in the absence of any wider claim to the effect that scrapie had transmitted to humans to cause CJD. A similar situation, I am arguing, pertains in the case of Hope et al.’s findings of molecular similarities between prion protein in BSE fibrils and prions in SAFs. These molecular similarities certainly support a nosological relationship between BSE and scrapie. However, they are much less able to support the type of

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aetiological relationship between these diseases that Wilesmith et al. are attempting to advance. We have now evaluated the histopathological, molecular and epidemiological evidence that was used by Wilesmith et al. to support their claim of an aetiological relationship between BSE and scrapie. Each of these strands of evidence, we have seen, is problematic in one or more respects. In some cases, essential knowledge was lacking (e.g. knowledge of the exposure of cattle to meat and bone meal). In other cases, greater significance was attributed to certain facts than a thoroughgoing assessment of these facts would have permitted (e.g. the overstated significance of changes in rendering practices). These various problems serve to weaken the supportive warrant that particular strands can confer on Wilesmith et al.’s aetiological conclusion. Yet, these individual strands and their attendant problems are less important to determining the supportive warrant of this aetiological conclusion than is the plausibility-raising capacity of these strands considered collectively.34 With each additional source of evidence, Wilesmith et al.’s claim of aetiological similarity between BSE and scrapie grew in epistemic stature. The epistemic evolution of this aetiological claim was at all possible because this claim had the status of a presumption, an epistemic category which, although tentative in nature, can improve its standing during inquiry. We will examine presumption in detail in the next chapter, where it will be seen that this notion is particularly well equipped to deal with the adverse epistemic conditions that characterize scientific inquiry in its early, emergent stage. The focus of this chapter, however, has been on an account of the evidential processes that were used by Wilesmith and his colleagues to forge an aetiological connection between BSE and scrapie, a connection that was to have a profound influence on all subsequent reasoning during the BSE crisis.

Notes 1. ‘In many cases of public health research, the emphasis is solely on data gathering (experimental, observational, surveillance, etc.) and the black-box operation of the techniques/instruments employed for this purpose, without any appreciation of the kind of substantive theoretical modelling that underlies these techniques/instruments and gives voice to the data’ (Christakos et al. 2005: 5; italics in original). 2. ‘Little attention has been given to the interdisciplinary nature of epidemic research and development. In this manner, important sources of knowledge available in the physical and life disciplines are ignored at the cost of profoundly inadequate epidemic and human exposure studies’ (Christakos et al. 2005: 4; italics in original). Clearly, Christakos et al. subscribe to the view that epidemic modelling requires the integration of knowledge bases from several disciplines. Savitz et al. (1999: 1159) make a similar point in relation to public health work in general when they remark that ‘[t]he phrase “the basic science of public health work” implies that the entire knowledge base underlying public health comes from epidemiology. . .it should be acknowledged that many other sciences serve public health as well. Among the basic public health sciences are clinical medicine, sociology, toxicology, molecular biology, anthropology, nutrition, sanitary engineering, policy analysis, risk assessment, industrial hygiene, economics, and political science’. 3. ‘The solution of mathematical models of epidemics has been viewed as a purely ontologic affair that focuses on abstract and dry formulas, whereas crucial factors – such as modes of perception and reasoning, and their integration – are neglected. . .’ (Christakos et al. 2005: 4; italics in original).

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4. ‘The fundamental spatiotemporal character of an epidemic under conditions of uncertainty has been mostly neglected. Intrinsically spatiotemporal phenomena, like disease propagation, are often modelled with “aspatial” and “aspatiotemporal” theories. . .This neglect has resulted in unsatisfactory analyses of major issues such as space-time prediction of disease distribution, epidemic explanation, and causation’ (Christakos et al. 2005: 4; italics in original). 5. In a 2003 interview with the eminent epidemiologist Mervyn Susser for the journal Epidemiology, Susser is asked for his opinion of the current state of health of epidemiology. His response conveys his concern that the field has become preoccupied with a focus on methods: ‘I have been writing a fair amount about this over the past dozen years, starting with “Epidemiology Today: ‘A Thought-Tormented World.’” I felt that we were at cross-purposes in formulating what epidemiology was. The academic center of the field was diverging from its concern with substance into the minutiae of methods. Not to say that methods are not essential, but to make methods a principal activity, to the neglect of the object of the activity, seems to me a travesty’ (Paneth 2003: 750). 6. The field of social epidemiology involves the ‘examination of the role of a broad array of social factors in the development and progression of many important health problems, and in the natural history of the risk factors for those diseases and conditions’ (Kaplan 2004: 124). 7. For Christakos et al. (2005: 68), stochastic modelling is the method of choice for dealing with multiple sources of uncertainty: ‘. . .in our view stochastic modelling is the primary conceptual and operational apparatus for studying fundamental uncertainties of the type happening in public health research, in general, and epidemics, in particular’. 8. That uncertainty is unavoidable in scientific inquiry is recognized by both scientists and philosophers. Christakos et al. (2005: 43) remark that ‘[u]ncertainty, in its various forms, is at the center of many scientific investigations and debates. Indeed, in the last few decades scientists have moved from seeing nature as inherently stable and deterministic to viewing it as uncertain, subject to unexpected shifts and changes. . .’. In this extract, Christakos et al. attribute uncertainty to nature. In Rescher’s philosophical account, uncertainty, in the form of incompleteness of knowledge, stems from the process of inquiry itself: ‘Certain fundamental features inherent in the very structure of man’s inquiry into the ways of the world thus conspire to indicate the incompleteness of the knowledge we can attain in this sphere’ (1980: 237). In Chapter 3, we will consider different sources of uncertainty during inquiry. 9. ‘If the development of SEP is going to produce rigorous rules for the integrated modelling of knowledge from different disciplines and levels of organization, it must rely on an adequate understanding of scientific intradisciplinarity and interdisciplinarity in an epidemic assessment context’ (Christakos et al. 2005: 14). 10. Of a paper by Adams et al. (2003) and responses to it by economists, epidemiologists and others in the same publication, Kaplan (2004: 126–127) remarks that ‘one is left with the impression that a number of the authors believe that the analysis of causal relations in observational data is so flawed as to potentially threaten even the conclusion that smoking causes lung cancer’. 11. Phillips et al. (2004) include the ‘critical analysis’ of epidemiology as one of the areas in which the new online journal Epidemiologic Perspectives & Innovations welcomes submissions. 12. Weed (1995: 916) sees the development of critical thinking skills among epidemiologists as one of the key benefits to emerge from a greater alignment of epidemiology with the humanities: ‘The ability to think critically is important to scientists. It is a broader ability than the concept of criticism alone, encompassing explanation, logic, creativity, and inquisitiveness. Critical thinking is useful for identifying bias, for finding hidden assumptions in causal criteria, and for developing new theories of disease causation that explain joint exposure effects. . .Critical thinking can be developed directly by studying the works of philosophers promoting it’. It is clear that an educational effort of the sort described in the main text is already underway in some public health circles. In a Technical Report prepared by the American Public Health Association (APHA), it is stated that ‘APHA should continue efforts

Notes

13.

14.

15.

16.

17.

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to strengthen training in schools of public health in the analysis of scientific evidence on public health problems’ (APHA 1990: 749). ‘In the epistemic cognition framework, the contribution of cognition is to identify basic knowledge-assimilation, belief-forming and problem-solving processes, which are then examined by means of the evaluative standards of epistemology’ (Christakos et al. 2005: 5). ‘[A]nother potentially significant departure of SEP from the traditional epidemic paradigm is the thesis that an epistemic cognition solution (which assumes that the relevant models describe incomplete knowledge about the epidemic and focuses on cognitive mechanisms) can lead to more adequate results than the conventional ontologic solution (which assumes that the models describe nature as is and focuses on form manipulations)’ (Christakos et al. 2005: 19–20; italics added). In developing a logic of error, Gabbay and Woods (to appear) subscribe to a form of fallibilism. They state that ‘[f]allibilism would be a harsh and pessimistic doctrine, and a stupid one, if it didn’t embed a further pair of assumptions. . .The one assumption says that the frequency with which we commit errors has not shut us down as would-be knowers; far from it. The other says that, notwithstanding the errors in which they land us, it is to the procedures in question that we owe our epistemic successes. They are not only the best that we can do, but they serve us rather well’. This neglect is a consequence of the concern not to conflate psychology with philosophy in the study of fallacies. In this way, Kahane (1980: 38) remarks that: ‘Well, then, do we overstep the bounds of logic and philosophy when we theorize about fallacious reasoning. Not, it seems to me, when we attempt to specify what fallacious reasoning consists in, nor when we specify the logical factors which make fallacious reasoning fallacious. These are questions of methodology, and thus of logic and philosophy. But we do overstep when we attempt to specify psychological mechanisms that lead to fallacious reasoning, and when we devise psychological categories useful in avoiding fallacious reasoning’. A theorist who explicitly acknowledges a role for cognition in the study of fallacies is Dale Hample (1982, 1985, 1988). Hample (1982: 59) states that ‘a message can only stimulate a fallacy; the actual fallacy is a cognitive event’ (italics in original). For further discussion of Hample’s views, see Cummings (2004b). Fallacy theorists have often advanced standards which actively eschew any role for the thinking agent (here, the user of argument) in argument evaluation. This can be seen in the following views of Biro and Johnson (the latter summarized by Walton): Both these approaches [Perelman’s rhetorical approach and Hamblin’s dialectical approach], in spite of their great interest, share the flaw we have seen to be fatal in Sanford’s treatment: relying, instead of on the necessary argument-relativity of the notion of knowability, on the essentially user-relative notions of assent and acceptance (Biro 1977: 270). Johnson’s claim is that mere “acceptance” or “effectiveness” in causing a listener to accept something she did not accept before is too weak a standard to do the job of providing a normative model of argument to help with analyzing fallacies (Walton 1993: 308).

At the root of such criticisms lies the concern that by assigning any significance to the user or recipient of an argument in judgements of argument acceptability, we are losing all sense of the objective from argumentative discourse. 18. Hansen and Pinto (1995) bring together the work of some of the key thinkers down the centuries who have engaged with the fallacies. Starting with Aristotle (384–322 B.C.), they include the authors of the Port-Royal Logic, Antoine Arnauld (1611–1694) and Pierre Nicole (1625–1695), John Locke (1632–1704), Isaac Watts (1674–1748), Richard Whately (1787– 1863) and John Stuart Mill (1803–1874). A further historical overview of the fallacies can be found in Charles Hamblin’s 1970 book Fallacies.

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19. See Lipsitch et al. (2009) for discussion of the uncertainty confronting scientists during the recent emergence of the influenza A (H1N1) virus that is responsible for swine flu. 20. As presented here, it seems that the tasks of argument reconstruction and evaluation are conceptually and temporally distinct activities with evaluation only occurring after the process of reconstruction has taken place. In reality, however, reconstruction and evaluation are interrelated stages in argument analysis. The task of argument reconstruction is already dependent on evaluative analysis, for example, when decisions concerning missing premises are made. We only accept as missing premises in an argument those claims which contribute to the deductive validity, plausibility or rational acceptability of an argument. And such notions are inherently normative and thus evaluative in nature. 21. An ‘implicit’ premise is also known by the terms ‘missing’ premise, ‘tacit’ premise, ‘unstated’ premise and ‘hidden’ premise. The standard role of these premises, according to Govier (1987: 82), is to ‘fill inference gaps’. 22. Bruce et al. (1997: 499) state that ‘[t]he BSE “signature”, based on both incubation periods and pathology, has only ever been seen in transmissions from animals suspected or known to have been infected with BSE. It has never been seen throughout an extensive series of transmissions, set up in Edinburgh between 1963 and 1994, of other naturally occurring TSEs (35 sheep and two goats with scrapie, two mink with transmissible mink encephalopathy, and a mule deer with chronic wasting disease)’. 23. Wells et al. (1987: 420) were the first investigators to call this new brain disease in cattle ‘bovine spongiform encephalopathy’: ‘Pathological and epidemiological studies, analyses of genetic data and experimental transmission studies have been initiated but until further characterisation is achieved the authors suggest for this disorder the provisional appellation: bovine spongiform encephalopathy’. 24. Patricia Merz was the first scientist to identify SAFs (Merz et al. 1981). Using electron microscopy, Merz demonstrated the presence of SAF ‘in all combinations of strain of scrapie agent and strain or species of host examined, regardless of their histopathology’ (1981: 63). 25. ‘In this report, we show the major protein of BSE fibrils is the bovine homologue of PrP as judged by its size, protease resistance, immunoreactivity, lectin binding and partial N-terminal protein sequence’ (Hope et al. 1988: 390). 26. ‘A number of factors have been identified which when combined are undoubtedly significant in the occurrence of this epidemiological phenomenon. These include: a dramatic increase in the sheep population in Great Britain which commenced in 1980 and has continued; a probable increase in the prevalence of scrapie infected flocks; the greater inclusion of sheep heads in material for rendering; the greater inclusion of casualty and condemned sheep in material for rendering as a result of the reduction in the number of knackers’ yards; the introduction of continuous rendering processes during the 1970s and 1980s which may have resulted in the rendering of animal material at a lower temperature and, or, a shorter time than previously and the decline in the practice of using hydrocarbon solvents and terminal heat treatment for fat extraction since the mid 1970s’ (Wilesmith et al. 1988: 643). 27. It should be emphasized that food-borne transmission of scrapie to these species is not suggested in the paper by Jeffrey and Wells (1988) or by the Report of the Chief Veterinary Officer (MAFF/ADAS 1986). In fact, Jeffrey and Wells (1988: 399) only appear to consider early feeding practice and direct and indirect (via paddocks) contact between this nyala and sheep (as well as mink and deer) as possible routes for the transmission of scrapie: ‘This nyala had no direct contact with sheep or goats, and its paddock had not previously been used by those species. It was bottle-reared on domestic cow’s milk by an attendant with responsibility for a small number of sheep grazed at a different location, but scrapie has not been reported in these sheep. Neither mink nor North American species of deer are kept at the wildlife park’. 28. This same point was made by Lord Phillips and his team when they remarked that ‘[t]he theory that BSE resulted from changes in rendering methods has no validity. Rendering methods have never been capable of completely inactivating TSEs’ (BSE Inquiry Report, Volume 1: xix).

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29. The Head of the Pathology Department and BSE research coordinator at the CVL, Mr Bradley, felt that an early approach to the feed industry would result in concealment of information. When asked on 27 November 1987 if an approach should be made, he responded ‘[n]ot yet. We must first identify the right questions to ask and we have more data to collect yet. We also need time to think. If we approach too early concealment of information is likely’ (BSE Inquiry Report, Volume 3: 61). 30. In a written statement to Lord Phillips and his team, Mr Rees (Chief Veterinary Officer, 1980–1988) remarked that ‘in these early stages we did manage to have some very informal discussions with a few advisers who we knew on a more personal basis, to determine the extent of the use of MBM in commercial feedingstuffs, and the distribution of MBM. These were really very informal chats as no one wanted to meet formally with MAFF at this stage’ (BSE Inquiry Report, Volume 3: 63). Mr Rees also told the inquiry team ‘of a single conversation that he had, on a personal and confidential basis, with an adviser to a feed manufacturer. While willing to assist, the adviser was not able to give very sound information as to the content of animal feed 4 or 5 years in the past’ (BSE Inquiry Report, Volume 3: 63). 31. From evidence given to Lord Phillips and his team, it is clear that Mr Wilesmith was more interested in contaminated vaccine than feed as a possible source of infection in June 1987 (BSE Inquiry Report, Volume 3: 60). However, by December 1987 Mr Wilesmith was ‘sufficiently confident’ that a feed-borne source was responsible for BSE (Volume 3: 62). Yet, it was 3 months later before feed industry representatives even became aware of a suspected link between feed and BSE. In this way, the UK Agricultural Supply Trade Association told the inquiry team that they did not learn of such a link until March 1988 (Volume 3: 61). Similarly, Mr Paul Foxcroft of Prosper De Mulder (the leading renderer in England and Wales) told Lord Phillips and his team ‘that he was absolutely certain that he was not aware of any suggestion of a link between BSE and animal feed until March 1988’ (Volume 3: 63). The time lag between Mr Wilesmith’s suspicion of a link and an opportunity to validate this suspicion through intensive investigation of the feed industry is responsible, I am arguing, for the lack of empirical validation of Wilesmith et al.’s food-borne hypothesis even by December 1988, when these investigators’ epidemiological findings were published. 32. Other studies in the same vein include Baron et al. (1988) who demonstrated immunoreactivity to rabbit antiserum raised against SAF protein in scrapie-infected mice and two familial cases of transmissible dementia. Manuelidis et al. (1985) tested protein blots of human, guinea pig and hamster CJD fractions with an antibody raised against a 29-kDa band from mouse scrapie. In all CJD and scrapie fractions, 29-kDa proteins were labeled. Bode et al. (1985) used antisera raised in rabbits and mice against SAF protein from hamster brain to test SAF proteins from hamster and mouse and from CJD. The antisera detected five bands in a Western blot analysis with molecular weights of 26, 24, 20, 18 and 16 K. By gel electrophoresis, these antigens seem to be identical in hamster, mouse and man. 33. A study by Brown et al. (1987), which concluded a 15-year investigation of CJD in France and reviewed the world literature, found no evidence whatsoever of a link between scrapie in sheep and CJD in humans. These investigators stated that although numerous cases of CJD had been observed in rural sheep-raising areas in Italy, Czechoslovakia and Chile, scrapie had not been recognized in sheep for at least a century in the latter two countries while there was no evidence that the Italian cases had been exposed to infected animals. In France, no increased risk of CJD was observed in people who were most exposed to sheep or sheep products, nor was there any relationship between CJD frequency and the distribution routes of sheep products from scrapie-endemic areas. CJD cases had occurred in France in people who had never eaten lamb or other sheep tissues and a life-long vegetarian in England also developed the disease. Furthermore, scrapie had been assiduously barred from Australia, where CJD occurs with the usual frequency, and Japan also experienced CJD cases even though scrapie had not been known until 1981. 34. This account differs from Rescher’s (1976) analysis of plausible reasoning in two significant respects. Firstly, Rescher (1976: 60–61) adopts a deductive approach to plausibility: ‘The

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presently envisaged approach to plausible inference thus proposes to assess the plausibility of a “merely plausible” piece of reasoning in terms of the plausibility of the added enthymematic premisses needed to transform it into a valid deductive argument’. As will become clear in Chapter 3, the model of reasoning that I am advancing in this book is essentially nondeductive in nature. Secondly, Rescher (1976: 61) states that the plausibility of an argument’s conclusion consists in the maximum plausibility among the various minimum plausibilities of the supplemental premises that are needed to turn the argument into a valid deduction: ‘the plausibility of the argument is to be the maximum value among the minima of the plausibilities of the enthymematic supplementations that enable a deductive derivation of the conclusion from the premisses’. My own model of reasoning adopts a cumulative approach to plausibility wherein no single premise determines the plausibility of the conclusion of an argument. Rather, all premises contribute to the raising of the plausibility of a conclusion, with high plausibility premises making a greater contribution to the plausibility-raising of the conclusion than low plausibility premises.

Chapter 3

Arguing Through Uncertainty

3.1 Introduction In the last chapter, the evidential basis of Wilesmith et al.’s aetiological claim was examined in detail. That claim sought to relate BSE and scrapie in the sense that BSE was caused by the transmission of scrapie to cattle. The evidence in support of this claim, I argued, was not without its weaknesses. The result was a rather tentative claim that was certainly grounds enough for proceeding in inquiry, but still fell some way short of the type of outright commitment that is associated with an established scientific thesis. I called this tentative claim a presumption and the evidential standard that attends it plausibility. Presumption has been something of a poor cousin in epistemological discussion. While concepts such as knowledge and belief have dominated epistemology, presumption has been the subject of much less philosophical inquiry. Yet, this notion has very direct relevance to a range of scientific deliberations, particularly where those deliberations are conducted against a backdrop of uncertainty. In this chapter, I demonstrate the epistemic resourcefulness of presumption within scientific inquiry that proceeds in a context of uncertainty. I will examine how the very features that have made philosophers overlook, if not altogether shun, this epistemic concept are the features that have made presumption a key ally of scientists in an emerging inquiry. These features include, most notably, presumption’s defeasibility and its association with error. A sound grasp of presumption on its own terms is vital if we are to proceed in delineating the type of argumentative strategies that were used by scientists during the first weeks and months of the BSE crisis. For presumption is the concept at the very heart of these strategies. Along with its bedfellow plausibility, presumption allows scientists to make gradual, but significant, epistemic gains at a time when conditions are adverse and the consequences of inaction, at least in the case of human health, are potentially catastrophic. The argumentative strategies which are integral to the reasoning of BSE scientists are very directly related to an old philosophical area. That area is the study of fallacies. The history of the fallacies has been an interesting one to say the least. Since Aristotle first examined the fallacies in Sophistical Refutations, and with the exception of contributions from medieval logicians and theorists such as Sidgwick,

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Whately and Mill, the fallacies have languished in a state of almost total neglect. In recent years, they have undergone something of a transformation, a transformation that was initiated by the publication in 1970 of Charles Hamblin’s landmark book Fallacies. Hamblin achieved a significant reinvigoration of the study of fallacies that is still being felt to the present day.1 One consequence of this reinvigoration is that logicians began to subject fallacies to the same systematic treatment that had long been evident in other domains of logic. It wasn’t long before this treatment began to bring forward results in the form of new frameworks for the analysis and evaluation of fallacies.2 Within these frameworks, investigators found increasingly elaborate ways of proscribing argument forms that had traditionally been characterized as fallacies. But an equally fortunate consequence of the development of these frameworks is that many so-called fallacies no longer appeared quite so fallacious when examined against new concepts (e.g. presumption) and standards of evidence (e.g. plausibility) in argument. In this way, non-fallacious variants of a number of traditional fallacies began to be described, including petitio principii (begging the question), argumentum ad ignorantiam (the argument from ignorance), and argumentum ad baculum (the argument from the stick or appeal to force) (Walton 1985, 1992; Woods 1995, 2004). The resurgence of interest in fallacies had effectively served as an impetus for investigators to characterize non-fallacious variants of these traditionally erroneous forms of argument. At the same time as fallacies were coming under renewed scrutiny, other developments were taking place that would change how theorists conceived of argument and reasoning. The first development was that theorists were increasingly beginning to challenge the relevance of formal (deductive) logic to the study of reasoning and argument.3 While it was recognized that reasoners and arguers were capable of drawing deductively valid conclusions, it was becoming increasingly evident that when making plans for the future, or arriving at a decision or assessing possible courses of action, arguers are much more likely to employ non-deductive modes of reasoning than accounts of reasoning had previously assumed.4 This decline in the traditional dominance of formal logic effectively cleared the way for investigators to begin describing forms of reasoning that had received little direct attention (at best) or that had been purposefully ignored (at worst) for no other reason than they did not attain deductive standards of validity and soundness. These forms included circular arguments, lack-of-knowledge reasoning and arguments based on analogies, amongst others. The second development was that philosophical accounts of science began to move away from the idea that scientific inquiry proceeded by means of deduction from certain and known theses to theses that are uncertain and unknown.5 Rather, scientific inquiry was as likely to contain a number of non-linear, non-hierarchical forms of reasoning in which the ordering of theses need not conform to strict epistemic priority requirements.6 Certainly, non-linear progression through scientific inquiry was no longer conceived as a subversion of the epistemic ground rules of inquiry and began to be viewed as a legitimate means of conducting inquiry, particularly in its earliest stages. Developments in epistemology have also served to create an intellectual context within which the view of scientific knowledge and reasoning expressed in this book

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may fit. Stanley (2005: 2) has recently challenged an epistemological orthodoxy – that the factors which make a true belief into knowledge are all truth conducive – by arguing for a role for practical interests in knowledge: ‘I will argue that the factors that make true belief into knowledge include elements from practical rationality. One consequence of my arguments is that the distinction between practical and theoretical rationality is less clear than one might wish’. To the extent that our practical interests have epistemic significance, we must countenance considerations such as the costs of being wrong within claims to knowledge. Where there is much at stake for an individual in a particular belief being true or false, this consideration is at least as relevant as any epistemic factor in whether that individual may be said to have knowledge: ‘There are cases in which two people are similarly situated, but one has knowledge, whereas the other does not, because one has greater practical investment in the truth or falsity of her beliefs. What makes true belief into knowledge is not entirely an epistemic matter’ (Stanley 2005: 2). The BSE affair saw practical interests intrude in a very direct manner onto what scientists did and did not know. There were considerable costs, particularly in terms of human health, of scientists being wrong. As subsequent chapters will demonstrate, there were numerous occasions in which BSE scientists confronted what Stanley characterises as a ‘high stakes’ scenario, a situation in which the cost of error precluded a claim to knowledge. It will also be evident from the discussion in these chapters that this practical consideration should have dissuaded scientists from making knowledge claims on many more occasions than was actually the case. Stanley’s epistemology captures a powerful intuition about why knowledge claims were not warranted under these conditions. A resurgence of interest in the fallacies, a reduction in the significance of deductive logic to reasoning and argument, a revision of the structure of scientific inquiry and the development of alternative epistemologies are the major developments that have made the analysis of scientific reasoning that will be presented in this book possible. Specifically, the argument forms that, I will argue, serve to advance inquiry under conditions of uncertainty are the very same argument forms that generations of philosophers have characterized as fallacies. Yet, these arguments are only fallacious when judged against standards which are based on deductive logic (and deductive logic, I am claiming, is no longer the only, or even the dominant, standard of argument evaluation). Moreover, these arguments can only subvert inquiry if the latter is construed along strictly linear lines in which certain and known theses have epistemic priority over uncertain and unknown theses (and such a linear model, I am claiming, is no longer the only, or even the dominant, conception of scientific inquiry). Indeed, I contend that the rational merits of these argument forms in scientific inquiry have been largely overlooked to date because of the distorting effects of the dominance of deductive logic on the one hand, and of models of scientific inquiry that assume epistemic priority, on the other hand. With these distorting effects removed from consideration, I intend to show that these argument forms directly facilitate scientific inquiry by conferring specific epistemic gains on this inquiry. But before we can describe these gains, we must first explore the epistemic concept that is the basis of these argument forms. That concept is called presumption.

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3.2 Presumption and Science Presumption is quite a remarkable concept. Few concepts that are as evident as presumption in our everyday discourse have received so little examination in epistemological discussion.7 Presumption has had a prominent and venerable presence in law but has been neglected, and even despised, in scientific contexts.8 A concept that can simultaneously inspire and infuriate is certainly worthy of further consideration. In this section, we will analyze presumption in detail as this concept is fundamental to the various argumentative strategies that were used by scientists during the BSE crisis. Central to this discussion will be an examination of five features of presumption that make this concept particularly suited to the work of science. These features variously draw upon aspects of the legal, dialectical and epistemic conceptions of presumption that have been discussed in the literature (see Rescher (2006) for discussion of these conceptions). In this section, we address those conceptions to the extent that they illuminate the particular features of presumption that are of relevance to scientific inquiry. Having discussed these features, we turn in the next section to consider how presumption is particularly well adapted to conditions of uncertainty in the emergent stage of a scientific inquiry. In Section 3.4, we will examine how presumptive frameworks are increasingly being used in the analysis of the various arguments that are integral to the model of reasoning which I am developing in this book. These frameworks provide a starting point for the exploration of the logical and epistemic attributes of the arguments that are the basis of this model. Also in this section, we identify examples of reasoning by BSE scientists that exemplify the argument forms in question in preparation for the evaluative analyses of Chapters 4, 5, 6, and 7. Notwithstanding the rather limited treatment of presumption in epistemological literature, definitions of presumption are commonplace. These definitions assume somewhat different emphases according to the legal, dialectical and epistemic conceptions within which they are advanced. A general characterization of this notion – and a good starting point for further discussion – is a definition advanced by Walton (1992: 42): [A] presumption is a kind of provisional concession or acceptance of a hypothesis that is reasonable to act on for the present, but that may have to be given up at some future point.

This definition reflects all five of the features of presumption that are operative in a scientific context. Chief amongst these features is presumption’s orientation to action (Feature 1). Presumption is a practical concept that permits agents to pursue a particular course of action. The action in question may be cognitive in nature (e.g. making a decision) or something which involves physical action (e.g. implementing disease control measures). The actions that are licensed by presumption are only warranted to the extent that there is some rational justification for the presumption in question (Feature 2). That it must be ‘reasonable to act’ on a presumption is essential to presumption’s claim to rational legitimacy both in scientific contexts and elsewhere. Notwithstanding this claim to rational legitimacy, a presumption may be shown by subsequent developments to be lacking or inadequate in some respect. In

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such an event, a presumption must be relinquished rather than stubbornly adhered to in the face of contrary evidence. The abandonment of a presumption is at all possible because of the inherent defeasibility of this notion (Feature 3). The conditions under which a presumption is first warranted are not always the conditions that may pertain at a later point in time. Presumption must display sensitivity to the wider contexts within which it operates and must be capable of responding to any changes in these contexts (Feature 4). Finally, a presumption is not a well established thesis but one which has a ‘provisional’ standing. Consequently, presumption has a rather lowgrade epistemic status (Feature 5). All five of these features will be examined in more detail below.

3.2.1 Feature 1: Presumptions Display an Orientation to Action Presumption’s orientation to action is very aptly demonstrated within a legal setting. Presumption rules in law, Ullman-Margalit (1983: 154–155) contends, function as a ‘means of extrication’ from some deliberation that cannot be resolved on the basis of the available evidence. They facilitate agents in coming to a decision and in taking a course of action in advance of completion of deliberation: A presumption rule. . .comes to the aid of a deliberating agent when he or she is called upon to act, when the choice of the course of action to be taken hinges in a material way on whether a certain state of affairs obtains, and when the agent is in a state of ignorance or doubt concerning the answer to the question. The significant factor in the description of the situation is that the person concerned is constrained to take action, some action, before his or her deliberation can be terminated: the time to act precedes the rational resolution of the deliberation process.

Ullman-Margalit (1983: 156) uses the legal presumption of innocence to demonstrate how ‘presumption rules function as, and are thus justified qua, means of extrication from unresolved deliberation processes’. In a criminal trial, where evidence clearly points to the guilt or innocence of a defendant, the deliberation process can be progressed to the point where a verdict is reached. However, in cases where evidence is inconclusive and some doubt exists about a defendant’s guilt or innocence, some method needs to be found of resolving the deliberation process. The presumption of innocence brings ‘triers of fact’ to the point where a verdict can be obtained. It thus avoids a situation in which deliberation must be aborted on grounds of failure to advance it. The action-oriented nature of presumption thus licences actions in practical and cognitive domains9 when the deliberative process encounters factors that risk throwing it into a state of indefinite suspension. Deliberation may be unable to proceed when there is a lack of evidence relating to the question-at-issue or when evidence is available but fails to conclusively establish one thesis over other, competing theses. Some means must be found of licensing action in the absence of a conclusion to the deliberative process. That means is presumption. In scientific inquiry, particularly when there is a pressing demand for action, the inquiry process may in itself represent an unacceptable delay on the initiation of such action. Presumption may then

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licence the implementation of a range of practical measures in advance of inquiry issuing forth in the type of theoretical knowledge that might be the basis of action under different circumstances. Walton (1992: 42) describes this circumvention of inquiry by presumption as follows: Presumption is basically a practical idea. Its use is to enable action to go ahead in a practical manner, instead of being stifled by lengthy investigations and inquiries that would delay any action past the point where action could be useful.

The action-oriented character of presumption comes into its own in the context of an inquiry into an emerging infectious disease. Diseases such as BSE and, more recently, SARS have posed a potentially serious, but at the time of their emergence largely unquantifiable, risk to humans. Scientists charged with responding to this risk have had the dual tasks of developing theoretical knowledge of the disease agents involved and of undertaking practical measures to contain the spread of an outbreak. The implementation of disease containment measures cannot await the outcome of inquiry, but must be initiated in advance of the attainment of complete or even partial knowledge of the disease processes that are responsible for an epidemic. Presumption warrants these actions in the practical sphere, actions that must proceed out of necessity and before the process of inquiry has terminated (and, in some cases, even started).

3.2.2 Feature 2: Presumptions Exhibit Rational Justification Although we only ever have a tentative commitment to presumption, that commitment must be rationally warranted. There must be some grounds in place to support a presumption. Godden and Walton (2007: 337) state that ‘presumptions can be based on practical, epistemic, moral, social, and prudential grounds, and each of these grounds befits a certain level of presumption’. In this way, moral and ethical considerations relating to the protection of human health warrant a presumption against the safety of new drugs and other medical interventions. Prudential considerations lead those who handle guns to adopt the presumption that they are loaded. The social norms and expectations that are implicit in our interactions with others warrant a range of communicative presumptions – that an interlocutor is being sincere, is contributing truthful, relevant utterances to the interaction, etc. A presumption in favour of our perceptual and cognitive resources is warranted on epistemic grounds – these resources are able to deliver true claims to us and are the basis of our various knowledge claims.10 Underlying each of these domain-specific justifications of presumption is a justification that is formulated in pragmatic terms. For presumptions are ultimately justified by virtue of the fact that they enable us to fulfil certain purposes and goals in a domain, should this be the safe handling of firearms, the successful containment of an infectious disease or the understanding of a speaker’s intended meaning in producing an utterance. Rescher (2006: 51) captures the pragmatic justification of presumption as follows:

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Our policies of presumption are justified through their purposive efficacy in facilitating realization of the inherent purposes and objectives of the domain in which they are instituted. Be it in matters of justice or inquiry or communication, these principles of presumption find their justification, insofar as they indeed are justified, through the common consideration that their operation is pragmatically effective.

According to Rescher, those presumptions that prove their purposive efficacy in a particular domain undergo retrovalidation whereby they can improve their epistemic standing in inquiry (see Feature 5 below). Some of the resentment towards presumption in science is a direct consequence of the mistaken belief that presumptions are little more than claims established on a whim, or at least not on any rational basis (certainly, this belief appears to motivate the comments about the place of presumption in science in note 8). Yet, the rational justification that attends presumption is similar to that which attends hypotheses in the context of a scientific inquiry. The rational justification of presumption inheres in evidential considerations, as Rescher (2006: 53) points out in the case of cognitive presumption: ‘The validation of a principle of cognitive presumption can – and ideally should – eventually come to rest on an experiential and evidential foundation’.11 The evidence in question is that of a ‘track record’ that the presumptions, which we have adopted, have served us well in fulfilling the goals of a domain. This track record, while ultimately a practical consideration, actually differs little from the evidential considerations at work in the acceptance of scientific hypotheses. For in accepting scientific hypotheses, we are favourably inclined towards those hypotheses that help us achieve certain cognitive and epistemic goals (e.g. we accept those hypotheses that provide the best explanation of the data). Although these goals are in the theoretical domain, their attainment is nonetheless a pragmatic consideration. So quite apart from being hostile terrain for presumptions, scientific inquiry has pragmatic considerations at the heart of its own processes of rational justification of hypotheses.

3.2.3 Feature 3: Presumptions are Inherently Defeasible Notwithstanding their very real claim to rational warrant, presumptions can be overturned as soon as evidence that is contrary to them emerges. Their capacity to be overturned by contrary evidence is the feature of defeasibility. While all presumptions are defeasible,12 the evidence that overturns them can only be determined on a case-by-case basis. For example, the evidence that leads me to doubt that a communicator is adhering to a presumption of sincerity in conversation is quite different from the evidence that will overturn a presumption against the safety of a new drug. While a lack of eye contact by my interlocutor may lead me to relinquish the former presumption, only extensive clinical trials that demonstrate no adverse effects of the drug will lead me to overturn the latter presumption. Clearly, a presumption’s defeasibility is a function of the significance of the particular issue under consideration13 – where the issue is one of safety and wellbeing, the evidence that defeats a presumption will be of a different order to that which defeats a presumption upon which little of significance rests. The defeasibility of presumption is thus

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intimately linked to the probative rules that operate in a particular domain. These rules specify the burden of proof14 that must be discharged by the opponent of a presumption in order for that presumption to be overturned. Presumption is closely tied to burden of proof in a dialectical conception of this notion.15 As Rescher (2006: 15) remarks: Presumption – and the idea of burden of proof that is indissolubly connected to it – also serves as a fundamentally dialectical conception and has figured as such from classical antiquity to Hegel and beyond.

A dialectical conception of presumption presupposes a context of argument. Within this context, two related conceptions of burden of proof can be seen to operate. On the first conception – what Rescher calls the probative burden of an original assertion – the arguer who initiates the assertion of a thesis has the burden of supporting it in argument. This burden remains upon this arguer throughout the course of argumentation. On the second conception of burden of proof – what Rescher calls the dialectical burden of further reply in the face of contrary considerations – the onus for advancing grounds in support of a thesis shifts between two arguers. In this way, when an arguer advances sufficient grounds in support of a thesis, that arguer has discharged his or her burden of proof. The thesis in question assumes the status of a presumption. The opponent of this thesis then has the right to advance grounds against it or in support of an opposing thesis. As well as advancing a dialectical conception of presumption, Rescher has emphasized the dialectical character of science itself. Scientists, he claims, are pursuing a form of rational dialectic in which scientific theses are subject to the critical examination of other scientists. This examination takes the form of a debate in which scientists assume the roles of proponents and opponents of various theses: [C]reative science appears in the light of an adversary procedure, with proponents and opponents carrying on a debate to secure the approbation of knowledgeable but “disinterested” (i.e., unaligned) parties – often as not the rising generation of specialists in the field (Rescher 1977: 111; italics in original).

The adversarial nature of scientific inquiry is well attested. Even established scientific theses may be subject to revision and rejection if sufficient grounds are adduced against such claims. And scientific theses grow in epistemic stature as they are seen to withstand the challenges of one’s scientific peers. These dialectical exchanges between scientists are only possible because of the existence of presumption and burden of proof. Their combined operation permits the progression of scientific inquiry – when sufficient evidence is adduced to overturn a presumption, the obligations of opposing scientists change and the inquiry enters a new phase of dialectic. The interlocking concepts of presumption and burden of proof therefore prevent a situation in which a single party to a scientific dispute can stall inquiry – their function is to regulate the actual conduct of inquiry.16 Also, as successive phases of dialectic are entered, the rational grounds of a thesis are progressively laid bare. As well as procedurally guiding inquiry, presumption and burden of proof thus make it possible to explore the rational basis of scientific theses.

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A dialectical conception of presumption has other important applications to scientific inquiry. Science is by its nature a fallible activity. As such, it must be able to respond to the emergence of error in a proportionate manner. The discovery of error should not normally entail the wholesale rejection of scientific theories – a complete unravelling of theories is both cognitively wasteful and likely to be unnecessary in particular cases. Dialectical presumptions can cope with the emergence of error on account of their defeasibility. Presumptions are highly sensitive to the onset of difficulties and can leave the dialectical scene as quickly as they entered it. The slightest unfavourable shift in the evidential warrant of a presumed thesis can trigger the rejection of that thesis. So the capacity of dialectical presumptions to be defeated and to fall by the wayside in scientific inquiry is an important feature of presumption’s response to scientific error. Where presumptions are beyond the reach of contrary evidence, they assume the status of immutable theses. Such theses are much closer to the presumption rules found in law than they are to the inherently defeasible presumptions that are required by science. However, even in science presumptions can be shielded from contrary evidence. Where emerging evidence cannot stand against a presumed thesis, this thesis becomes fossilized in inquiry. A fossilized presumption persists in inquiry regardless of the evidence that is adduced against it. It is thus a distortion of presumption, an aberrant presumption that outlives its warrant. In Chapters 4, 5, 6, and 7, we will consider examples of fossilized presumptions in the inquiry into BSE, as well as discuss instances in which presumptions were appropriately overturned by contrary evidence.

3.2.4 Feature 4: Presumptions Display Context Sensitivity Thus far, we have seen a number of ways in which presumption is linked to aspects of context. Presumptions, we argued above, were justified in the final analysis in pragmatic terms through their fulfilment or otherwise of the purposes and goals in a particular domain. The presumption of sincerity in conversation is ultimately justified by whether or not it permits communicators to successfully understand each other’s utterances. The goal of successful comprehension between communicators confers rational legitimacy upon communicative presumptions but would hold little sway in justifying the presumptions of other domains such as the law (e.g. the presumption of innocence). The rational justification of presumption is a context-sensitive business with justification residing within the unique features that pertain in a particular domain or setting.17 Similarly, the evidence that can overturn a presumption cannot be determined apart from the particular context in which that presumption has been used. The defeasibility of presumptions rests on a multitude of factors in a given situation (e.g. the seriousness of the contention at issue) and is thus a context-sensitive affair. Walton (1996: 41) remarks upon the context sensitivity of presumption in reasoning as follows: [T]he job of evaluating presumptive reasoning is inherently pragmatic, in that it depends on the particular circumstances of a given case, as far as these are known, to a given point.

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3 Arguing Through Uncertainty This context-sensitivity and openness to revision is also characteristic of practical reasoning generally – a kind of reasoning that takes as its object an inherently variable situation unfolding in time.

Context sensitivity poses considerable difficulties for investigators who wish to develop a theory of presumption. It precludes the attempt to state in general terms the conditions under which presumptions are rationally justified, defeated and much else besides. Even in a single domain such as science, presumptions stand and fall on the basis of context-specific considerations that vary across and within different inquiries. We will see that during the BSE affair, the emergence of experimental and other findings over time profoundly changed the evidential context in which the inquiry into BSE was conducted. To the extent that scientific presumptions are context sensitive, this evolving evidential context might be expected to have implications for the rational standing of theses in this inquiry. On some occasions, this context sensitivity was reflected either in an increase in the epistemic stature of theses as confirmatory evidence emerged from experimental studies or in the revision and rejection of theses as disconfirming evidence was forthcoming from studies. However, on a significant number of occasions presumptions became detached from the evidential contexts in which they operated. In failing to reflect the available evidence relating to some aspect of the BSE problem, these presumptions were essentially context insensitive. We will see in Chapter 5 that this detachment of presumption from context served to distort the operation of presumption and burden of proof in BSE inquiry and with it the dialectical progress of this inquiry.

3.2.5 Feature 5: Presumptions Have a Low-Grade Epistemic Status Another feature of presumptions is their low-grade epistemic status.18 A presumed thesis is not a known thesis.19 However, for those presumptions that prove their worth to inquiry, some improvement in their epistemic standing is possible. At the outset of inquiry, presumption occupies a rather lowly epistemic status. While this status is inadequate as a basis for theory construction in science,20 it presents a distinct advantage for scientists in the initial stage of inquiry. For the scientist who is setting out on a new scientific inquiry, presumption represents an important route into that inquiry. Our minimal commitment to presumption means that scientists can embark on inquiry when a requirement for more established theses would make the initiation of inquiry impossible. Our attitude to presumption is one of forging ahead on an almost exploratory basis with no expectation of where that exploration will take us. Of course, our chosen presumptions may lead us into error (see Feature 3). Alternatively, they may be validated by evidence that emerges during the conduct of inquiry. Validated presumptions grow in epistemic stature and improve their standing in inquiry. According to Rescher (1977: 56), this improvement comes about through a process of retrospective revalidation: We begin by provisionally accepting certain theses whose initial status is not that of certified truths at all, but merely that of plausible postulations, whose role in inquiry is (at

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this stage) one of regulative facilitation. Eventually these are retrovalidated (retrospectively revalidated) by the results of that inquiry. At that stage their epistemic status – though not their content – changes. In the first instance these presumptions have a merely provisional and regulative standing, though in the final instance they attain a suitable degree of factual-constitutive substantiation. (italics in original)

The picture to emerge is one of certain presumptions undergoing an epistemic evolution from their earliest, tentative beginnings to their subsequent upgrading in inquiry. This evolution is consistent with the long-standing philosophical idea that scientific inquiry proceeds in phases or stages, each of which contains a distinct type of intellectual activity.21 The first of these stages involves the generation of hypotheses. Hypothesis generation is essentially a creative process that can draw upon information from a range of sources.22 Its unconstrained character has led some philosophers to question whether any progress can be made in understanding the global processes at work in this stage of scientific inquiry.23 Once generated, a hypothesis must be tested for its ability to explain the data that is available in a case. A hypothesis that explains these data is confirmed and is assimilated into a body of scientific knowledge. This stage of scientific theory construction involves certain and known theses that have been rigorously validated by preceding phases of inquiry. Theory construction is not receptive to untested presumptions which, although plausible, may have little value to inquiry in the long run. Presumptions are thus most prominent in the initial, hypothesis generation stage of inquiry and least evident in the final inquiry stage of theory construction. Walton (2005: 73) captures these different phases of scientific inquiry, and the role of plausible (presumptive) argumentation and reasoning within them, as follows: Plausible argumentation in science is typical of the initial discovery stage of an investigation where a hypothesis is formed, even though it has not yet been verified by collecting enough data. At a later stage, once more information is in, testing and further verification of the initial hypothesis may lead to a point where it can be evaluated as probably true or probably false by inductive reasoning. Or still later, no reservations may need to be expressed, once a precise theory has been constructed and deductive arguments can be used to prove it. Plausible reasoning can be useful as a way to move forward provisionally and narrow down the number of hypotheses that need to be experimentally tested.

To appreciate the epistemic evolution of presumptive theses during the scientific inquiry into BSE, it is important to avoid conducting an examination of this inquiry at one or more discrete points in time. As with all inquiries, the inquiry into BSE possesses a temporal context and it is to that context that we must turn in order to track the trajectory of scientific presumptions. We will see that some presumptions were relatively short-lived during the BSE affair while others persisted throughout most of the course of inquiry (e.g. the presumption that beef was safe to eat). Some presumptions that persisted in inquiry achieved an epistemic standing that was not always warranted by the available evidence (e.g. the presumption that BSE was bovine scrapie). An examination of these and other presumptions will reveal some critical uses and abuses of presumption by scientists and government ministers alike.

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3.3 Presumption and Uncertainty Management Clearly, presumption is a complex concept with many attributes that warrant a much greater integration of this notion with the concerns of science itself. Yet, if the argument that I am advancing is correct, the ultimate value of presumption to science resides in this concept’s unique capacity to navigate a safe route through the treacherous waters of uncertainty. While philosophical and scientific analyses of uncertainty24 abound, few if any of these contributions have thus far produced a viable framework for the management of uncertainty in a public health context. In this way, Christakos et al. (2005: 9) remark that ‘no systematic methodological framework exists for integrated epidemic modelling in a realistic space-time domain under conditions of multi-sourced uncertainty’. In this section, we examine what uncertainty consists in within a public health setting. This discussion reflects a much wider range of considerations than have traditionally been encountered in work on uncertainty. Specifically, it will be argued that although uncertainty is typically manifested in a lack of knowledge in a particular domain, that lack of knowledge can have its source in a range of conceptual, empirical, cognitive and technical issues. The successful management of uncertainty, I contend, will require investigators to embrace an equally eclectic mix of considerations in whatever frameworks are instituted. Central to my argument will be the claim that a model of reasoning that has presumption at its centre is particularly well equipped to deal with the multidimensional concept of uncertainty that pertains in public health science. Certainly, some such model, it will be argued, can go a considerable way towards addressing the substantial dissatisfaction that is experienced by public health researchers with attempts to manage uncertainty.25 A few preliminary remarks are in order. The phrase ‘the management of uncertainty’ has a significance which will have an important bearing on what will subsequently be said about uncertainty. That significance concerns the existence of uncertainty. In this discussion, it will be assumed that uncertainty is omnipresent in public health science. Scientists can never eliminate uncertainty;26 rather, they can at best more or less successfully manage it. The elimination of uncertainty is not an attainable scientific aim, if for no other reason than nature is itself not a certain entity: Uncertainty, in its various forms, is at the center of many scientific investigations and debates. Indeed, in the last few decades scientists have moved from seeing nature as inherently stable and deterministic to viewing it as uncertain, subject to unexpected shifts and changes, which can suddenly create huge opportunities for the prepared and sometimes fatal threats for the slow movers (Christakos et al. 2005: 43).

Scientists are increasingly acknowledging the inevitability of uncertainty in their work. This acknowledgement takes many forms. In a report of a World Health Organization meeting held in Copenhagen in December 2005, the lack of certainty in science was highlighted. A recommendation to emerge from this meeting was that scientists should make efforts to educate the public and decision makers on the essentially uncertain nature of much of their work and challenge the

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pronouncements of politicians where these misrepresent the uncertain nature of science: Underlying the concept of uncertainty is a belief that “certainty” exists, which. . .is more of a myth than a fact when it comes to evidence on environment and health. Science has contributed to creating this myth in the past focusing on what we know and not so much on what we do not know. . .This has led policy makers to choose the courses of action that appear to be based on the most certain information, which might not be the best overall option. It was recommended that scientists be clearer to the public and decision-makers about the underlying lack of certainty of their work. It was proposed that scientists “deny” politicians clear-cut recommendations in order to make them accept fundamental uncertainty. . . (World Health Organization 2006: 9–10).

An important proviso attends the inevitability of uncertainty in science. In admitting that uncertainty is inevitable in science, we are not leaping into a sceptical abyss whereby the very possibility of acquiring knowledge in science is immediately foreclosed. Certainly, the knowledge sceptic uses a ‘no certainty’ claim of sorts to justify such foreclosure.27 However, his abandonment of the entire enterprise of knowledge is motivated by a transcendental conception of certainty which is foreign to the concerns of science.28 The scientist is concerned to tackle uncertainty from within the project of knowledge. In this way, he is prepared to concede that there are truths which could be known, even if we do not currently know them. For the sceptic who is subscribing to a transcendental notion of certainty, there are not even truths which could be known. In science, the omnipresence of uncertainty is a feature of our epistemic dispensations that could in principle yield to the best inquirers (even if this doesn’t always happen in practice). The omnipresence of uncertainty for the knowledge sceptic is the consequence of the hyperbolic requirement that we must be able to step outside of our minds and assume a metaphysical standpoint in making claims to knowledge. To the extent that we cannot remove ourselves from our cognitive standpoints, the sceptic argues that we can never satisfy knowledge’s requirement for absolute certainty with the result that we cannot claim to know anything at all. The sceptic places himself outside the knowledge enterprise through his imposition of an unattainable form of certainty on the concept of knowledge. For the scientist, such certainty is no part of the knowledge concept that is integral to scientific inquiry and its imposition constitutes a distortion of knowledge itself. So the picture to emerge is one in which uncertainty is omnipresent in public health science without this claim raising the spectre of knowledge scepticism. The uncertainty that confronts the public health scientist is a manageable attribute of scientific inquiry, notwithstanding its resistance to resolution in particular cases. Yet, resolution is possible and not only in exceptional circumstances. The central plank of the scientific response to uncertainty must be the cognitive concepts that the knowledge sceptic assumes we can somehow transcend. Chief amongst these concepts is reasoning, although perception (a cognitive process particularly distrusted by the sceptic), memory, visual imagery and linguistic features could equally be added.29 Modes of reasoning, which are much broader than those traditionally characterized as deduction and induction, have a key role to play if for no other

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reason than deduction demands the type of certain theses that are somewhat thin on the ground in a context of scientific uncertainty. Similarly, the probable theses of induction are a considerable luxury in the uncertain terrain of an emerging scientific inquiry. Reasoning based on presumption, I contend, is ideally placed to counter uncertainty. However, in order for this last claim to stand, presumption must be shown to be able to accommodate the types of uncertainty that are inherent in scientific inquiry. Such demonstration will be the focus of the remaining discussion in this section. Public health scientists have variously construed the concept of uncertainty that confronts them in their work. For some of these scientists, uncertainty is a psychologically laden notion that captures a certain imprecision or lack of clarity in our own thought processes.30 For other scientists, uncertainty is best construed in ontological terms where it captures certain objective features of reality itself.31 For still other scientists, uncertainty is a technical notion that results from various limitations in our measurement and other techniques.32 Each of these forms of uncertainty is in evidence in scientific inquiry with the inquiry into BSE no exception in this regard. But there is a significant sense in which uncertainty during scientific inquiry has sources that are not fully captured by these psychological, ontological and technical conceptions of the notion. These additional sources must also be addressed by public health scientists.33 In an interdisciplinary inquiry, such as occurred during the BSE crisis, uncertainty can arise when investigators from a range of different fields are contributing their respective expertise on a particular problem or issue. The differences between these fields are more than merely terminological in nature. Everything from types of evidence and burdens of proof through to modes of reasoning and processes of knowledge generation set these fields apart. Yet, their integration is needed in order for scientists to be able to address an interdisciplinary problem such as the risk that an animal disease like BSE poses to human health. Where this integration does not occur, or occurs only inadequately, uncertainty with all its pernicious consequences is the result. The question now is whether presumption has the requisite conceptual resources to achieve this integration. This question can be answered, I believe, in the affirmative. But before doing so, we want to establish if there are other features of scientific uncertainty which must be captured by presumption. More often than not during inquiry, forms of uncertainty are interrelated with the result that it is not always clear which of several uncertainty sources is the main or primary obstruction to the resolution of an issue. Where a primary form of uncertainty cannot be addressed for whatever reason, there is little prospect of scientists successfully managing other forms that are related to, or dependent upon, it. For example, during the BSE inquiry, the results of a study designed to investigate maternal transmission of BSE could not be clearly interpreted (uncertainty 1) because it was not possible to exclude the possibility that calves had been exposed to infected feed (uncertainty 2) and there was a lack of knowledge of the genotype of the calves in the study (uncertainty 3). To the extent that ingestion of contaminated feed could not be eliminated as a cause of the increased incidence of BSE in the offspring of infected dams and given that the genetic studies required to establish

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the genotype of subject and control calves were not available in 1989, the results of this maternal transmission study remained essentially uncertain: When the results were obtained, there was a difficulty in analysing them. Although the experiment had been designed to be large enough to give an answer despite the possible exposure of the animals to infected feed, it was not possible to establish with certainty whether the increased incidence in offspring of affected dams was the result of maternal transmission of BSE, or maternal transmission of genetic susceptibility to BSE. . .a complex genetic association study using multiple polymorphic genetic markers would have been needed to determine if there were significant differences in genotype between subjects and controls. Such a study would not have been possible in 1989. However, the consequence is that uncertainty remains about the interpretation of the results of the study (BSE Inquiry Report, Volume 2: 209; italics in original).

Clearly, a lack of scientific knowledge of the genotype of the calves in this maternal transmission study is responsible for the uncertainty in the experimental results of this study. This case reveals how concept-related uncertainty and fact-related uncertainty are intimately linked in scientific inquiry.34 However, it demonstrates something altogether more fundamental that a concept of presumption which is equipped to deal with uncertainty will have to address. That is the question of the order in which uncertainties should be addressed in scientific inquiry. In most cases, that order is epistemically determined. In the example above, the forms of uncertainty represented as ‘uncertainty 2’ and ‘uncertainty 3’ are epistemically prior to the form of uncertainty represented as ‘uncertainty 1’ – investigators cannot know if maternal transmission is responsible for BSE in the calves in this study without first knowing if the calves had been exposed to infected feed, etc. To make progress on ‘uncertainty 1’, scientists must first tackle these prior forms of uncertainty. But this epistemic ordering of uncertainties is no more set in stone than is the requirement that we proceed in inquiry from well known theses to less well known theses (see Section 3.1). This maternal transmission study also demonstrates that where one or more of these prior forms cannot be resolved in either the short or longer term, investigators are confronted with intractable uncertainty. Such uncertainty may have to be held in abeyance while other uncertainties, which can be addressed, are given priority. In such a case, pragmatic considerations relating to the forms of uncertainty that investigators can address in a particular context assume precedence over epistemic considerations. We will see subsequently that there were episodes during the BSE inquiry where just such a prioritising of uncertainties occurred on pragmatic grounds. As well as coping with the uncertainty that attends the convergence of different disciplines on a scientific inquiry, and managing the prioritization of uncertainties in inquiry, presumption must also address the temporality of uncertainty. Some uncertainties during scientific inquiry are particularly enduring. We will see, for example, that uncertainty surrounded the question of whether BSE could be transmitted to humans right up until 1996, when the disease was first definitively diagnosed in ten young people. Other uncertainties have a transitory quality and are relatively shortlived in inquiry. For example, the uncertainties surrounding the host range of BSE were beginning to be resolved by the summer of 1990, when cats were first observed

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to have a TSE (this was clear demonstration that BSE did not have the same host range as scrapie). These varying temporalities are intimately connected with the developing evidence base of an inquiry with uncertainties persisting or resolving as and when evidence becomes available. The temporality of uncertainty serves to emphasize once more the importance of the temporal context in which a scientific inquiry is conducted (see Section 2.2.4). This temporal context was often a foe to investigators during the BSE inquiry. Much of the uncertainty that BSE scientists had to confront was a direct consequence of the need to take decisions about the management of the disease in advance of obtaining results from experimental studies. Some of these studies took several years to complete such as a BSE pathogenesis study, which was initiated in December 1991 at the CVL and produced significant results in June 1994. These results showed that BSE pathogenesis differed from that of scrapie. However, in November 1989 a more limited ban of specified bovine offals (SBO) was implemented than was necessary to protect human health. So it emerges that presumption must be able to integrate the disciplines that converge on a scientific inquiry, accommodate the prioritization of uncertainties in inquiry and capture the temporality of uncertainty. It can be readily demonstrated that presumption can address each of these scientific applications. A range of scientific disciplines and sub-disciplines converged on the investigation of BSE. They included human and animal neuropathology, genetics, molecular biology, histopathology, biochemistry, epidemiology, zoology and virology, to name just a few. To these, one must add knowledge of animal husbandry, industrial processes relating to meat production and human food production processes. With so many specialisms contributing to questions about BSE, some means needed to be found of successfully integrating the knowledge bases of each. Presumption, I contend, is that means. In Chapter 2, we saw how studies investigating the histopathology, molecular biology and epidemiology of BSE collectively served to raise a presumption regarding the aetiological basis of this bovine brain disease. The plausibility of this presumption was a function of its entire evidential base: its supportive warrant lay in the presence of several interlocking strands of evidence. Presumption thus derives its tentative strength by drawing upon multiple sources of evidence often across different disciplines. By itself, each individual source has a rather limited presumption-raising capacity – we saw in Chapter 2 that the studies which investigated the histopathology, molecular biology and epidemiology of BSE individually fell short of supporting the aetiological claim that John Wilesmith and his colleagues went on to advance. Through the integration of these evidence sources, presumption was able to attain a level of warrant that would not otherwise have been possible. Presumption thus serves to integrate disciplines through its own requirement to interrelate evidence sources and, in so doing, establish the strongest possible supportive warrant for presumed theses. The different disciplines that converged on the study of BSE are unified by virtue of the fact that they are the sorts of rational activities that are capable of raising presumptions. Indeed, it is from these disciplines that presumptions receive their rational validation – these disciplines provide evidential support for the presumptions that they individually and collectively generate. If we consider the type of

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disciplines involved, we can see why this is the case. There has been a longstanding recognition that science has a uniquely successful track record in delivering truths to us about the natural world. This special status of science is acknowledged through the extensive range of scientific principles, techniques and methods to which we are prepared to grant either the status of presumptive truths or a presumption-raising capacity. In this way, a presumption of truth operates in favour of inductive parameters in science such as simplicity and uniformity (Rescher 1977: 37). Continuing the scientific methodology theme, we also accept as presumptively true the pronouncements of scientific experts,35 the information made available to us through the use of scientific instruments (e.g. microscopes, telescopes) and the results of scientific experiments. Further still, the history of our various cognitive practices clearly shows that we are prepared to reject any presumptive status for those sources that set themselves apart from the rational methodology of science.36 Put quite simply, the scientific disciplines that investigated BSE are integrated by virtue of their adherence to the entire probative framework that is given effect by means of the operation of presumption and plausibility. It is this framework that ultimately unifies these disciplines and makes substantive conceptual interchange between them even possible. We have seen how scientists must be able to prioritize the uncertainties that they encounter in inquiry. Such prioritization occurs by and large along epistemic lines with the uncertainties that are epistemically prior to other uncertainties among the first to be addressed by scientists. We saw above, for example, that scientists first needed to have some knowledge of the genotype of the calves in the maternal transmission study before they could conclusively say if maternal transmission of BSE, rather than inheritance of a genetic susceptibility to BSE, was responsible for the increased incidence of this disease in the offspring of infected dams. But this epistemic prioritization of uncertainties, it was emphasized, is not immutable and readily yields to other factors that are operative in the context of inquiry. Some uncertainties present greater urgency to investigators because their lack of resolution poses a significant risk to human health or has some other equally grave consequences. But even these more urgent uncertainties may be subordinated in a particular context to uncertainties that are addressed for no other reason than that they can be tackled. This continuous adjustment in the prioritization of uncertainties during scientific inquiry can only be accommodated by a concept that is sensitive to changing contextual factors. Presumption is such a concept. Through its context sensitivity, presumption is ideally placed to respond to the competing priorities of addressing those uncertainties which it is most urgent to manage, or addressing those uncertainties which have epistemic priority over other uncertainties, or addressing those uncertainties which can be tackled practically in a particular context. The relative significance of these various factors within an inquiry is most readily accommodated by a concept of presumption that is responsive to features of context. Where the prioritization of uncertainties is subject to the competing influences of several contextual factors, the temporality of uncertainty relates only to the temporal dimension of context. This aspect of uncertainty management reflects the

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importance of temporal context in scientific reasoning in general, particularly where that reasoning is concerned to address the rapidly evolving dynamics of an emerging infectious disease. During some episodes in the BSE inquiry, expert scientific deliberation proceeded at a pace that was largely blind to temporal context. For example, it took from February 1991 to September 1994 for a Working Group of the Advisory Committee on Dangerous Pathogens to complete and issue guidance to those handling risk tissues in laboratories, hospitals and mortuaries (BSE Inquiry Report, Volume 1: xxvii). Of course, uncertainty about the risks that these workers might be exposed to contributed in no small part to this inordinate delay. But this case amply demonstrates that uncertainty management cannot proceed in a manner that is divorced from temporal context. With its emphasis on context sensitivity, presumption is ideally placed to handle the temporal dimensions of uncertainty in such a case. But another feature of presumption, its defeasibility, also comes to the fore when we are discussing the temporality of uncertainty. BSE scientists arrived at the decision to exclude certain tissues from the human SBO ban on the basis of an uncertainty, namely, that the pathogenesis of BSE was similar to that of scrapie. At the point in time at which it became apparent to investigators that the pathogenesis of BSE differed in significant respects from that of scrapie, the presumptions that were the basis of the decision to exclude certain tissues from the human SBO ban were swiftly rejected. Such rejection was at all possible on account of the defeasibility of presumption. It emerges that along with the integration of disciplines in inquiry and the prioritization of uncertainties, presumption is also equipped to deal with temporal aspects of uncertainty management.

3.4 Presumption, Reasoning and Fallacies Thus far, it has been argued that presumption has a central and valuable role to play in scientific methodology and that presumption is quite substantially equipped to deal with the challenges inherent in uncertainty management. To the extent that these contentions are well grounded, there is a strong case for saying that presumption is a most important concept for investigators whose task it is to deal with uncertainty in the context of a scientific inquiry. But although presumption is a key concept in this context, it can only be pressed into operation through its inclusion within a model of reasoning. This essentially epistemic concept must assume a cognitive character for this to be possible. In this section, we examine reasoning frameworks that are based on presumption. Although these frameworks have been discussed in fields as diverse as computer science (particularly artificial intelligence),37 linguistics38 and jurisprudence, it is in the sub-discipline of logic called informal logic that we find models of presumptive reasoning that are best equipped to handle the informal fallacies. Historically, presumptive analyses of the fallacies have been slow to emerge. Although they are still far from commonplace, there are now a number of theorists who are casting the fallacies in explicitly presumptive terms (see Cummings 2009). We examine these analyses as they relate to

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the fallacies that will be discussed in Chapters 4, 5, 6, and 7. We will then be in a position to undertake the evaluative treatment of the fallacies in those chapters. While deductive and even inductive reasoning has had a long and distinguished history in logic, presumptive reasoning has been largely overlooked by logicians. Walton (1996: 17) remarks that ‘[a]lthough presumptive reasoning is very important in philosophy, it has tended to be neglected by logicians’. One reason for this neglect is that presumption itself is a relatively unexplored concept.39 However, an equally significant reason for this lack of logical interest in presumptive reasoning is that such reasoning is viewed as being inherently inferior to deduction and is, accordingly, not worthy of investigation. On this view, the true premises and valid inferences in deductive arguments (and even the probable premises and inferences in inductive arguments) represent a more rigorous standard of reasoning than is achievable in presumptive reasoning. The latter is, by its nature, a tentative form of reasoning that is subject to defeat should specific counter-indications emerge.40 Such attributes are clearly demonstrated by the following example which is based upon events that took place during the BSE inquiry: In November 1989, the human Specified Bovine Offal (SBO) ban came into force. This ban was intended to protect human health by removing infective bovine tissues from the food chain. The decision to include some tissues within the ban and exclude other tissues was based on what was known about the pathogenesis of scrapie. However, it became apparent to scientists in June 1994 that tissues which had not been infective in lambs (e.g. distal ileum) displayed infectivity in calves. As a result, the decision was taken in the same month to extend the human SBO ban to include these additional, infective tissues.

The tentative nature of the reasoning in this example derives from the uncertainty of the following major premise which is implicit in the above extract: the pathogenesis of BSE is similar to the pathogenesis of scrapie. This premise is a defeasible presumption that was not without evidential support, albeit of an indirect kind (this premise derives tentative support from the aetiological claim that was examined in Chapter 2). To this extent, there is some degree of presumptive warrant for the conclusion that certain bovine tissues, such as the distal ileum, will not contain infectivity. The structure of this presumptive argument is as follows: MAJOR PREMISE: MINOR PREMISE: CONCLUSION :

The pathogenesis of BSE is similar to the pathogenesis of scrapie. The distal ileum is not infective in lambs. The distal ileum will not be infective in calves.

The presumptive warrant for the conclusion of this argument derives from the strength of the major premise. As soon as that premise could no longer be supported – experimental results revealed that the pathogenesis of BSE was dissimilar to scrapie – investigators were compelled to reject it, along with the conclusion which was the basis for the exemption of the ileum from the human SBO ban. This presumptive argument has the form of an argument from analogy. In analogical arguments, it is argued that a proposition is true in one case because it is true in a case that is similar in some respects. Problems arise when the similarity between these cases can be shown, as in this example, not to hold or when the two cases can

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be shown to be dissimilar in some other, relevant aspects. The inherently presumptive nature of analogical arguments means that there is an ongoing requirement for investigators to keep this type of argument under review. At the first onset of difficulties, investigators must be prepared to reject any conclusion that is arrived at through these arguments. Although such rejection occurred swiftly in the example above, we will encounter in subsequent chapters many more instances during the BSE inquiry in which analogical conclusions persisted in the face of significant counter-indications. With presumptive reasoning demonstrated in outline, it is now possible to say something about the theoretical frameworks that have been advanced to capture this process. One of the most prominent theorists to discuss this type of reasoning is Douglas Walton. Although Walton has for some years examined the full gamut of approaches to presumptive reasoning, it is clear that his approach of choice is to view presumption as a speech act within argumentative dialogue.41 He explains his rationale for doing so as follows: A theory showing how presumption functions as a type of speech act put forward in argumentative dialogue is set out. The goal of the analysis is not to aid research in artificial intelligence specifically, but more generally, to provide a concept of presumption that is useful for the evaluation of argumentation in everyday conversations, and especially for the analysis and evaluation of informal fallacies (Walton, 1996: 18).

To the extent that Walton’s approach promises to address a concern of interest in the present context – the informal fallacies – it is worthy of further consideration. For Walton (1996: 18), presumption is a ‘distinctive kind of speech act halfway between assertion and mere assumption (supposition)’. Unlike assertion, it can be brought forward in dialogue without a requirement that the proponent who advances it must prove it. Rather, the proponent must merely show that the presumption has some practical value in the sequence of argumentation. Once it is in place as a working presumption, the burden is on the respondent to refute it. If refutation is not possible, the presumption becomes established as a commitment in dialogue. In keeping with its defeasible nature, presumption is not a non-retractable commitment for either of the parties in a dialogue, although it will typically stay in place for a particular round of argumentation. The points in a dialogue at which a presumption can be advanced and retracted as well as the obligations on the proponent and respondent are stipulated within a set of speech act conditions. These conditions provide ‘a general normative framework for the use of presumptive reasoning in dialogue which can help in the determination of certain kinds of argumentation as fallacious or nonfallacious’ (Walton, 1996: 30). In demonstration of this framework, we will examine another argument form that will be discussed at length in Chapters 4, 5, and 6. The argument in question is the argument from ignorance (argumentum ad ignorantiam). Although this argument has several forms,42 it consists in arguing from a lack of knowledge that a proposition is true (false) to the conclusion that this proposition is false (true). This argument can be more or less warranted in particular contexts. In a setting where a knowledge base is closed and we can be reasonably confident that if a particular

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proposition were true, then we would know about it, the lack of knowledge of the truth of a proposition can be used as grounds to conclude that a proposition is false. Such epistemic closure43 can be seen in the case of expert knowledge systems44 but is also evident in more mundane contexts.45 Fallacious variants of the argument arise when such closure does not exist in a particular case, but a reasoner nevertheless concludes to the truth or falsity of a proposition as if it did exist. During a critical discussion, a lack of closure is evident when the respondent, whose task it is to hold the proponent of a thesis to his requirement to defend that thesis (let’s say T), is suddenly asked by the proponent to prove the opposite of that thesis (i.e. not-T). To the extent that the respondent is not obliged by the rules of a critical discussion to defend not-T, it is likely that he will be unable to do so. His failure to prove not-T cannot be taken, however, as proof of T. During inquiry dialogue, a lack of closure is evident at the start of an inquiry when none or very few of the facts of a case are present. At this stage, as in critical discussion, the argument from ignorance is used fallaciously. However, at a later stage of inquiry, when exhaustive investigation of a question has been completed, it is perfectly reasonable for investigators to conclude to the falsity of a proposition from a lack of knowledge of the truth of that proposition. So it emerges that presumption can be implemented within a model of reasoning which has unique characteristics that set it apart from traditionally dominant deductive and inductive forms of reasoning. Presumption can also be readily integrated within normative dialogical frameworks which can be used to capture fallacious and nonfallacious forms of argument. But there is a significant sense in which these presumptive analyses do not go far enough for the type of work that will be undertaken in Chapters 4, 5, 6, and 7. Implicit in these analyses is the assumption that while certain of the fallacies can be shown in context to confer a practical or other advantage on reasoners, that this advantage is not somehow a consequence of the workings of cognitive rationality. This is evident in the following comments by John Woods (2004: 13) in relation to one inductive fallacy called hasty generalization: [H]asty generalization is sometimes a prudent strategy, especially when the risks are high, even though the haste of the generalization might attract a charge of fallaciousness. If fallacies are violations or failures of rationality, then we could expect to have it that survival skills are sometimes exercised successfully but not rationally. (italics in original)

Woods appears to be saying that success in making decisions and taking actions in the practical sphere, especially when that success is predicated upon the use of a so-called fallacy, is not ordained by cognitive rationality. There can be little doubt that the fallacies have managed in the last 40 years to shrug off to a considerable extent the largely negative characterizations that philosophers and logicians have been wont to make of them. But it is equally clear that they still have some way to go on their journey towards full integration within cognitive rationality as long as views of this type remain. Such integration would represent an important opportunity for the fallacies on the one hand and for models of scientific reasoning on the other hand. In relation to the fallacies, integration could only really be achieved if there was a significant cognitive reorientation in the study of the fallacies.46

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One cannot go far in the literature on the fallacies without realizing that there is a widespread tendency on the part of investigators to overlook the cognitive character of the fallacies.47 An emphasis on cognitive agency would certainly serve as a useful corrective to some of the more untenable analyses that have been undertaken in relation to the fallacies.48 With recent developments in logic,49 such a cognitive reorientation in the study of the fallacies appears more likely now than at any point in the past. Models of scientific reasoning are also likely to gain from the integration of the fallacies within cognitive rationality. These argument forms represent a rational cognitive resource that has been largely unexploited to date in accounts of scientific reasoning in contexts of uncertainty. But if public health scientists are to make significant gains in managing uncertainty, then they must take seriously the call by Christakos and others for investigators to engage with new and different modes of reasoning and to place ‘the science of the mind’ at the centre of attempts to deal with public health problems.50 The account of the fallacies that I will pursue in subsequent chapters thus has the ascendance of the fallacies within rationality at its heart. In casting the fallacies as rational strategies that bestow epistemic gains on scientific inquiry in contexts of uncertainty, the approach taken in this book is consistent with the work of certain rationality scholars. These scholars subscribe to the view that some mental short cuts and heuristics are beneficial to agents in that they are economical with respect to cognitive effort and effective in achieving cognitive goals: ‘at least some heuristics earn their keep by being not only fast and frugal, but also sufficiently accurate to be effective or adaptive’ (Smithson 2008: 210). For example, Todd and Gigerenzer (2000: 727) demonstrate how certain heuristics, by exploiting the way in which information is structured in particular environments, can enable ‘living organisms and artificial systems to make smart choices quickly and with a minimum of information’. Moreover, the performance of these simple heuristics is comparable to that of more complex algorithms.51 Theorists who subscribe to this adaptive heuristics view of some of our cognitive processes additionally contend that these processes have a strong evolutionary basis. Cosmides and Tooby (1992), for example, make this claim of the specialized inferential processes that are involved in social cognition.52 I will not directly argue in support of these claims in relation to my own account of the informal fallacies. However, the reader should be aware that implicit in my analysis of these fallacies is a view in which these argument forms are operating as adaptive heuristics in all but name.53

Notes 1. Hamblin (1970: 12) was concerned to challenge the so-called standard treatment of the fallacies that was found in logic textbooks: ‘And what we find in most cases, I think it should be admitted, is as debased, worn-out and dogmatic a treatment as could be imagined – incredibly tradition-bound, yet lacking in logic and historical sense alike, and almost without connection to anything else in modern logic at all. This is the part of his book in which a writer throws away logic and keeps his reader’s attention, if at all, only by retailing traditional puns, anecdotes, and witless examples of his forbears’. Where Hamblin led, other fallacy theorists

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followed. Massey (1981: 489) stated that ‘[t]extbooks are parasitic upon journals and scholarly tomes, and properly so. Cut off from their natural source of nourishment, textbooks are likely to suffer from conceptual malnutrition. Some of its symptoms: aimless or directionless thinking, exaggerated fascination with taxonomies, and shoddy reasoning. Alas but not unexpectedly, textbook treatments of fallacy exhibit all three symptoms’. Finocchiaro (1981: 18) remarked that ‘textbook accounts of fallacies are basically misconceived, partly because their concept of fallacy is internally incoherent, partly because the various alleged fallacious practices have not been shown to be fallacies, partly because their classification of fallacies is unsatisfactory, and partly because their examples are artificial’. Walton (1992: 383) directly attributes the presumptive framework that is the basis of his analysis of nonfallacious arguments from ignorance to Hamblin’s formal dialectic: ‘This analysis of presumption clearly itself presumes the existence of a dialectical framework for the evaluation of arguments where two parties “reason together”. But such a framework is given in the outline of formal dialectic presented by Hamblin (1970). . .’. Logicians had typically viewed deductive logic as the most significant form of logic or even the only form of logic. Against deductive logic, all other forms of logic and reasoning were viewed as being inadequate. This is evident in comments made by Rescher in his account of plausible reasoning. Rescher (1976: 99, 101) states that inductive inference is ‘an aspiring but failed deductive inference’ and that ‘[d]eductive logic is seen as the only genuine logic’. The theorists who challenged deductive logic’s dominance had several motivations for doing so. They included those who were charged with teaching introductory logic courses to students (see note 4), and authors such as Chaïm Perelman who were dealing with more abstract concerns (in Perelman’s case, developing a theory of justice). Perelman (1963: 142) states that ‘[m]odern formal logic was set up as the study of the means of demonstration used in the mathematical sciences. But as a result its domain is limited, for whatever is ignored by the mathematicians is foreign to formal logic. The logicians should complete their theory of demonstration by a theory of argumentation. They face the task of analysing the means of proof which the human sciences, law and philosophy make use of. They must analyse the argumentation presented by publicists in their journals, by politicians in their speeches, by lawyers in their briefs, by philosophers in their treatises’. The lack of relevance of deductive logic to the study of everyday reasoning was starkly brought home to Howard Kahane during an introductory logic course. Kahane (1971: v) recalls that ‘[i]n class a few years back, while I was going over the (to me) fascinating intricacies of the predicate logic quantifier rules, a student asked in disgust how anything he’d learned all semester long had any bearing whatever on President Johnson’s decision to escalate again in Vietnam. I mumbled something about bad logic on Johnson’s part, and then stated that Introduction to Logic was not that kind of course. His reply was to ask what courses did take up such matters, and I had to admit that so far as I knew none did. He wanted what most students today want, a course relevant to everyday reasoning, a course relevant to the arguments they hear and read about race, pollution, poverty, sex, atomic warfare, the population explosion, and all the other problems faced by the human race in the second half of the twentieth century’. The lack of relevance of deductive logic to these different forms of mundane reasoning extended to areas such as the recovery of implicatures during utterance interpretation. In this way, Leech (1983: 30–31) states that implicatures are ‘probabilistic’, and that the process by which they are recovered ‘is not a formalized deductive logic, but an informal rational problem-solving strategy’. These accounts have their origins in Aristotle’s Posterior Analytics, where the idea of scientific knowledge obtained by means of demonstration is described: ‘What I now assert is that all events we do know by demonstration. By demonstration I mean a syllogism productive of scientific knowledge, a syllogism, that is, the grasp of which is eo ipso such knowledge. Assuming then that my thesis as to the nature of scientific knowing is correct, the premises of demonstrated knowledge must be true, primary, immediate, better known than and prior to the conclusion, which is further related to them as effect to cause. Unless these conditions

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8.

9.

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3 Arguing Through Uncertainty are satisfied, the basic truths will not be “appropriate” to the conclusion. Syllogism there may indeed be without these conditions, but such syllogism, not being productive of scientific knowledge, will not be demonstration’ (Posterior Analytics, Book I, Part 2). A particularly significant proponent of this alternative view of scientific inquiry is Nicholas Rescher. For some years, Rescher (2005a: 38) has advanced a dialectic of inquiry, scientific inquiry specifically included: ‘In deduction we move uni-directionally from accepted premises to a conclusion. Inquiry dialectic, by contrast, is a far more complex process. In dialectic we move cyclically, testing the acceptability of premises in terms of the acceptability of the conclusions to which they lead’. Writing in 1983, Ullman-Margalit (1983: 143) remarks of presumption that ‘the notion itself has not so far been the focus of proper philosophical attention. I shall in this paper give it the attention I think it deserves’. Ullman-Margalit cites only three papers that use ‘presumption’ in their titles: Llewelyn (1962), Lamb (1972) and Katzner (1973). There is little evidence that this situation has changed in the 25 years since Ullman-Margalit wrote ‘On Presumption’. Recently, Rescher (2006: xii) has remarked of presumption that ‘their foothold in epistemology is still rather insecure’. Also, in the 5 year period between January 2003 and December 2007, not a single article on presumption has been published in The Journal of Philosophy (the source of two of the three articles cited by Ullman-Margalit). Douglas Walton (1992: 43) captures science’s uneasy relationship with presumption as follows: ‘Presumptions are also used in scientific investigations and inquiries. . .but scientific methodology tends to be unfriendly to presumptions if they can be avoided or dispensed with by gathering evidence to confirm or disconfirm the hypothesis, one way or the other. Presumptions are often necessary in scientific investigations, but science is a quest for evidence, and therefore scientists tend to be uncomfortable with presumptions and try if possible to turn them into hypotheses where some hard evidence can be found either to confirm or disconfirm them. Presumptions exist in science but the goal of scientific inquiry is to eliminate them (as presumptions) if possible’. Fuller and Collier (2004: 301) state that ‘scientists are professionally mandated to treat presumptions not as positive accomplishments in their own right, but as way stations to be superseded on the road to inquiry’. The importance of the cognitive domain in the context of presumption is acknowledged by Rescher (2006: 11) who states that ‘[s]ome writers see presumption as merely an actionguiding device. But this does not do full justice to the matter. For while a practice is indeed at issue with presumption, this can also include the practice of information management – of epistemic or cognitive procedure’. Rescher (2006: 93) states that ‘[o]ur standard cognitive practices incorporate a host of fundamental presumptions of initial credibility, in the absence of concrete evidence to the contrary’. Rescher extends the scope of cognitive presumptions by including scientific instruments such as telescopes. In this way, he states that there is a presumption ‘[t]o accept the reliability of the standardly employed cognitive aids and instruments (telescopes, calculating machines, reference works, logarithmic tables, etc.)’ (Rescher 2006: 94). Rescher (2006: 49) states that cognitive presumptions are ‘validated on the basis of their utility in fostering the aims of the cognitive enterprise – obtaining appropriate answers to our questions and securing useful information’. Some so-called legal presumptions are indefeasible. However, as Rescher (2006: 5) points out, these indefeasible presumptions are presumptions ‘in name only’; they actually have the status of legal postulates: ‘To be sure, certain legal principles are sometimes characterized as “conclusive presumptions” (for example, that a child of less than 7 years cannot commit a crime or that a crime exists only with establishment of circumstances “beyond reasonable doubt”). But these indefeasible “presumptions” are presumptions in name only – in actual fact they are incontestable legal postulates’. Rescher (2006: 17) states that ‘what will be evidentially sufficient in shifting a burden of proof hinges on the inherent seriousness of the contention at issue’.

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14. The concept of burden of proof is integral to the precautionary principle: ‘The precautionary principle asserts that the burden of proof for potentially harmful actions by industry or government rests on the assurance of safety and that when there are threats of serious damage, scientific uncertainty must be resolved in favor of prevention’ (Goldstein 2001: 1358). This principle characterised the public health response to the BSE problem, at least according to the various actors who participated in this response (see note 38, Chapter 7). The precautionary principle is discussed further in Section 8.3.1. 15. Godden and Walton (2007) attribute the first detailed account of presumption in a dialectical framework to Rescher (1977). 16. Rescher (2006: 19; italics in original) makes this point as follows: ‘The workings of the conception of burden of proof represent a procedural or regulative principle of rationality in the conduct of argumentation: a ground rule, as it were, of the process of rational controversy – a fundamental condition of the whole enterprise’. 17. Walton (1992: 43) makes this point in relation to dialogue as follows: ‘To understand any presumption as reasonable or not, you have to look at the context of dialogue in which the presumption has supposedly been made, and you have to understand the purpose of making the presumption in that context’. 18. Rescher (2006: xii) describes presumptions as low-grade data. 19. ‘[P]resumption is certainly not knowledge: we do not know what we merely presume to be so. As an informative resource its standing is quite different from that of knowledge’ (Rescher 2006: 6; italics in original). 20. Scientific disdain for presumptions in theory construction is related to the increased likelihood of error for the theses in this epistemic category. Erroneous presumptions, it is argued, necessitate costly revisions of scientific theories. Walton (1992: 42) captures this point as follows: ‘In a scientific investigation where the researchers want to establish the facts conclusively as a basis for building up a solid body of evidence, it may be thought desirable to avoid presumptions if at all possible. For presumptions may have to be withdrawn as further evidence builds up in the inquiry, thereby necessitating revisions that could complicate a well-established theory that has been carefully constructed and developed’. However, with few, if any, of their most central theoretical commitments resting on presumptions, scientists can afford to dispense with presumed theses as soon as they become problematic without scientific inquiry incurring widespread adverse epistemic consequences. Scientific error can thus be absorbed by low-grade presumptions, leaving the better established theses and theories of science relatively unscathed. 21. The logical positivists held the view that scientific practice could be divided into two distinct types of activity – a context of discovery, in which scientific hypotheses were developed and a context of justification, in which they were rationally assessed. They believed that the factors which were operative in the development of hypotheses were essentially non-logical in nature, while the correctness of an idea required a logical relation between a hypothesis and its supporting evidence. 22. Bechtel (1988: 18) describes a famous example of how the initial, discovery phase of scientific inquiry may be influenced by an indefinable range of non-logical factors: ‘Kekule is supposed to have developed his proposal for the structure of the benzene radical while gazing upon the pattern of a flame from a burning log. He interpreted the flames as atoms dancing in snakelike arrays, and when one of the snakes seemed to grasp its tail, forming a ring structure, that suggested to him the ring structure for benzene’. 23. One such philosopher is Jerry Fodor. Fodor (1983: 129) believes that we are very far from having an adequate account of the psychology of hypothesis formation and confirmation because both processes require the involvement of global processes: ‘[T]he reason that there is no serious psychology of central processes is the same as the reason there is no serious philosophy of scientific confirmation. Both exemplify the significance of global factors in the fixation of belief, and nobody begins to understand how such factors have their effects’.

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24. Uncertainty is only one of five dimensions of non-knowledge that Dressel and Wynne (1998) use in their analysis of the BSE crisis. This analysis draws upon Beck’s (1992) theory of the risk society. Beck identifies five dimensions of non-knowledge in the risk society: selective perception; uncertainties; possibilities of mistakes; inability to know; and unwillingness to know. See Bammer et al. (2008: 292) for discussion of ‘two attempts to put structure on uncertainty’. 25. Several authors have remarked upon this dissatisfaction. Graham (1995: 30) states that ‘[i]n light of the growing importance of risk assessment, it is disconcerting that America’s current risk assessment processes do not command a high degree of respect within the scientific community, interest groups and the public at large’. One reason given for this lack of respect is that ‘[t]he degree of uncertainty in risk estimates is poorly characterized’ (1995: 42). 26. Indeed, according to Michaels and Monforton (2005: S40), uncertainty is often purposefully generated in a public health context. The generation of uncertainty is pursued with a view to obstructing regulatory action against certain products and processes: ‘manufacturing uncertainty and creating doubt about scientific evidence is ubiquitous in the organized opposition to the government’s attempts to regulate health hazards’. 27. Rescher (2005b: 75) captures the sceptics ‘no certainty’ argument as follows: ‘All knowledgeclaims are committed to a demand for absolute certainty. Objective factual claims are always evidence-transcending: they are never in a position to meet absolutistic demands. Our objective factual claims can never amount to actual Knowledge’ (italics in original). 28. The sceptic’s transcendental conception of certainty requires that we step outside of our cognitive skins and eliminate all possibility of error in making a knowledge claim, not just any realistic possibility of error. In this way, before we can claim to know anything, we must first be able to eliminate the possibility that some evil scientist or demon is manipulating our perception and thoughts. However, Rescher (2005b: 82–83) contends that ‘we need not in the usual course of things exert ourselves in an endeavor to rule out the imaginative sceptic’s recourse to the whole demonology of uncannily real dreams, deceitful demons, powerful evil scientists, etc. . .To claim knowledge in specific cases, all we need do is eliminate those case-specific considerations which would countervail against the claim at issue’. 29. Christakos et al. (2005: 17) envisage an equally broad set of cognitive considerations within their synthetic epidemic paradigm: ‘It could be a constructive approach. . .that the SEP views interdisciplinarity as a reasoning process that entails rigorously formulated logical and cognitive mechanisms (scientific argumentation modes, conceptual metaphors, epistemic principles, mathematical techniques, etc.) in a composite space-time manifold (in which space and time are intimately connected)’. 30. ‘Some public health policy studies assume a purely subjective interpretation of uncertainty and associate it with preferences, subjective decisions, beliefs and linguistic imprecision’ (Christakos et al. 2005: 44; italics in original). 31. ‘[U]ncertainty characterizing a public health system can be seen both as an epistemic concept describing one’s state of incomplete knowledge regarding the system and an ontologic concept that reflects certain objective aspects of reality’ (Christakos et al. 2005: 65; italics added). 32. ‘[I]n the eyes of many practicing public health scientists the uncertainty encountered in realworld situations should be described as a technical notion linked with measurement errors, heterogeneous data bases, erratic fluctuations of the underlying processes’ (Christakos et al. 2005: 44–45; italics in original). 33. Christakos et al. (2005: 45) express a similar view: ‘In our view. . .a sound public health model should go beyond these common uses of the uncertainty concept. Uncertainty is of far greater importance in scientific thought than merely a technical notion reflecting error measurements and observation biases or a subjective kind of a variable associated with decisions and preferences’. 34. ‘Uncertainty in concept formation will be reflected into a corresponding uncertainty in experimental results. An adequate representation of the uncertainty related to proposed concepts

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39. 40.

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can improve the accuracy of the facts gathered through experimentation; similarly, a meaningful calculation of the uncertainty of the experimental facts can offer valuable information in our representation of the uncertainty of the corresponding concepts. This twofold argument is summarized as follows: concept-related uncertainty and fact-related uncertainty are closely linked and can enlighten each other’ (Christakos et al. 2005: 64). The role of presumption in appeal to authority arguments will be discussed in Chapter 7. Although ‘argumentum ad verecundiam’ is often used to describe arguments that appeal to authority, Walton (1995: 278) remarks that this expression should be used only to refer to fallacious appeals to authority. Rescher (1977: 57) states that ‘one can, without problems, invalidate an entire source that has provided a basis of presumptions, as, for example, abandonment of the longstanding practice of giving probative weight to dreams, omens, signs, portents, etc.’. The defeasibility of presumption is the basis of a feature of presumptive reasoning called nonmonotonicity. Deductive reasoning is monotonic in that a valid argument cannot be rendered invalid by the introduction of new premises. Such reasoning is unresponsive to changes or fluctuations in the context in which reasoning occurs. A quite different situation pertains in presumptive reasoning where the emergence of new evidence, facts or findings has the potential to bring about the revision or rejection of presumptive conclusions (as we will see in the main text). Non-monotonicity is of interest to workers in artificial intelligence, where a range of defeasible inferences have been studied. These inferences are often based on defaults which capture what is typically or normally the case. In this way, reasoners know that it is normally or typically the case that birds can fly, so they are likely to conclude that Tweety, a particular bird, can also fly. However, this conclusion, based on a default, will be overridden if it is discovered that Tweety is a penguin or an ostrich, i.e. a bird that does not fly (Reiter 1987: 149). In linguistic pragmatics, presumption is integral to Stephen Levinson’s theory of generalized conversational implicature. For Levinson, presumed meanings are the basis of utterancetype meaning which is the middle level of three levels of meaning: sentence meaning, utterance-type meaning, utterance-token meaning. The presumptive meanings that constitute this middle level of meaning are neither semantic nor pragmatic. Rather, they are ‘presumed, default interpretations, arrived at by virtue of the repeated scenarios from the past, knowledge of language and the world, and other salient information, processed with the aid of some general principles of reasoning. They correspond loosely to Grice’s generalized conversational implicatures and hence Levinson’s theory of presumed (“presumptive”) meanings is also called a theory of generalized conversational implicature’ (Jaszczolt, in press). ‘Although philosophers are familiar with defeasible reasoning, there would appear to be no very influential or well-developed theories of presumption’ (Walton 1996: 17–18). ‘Presumptive reasoning is always tentative or provisional in nature. . .Presumptive reasoning is inherently defeasible in nature, meaning that it is suppositional and is subject to defeat by exceptional cases’ (Walton 1995: 132). Nor is he the only theorist to do so. Frans van Eemeren and Rob Grootendorst are the forerunners of this type of speech act approach to the study of argument and the fallacies. In their pragma-dialectical framework, van Eemeren and Grootendorst associate speech acts with moves in a critical discussion that is aimed at resolving a difference of opinion: ‘The theory of speech acts is ideally suited to provide the theoretical tools for dealing with verbal communication that is aimed at resolving a difference of opinion in accordance with the pragma-dialectical principles’ (van Eemeren and Grootendorst 2004: 62). Moreover, speech acts that violate one of the rules for a critical discussion and undermine attempts to resolve a difference of opinion are characterized as fallacies: ‘Any infringement of one or more of the rules, whichever party commits it and at whatever stage in the discussion, is a possible threat to the resolution of a difference of opinion and must therefore be regarded as an incorrect discussion move. In the pragma-dialectic approach, fallacies are analyzed as such incorrect discussion moves in which a discussion rule has been violated’ (van Eemeren and Grootendorst 1995: 136).

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42. Woods and Walton (1978) described three forms of the argument from ignorance: (1) the argument occurs where there is an illicit shifting of the negation operator in a knowledgebased inference, e.g. A is not known to be true; therefore, A is known not to be true; (2) the inductive form of the argument occurs where a lack of confirming (disconfirming) evidence for a thesis A leads one to conclude that A is disconfirmed (confirmed); (3) the dialectical form of the argument occurs where the burden of proof in dialogue is illegitimately shifted onto the respondent as opposed to the proponent of a thesis. 43. The phrase ‘epistemic closure’ is from de Cornulier (1988: 182) who defines this notion as follows: ‘If one knows that it cannot be the case that P without his knowing it, then, if not-P, he can infer that not-P’. Epistemic closure is functionally equivalent to the closed world assumption in the theory of databases. This assumption states that ‘all relevant positive information has been explicitly represented. If a positive fact is not explicitly present in the database, its negation is assumed to hold’ (Reiter 1987: 150). 44. A computer program called SCHOLAR is using an argument from ignorance in the example below. Its use of this argument is non-fallacious because its knowledge base is closed: ‘SCHOLAR does not have any specific item of knowledge saying that Guyana produces rubber or not. However, SCHOLAR does know that Peru and Columbia are the major rubber producers in South America. SCHOLAR also knows that rubber is an important product, so if Guyana did produce rubber, SCHOLAR would presumably know it. SCHOLAR concludes: “I know enough that I am inclined to believe that rubber is not an agricultural product of Guyana”’ (Collins et al. 1975: 398). 45. A mundane example in which the argument from ignorance is being used non-fallaciously is given by Walton (1996: 112): ‘We want to determine whether the train stops at Schipol. We can reason as follows: Since the schedule did not indicate that the train stops at Schipol, we can infer that it does not stop at Schipol. In other words, we can presume that the knowledge base is complete (epistemically closed) on the ground that if there were additional stops, they would be specified on the schedule posted’. 46. Nor am I alone in thinking such a cognitive reorientation is necessary. For example, Woods (2004: xxvi) states that ‘an account of fallacies needs to be set in a more general theory of cognitive agency’. 47. A notable exception is Dale Hample’s work on fallacies. Hample (1982: 59) states that ‘a message can only stimulate a fallacy; the actual fallacy is a cognitive event’ (italics in original). 48. There are a number of ways in which fallacy analyses are untenable, several of which are related to distrust of the cognitive agent. Firstly, theorists have tended to reject notions that make reference to a cognitive agent as normative criteria for the evaluation of the fallacies (see Chapter 2, note 17). The assumption behind these rejections is that agent-based criteria are somehow inadequate to the task of argument evaluation (these criteria lack objectivity, etc.). Secondly, one cannot proceed to analyze and evaluate fallacies without drawing upon further logical concepts such as argument, inference and proof. But as Scriven (1980: 150) points out, theorists have also tended to eschew any role for cognitive considerations within these related concepts: ‘I find the same point to hold throughout informal logic – the notion of proof, of assumption, of fallacy, of truth, of reason, of argument, of persuasion, of consideration, of inference, of probability – all of them are at least dualistic notions whose mentalistic face has been veiled for too long’. Thirdly, the working assumption of dialectical frameworks appears to be that fallacy analysis can proceed in isolation from the cognitive concerns typically associated with monolectical (i.e. inferential) frameworks. In this way, dialectical accounts of ad ignorantiam argue that the fallacy consists in the subversion of burden of proof – the respondent in argument is called upon to defend the opposite claim to that advanced by the proponent. But the illicit shifting of the burden of proof from proponent to respondent, and the respondent’s ensuing failure to discharge this burden, cannot in itself produce an ad ignorantiam conclusion – only an inference of the form ‘failure to prove that a proposition is true (false) implies that this proposition is false (true)’ can generate such a conclusion.

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49. One development in particular, the empirically sensitive logic (ESL) advanced by Gabbay and Woods (to appear), has a logic of error in its sights (fallacies are thus a major concern in ESL) and places emphasis on the cognitive resources that reasoners bring to the task of reasoning: ‘As an agent-centred enterprise, ESL takes into account the resources an agent has at his (or its) disposal for the discharge of that class of tasks – chiefly belief-revision and decision – in which logic has historically shown an interest. Related considerations are those affecting the cognitive constitution of reasoning agents, what they are like as knowers’. 50. Christakos et al. (2005: 17) state that their synthetic epidemic paradigm (SEP) should contribute ‘to the emergence of a cognitive science of human health that involves the application of the science of the mind to epidemiologic ideas and methods. At the center of this effort is learning to think about thinking in an interdisciplinary arena. More to the point, the SEP will be confronted with different modes of reasoning (or styles of scientific thinking)’ (italics in original). 51. ‘[W]e show how simple building blocks that control information search, stop search, and make decisions can be put together to form classes of heuristics, including: ignorance-based and one-reason decision making for choice, elimination models for categorization, and satisficing heuristics for sequential search. These simple heuristics perform comparably to more complex algorithms, particularly when generalizing to new data – that is, simplicity leads to robustness’ (Todd and Gigerenzer 2000: 727). 52. ‘Our view. . .is that humans have a faculty of social cognition, consisting of a rich collection of dedicated, functionally specialized, interrelated modules. . .organized to collectively guide thought and behaviour with respect to the evolutionarily recurrent adaptive problems posed by the social world’ (Cosmides and Tooby 1992: 163). 53. It is interesting to note that heuristics also feature in discussions of how people assess risk in matters relating to public health. Johnson (2005: 632) states that ‘[a]. . .heuristic-systematic model (HSM) separate[s] systematic from heuristic information processing. The systematic approach. . .is deliberative, attends to detail, weighs alternative views, and assesses argument quality in judging the validity of persuasive messages. The heuristic approach is alert to cues (e.g., trusted groups’ evaluation of the information) and simple decision rules (if encoded in memory, accessible to recall, and deemed reliable) justifying quick intuitive judgment’. Johnson examines the HSM model in a study of how subjects assess the risks posed by a semi-hypothetical industrial facility. Wilson et al. (2004) examined heuristic processing in a study of how adults assessed risks associated with genetically modified food crops.

Chapter 4

Good Arguments During the BSE Inquiry

4.1 Introduction At this stage of discussion, we have all the raw materials in place to construct a model of scientific reasoning that is adapted to contexts of uncertainty. At the conceptual heart of this model is presumption. Through its unique features of defeasibility, context sensitivity and much else besides, presumption, it was argued, is equipped to handle the full range of demands that uncertainty imposes on investigators during scientific inquiry. But presumption could not act alone in this endeavour. Several argument forms that have traditionally been characterized as fallacies became the vehicle through which presumption was given effect in a model of reasoning. These argument forms, it was contended, served to facilitate scientific inquiry when widespread uncertainty threatened to halt inquiry in its tracks. The purpose of this chapter will be to demonstrate in quite specific ways how certain of the fallacies achieved this facilitation in the case of scientific inquiry into BSE. The presumptive analyses of fallacies that have been advanced to date have certainly served to reveal rational features of the fallacies. These features have been largely obscured from view under traditionally dominant deductive and inductive conceptions of argument. To this extent, these analyses have helped to move the fallacies a bit further along the road towards full integration within cognitive rationality. But there are lingering suspicions amongst theorists that these argument forms, despite their demonstrated practical and other benefits in inquiry, may still not somehow fully warrant the type of rational legitimacy that routinely attends deductive and inductive modes of reasoning. In this chapter, I aim to dispel those suspicions once and for all by arguing in support of a clear role for the fallacies within cognitive rationality. To the extent that presumption is at the heart of the analytical framework that we are using to examine the reasoning of BSE scientists, normative considerations that are more or less directly related to this concept will assume significance in our analysis of particular episodes within that reasoning. On some occasions, it may be helpful to think of the rational merits or weaknesses of a piece of reasoning in terms of the (in)correct application of burden of proof. On other occasions, it may assist us to evaluate an extract of reasoning in terms of the cognitive or practical gains it bestows on inquiry or in terms of certain epistemic goals that it allows investigators L. Cummings, Rethinking the BSE Crisis, DOI 10.1007/978-90-481-9504-6_4,  C Springer Science+Business Media B.V. 2010

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to achieve. On still other occasions, the premises in scientists’ reasoning may be evaluated as lacking plausibility while conclusions may be judged to have insufficient presumptive warrant. All these dialectical, epistemic, cognitive and pragmatic criteria relate in one way or another to the concept of presumption and reveal, yet again, the multi-faceted nature of this concept. Their role as normative criteria in an assessment of the rational acceptability of the reasoning of BSE scientists necessarily takes us well beyond traditional deductive standards of truth, validity and soundness in an assessment of that reasoning, so much so in fact that the various arguments we will examine do not satisfy these deductive standards. However, as we argued in Section 3.1, this failure to satisfy deductive standards is only a problem for our account of scientific reasoning if it is assumed that deduction is the only (or even dominant) mode of reasoning in scientific inquiry. And this particular assumption, it was contended, is less tenable now that at any point in the past. The reader can therefore expect in the evaluative analyses that follow to be exposed to all sorts of reasoning patterns, strategies and standards that would offend the sensibilities of the deductive logician. The evaluative analyses in the current and subsequent chapters will be facilitated by drawing a distinction between an argumentative strategy on the one hand and component arguments on the other hand. As used in the present context,1 an argumentative strategy describes an overarching structure that embodies features such as the goals of reasoning and how reasoners are undertaking to fulfil those goals. This structure can be consciously teased out at the onset of inquiry or it can develop organically, without much forethought, as inquiry proceeds. An argumentative strategy will span an entire sequence of argumentation, rather than individual arguments within this sequence. It is thus something of long duration that can persist in inquiry, often over a number of years, despite rejection or revision of the individual arguments that constitute the strategy. This said, an argumentative strategy should not be entirely insensitive to revisions that occur in the arguments that constitute its sub-structure. When these revisions are sufficiently wide-ranging, there should be a corresponding reformulation of the argumentative strategy itself. If this reformulation does not occur, the argumentative strategy has become divorced from the individual arguments that are its rational basis. At this stage, the argumentative strategy has been misappropriated by certain reasoners for their own ends, which could include personal interests such as political and commercial gain. We will see that this distinction between argumentative strategy and component arguments has very direct relevance to the scientific inquiry into BSE. The overarching argumentative strategy in that inquiry was to argue that BSE would not transmit to humans and that beef was safe to eat. At least initially, this strategy had a rational basis in a number of arguments that were advanced by scientists. However, as inquiry proceeded and it became apparent that this strategy could no longer be defended, its persistence became a source of fallacious arguments during that inquiry. The arguments that were subsumed by the argumentative strategy of the BSE inquiry were often among the standard list of so-called informal fallacies.2 In this way, we will see examples of ad ignorantiam reasoning, question-begging argument, ad verecundiam argument, faulty analogy and much else besides. But the

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whole thrust of the analyses to follow serves to undermine the idea that there exists some invariant list of fallacies that are inherently problematic. For a start, many of the fallacies on the standard list will be shown to be anything but fallacious when we consider them within their particular contexts of use. We will see, for example, that ad ignorantiam conferred significant gains on inquiry into BSE, particularly in the early stages of that inquiry. Furthermore, although this standard list includes the most commonly encountered fallacies, it is by no means exhaustive of the many ways in which reasoning can be found to be lacking. Accordingly, we will see in subsequent chapters a number of novel fallacies that have not been discussed in the literature to date. At least one of these fallacies – failure to use authority – involves an extension in the traditional analyses of what can go wrong with appeals to authority. With so many fallacies in the standard list not fallacious within particular contexts of use, and other arguments not included in the list but which are still evidently weak, it is clear that the standard list is something of a fallacy theorist’s fiction. In saying this, I am not making the altogether stronger claim that there is no such thing as the fallacies.3 However, what I am challenging is the idea that there is just something inherently problematic with certain argument forms and that a theory of fallacy must proceed to legislate against those forms. A few further comments are in order before we embark on the main business of the chapter. During the BSE inquiry, policy decisions were often taken and health pronouncements made by government ministers. These decisions and pronouncements were the outcome of an extensive (but not always efficient) consultation process that involved civil servants at the Department of Health and the Ministry of Agriculture, Fisheries and Food on the one hand and scientists from a range of medical and veterinary disciplines on the other hand.4 Scientists often delivered their advice and opinions, not as individuals, but as a group of experts that met under the auspices of several expert scientific committees or working groups. These bodies were convened to offer expert scientific advice on specific aspects of the BSE problem, which were usually specified in explicit terms of reference for the committee or working group in question. In this way, the BSE Working Group was established in 1989 ‘[t]o advise the Section 4 Committees5 on the implications of BSE to human medicinal products’ (BSE Inquiry Report, Volume 7: 135). In the evaluative analyses of this chapter and subsequent chapters, it is important to make a distinction between the scientific advice that went forward from these expert groups and the health advice that government ministers subsequently released to the general public. As will be seen in Chapter 7, the content of this latter advice cannot simply be assumed to accurately reflect the advice that was issued by scientific experts. More often than not, the scientific advice that went forward from expert advisory groups was tainted by political, commercial and other influences which had the effect of altering the nature of that advice. To the extent that we are evaluating the reasoning of BSE scientists, it is important to use as premises and conclusions in that reasoning only those propositions that were actual claims of these scientists. In examining the reasoning of BSE scientists, we are constantly reminded of the acutely difficult epistemic conditions under which these scientists were compelled to operate. Decisions about the risks that BSE posed to human health often had to be

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made before the results of experimental studies were available. Pre-existing knowledge of TSEs was at best an indirect guide as to how BSE would behave. By virtue of the risk assessments that scientists were required to make, they were often forced to pass judgement on matters that took them beyond their particular areas of expertise. By any standard, the situation confronting scientists charged with handling the BSE crisis was not an easy one. In full cognizance of this fact, we must employ a principle of charity in our consideration of the reasoning of these scientists. As used by argumentation theorists, this principle describes how one should proceed to add statements to the premises of an argument during the task of argument reconstruction. Johnson and Blair (1994: 34) state that ‘your objective is to add to the stated premises the most plausible statement (consistent with the rest of the passage and likely to be believed by the arguer and used in addressing that audience) needed to make the whole set of premises relevant to the conclusion’. This simply stated principle precludes a number of activities on our part that could be reasonably described as being unfair towards the scientists whose reasoning we are examining. We cannot attribute premises to these scientists that they could not possibly have known given the state of knowledge present at a particular point in time. Nor can we criticize the reasoning upon which scientists based decisions using evidence that emerged at a subsequent point in inquiry. And we are definitely not permitted to expect scientists to revise or relinquish beliefs that were ultimately shown to be incorrect when those beliefs were supported by the best evidence available at the time they were formed. In recognition of the importance that we are attributing to the temporal context in which inquiry into BSE was conducted, I want from the outset to demarcate three phases in that inquiry. The first phase (‘the early years’) marks the period between the emergence of cases of BSE in 1986 and the introduction of the first significant measure designed to protect human health, the human Specified Bovine Offal ban of November 1989. The second phase (‘the middle years’) charts the time following the introduction of the human SBO ban until the discovery in June 1994 that the pathogenesis of BSE was significantly different from that of scrapie. The third phase (‘the final years’) marks the time between the release of the results of the CVL’s pathogenesis experiment and the announcement in British Parliament in March 1996 that BSE was responsible for a new variant of CJD in a number of young people. Any attempt to mark out distinct phases in the scientific inquiry into BSE is necessarily problematic. By its very nature, scientific reasoning is a continuous process that is coextensive with the entire duration of the inquiry into BSE. However, these phases are not entirely arbitrary either; rather, they are each mediated by quite distinct evidential considerations. In this way, the first phase is noteworthy for its evidential bereftness which found scientists making decisions relating to the protection of human health on the basis of very scarce evidence indeed. The second phase is distinguished by a marked increase in the evidence that was available to scientific investigators. Specifically, experimental studies and natural transmission of BSE began to reveal certain anomalies in the dominant scientific view of this disease during this phase of inquiry. The third phase is noteworthy for how scientists responded to the burgeoning contrary evidence that began to emerge in the second phase of inquiry.

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4.2 The Early Years: 1986–1989 Most of the reasoning that will be examined in this chapter falls within a period of the BSE inquiry that is marked by considerable scientific uncertainty. That period spans the time from the emergence of the first cases of BSE in 1986 to the introduction of the human SBO ban in November 1989. This was a phase of inquiry in which it became clear to investigators that they were confronting an increasingly serious animal health problem. From the initial identification of BSE in diseased cattle from two herds at the end of 1986, the situation had escalated to 10,091 confirmed cases of BSE by the end of the period we are considering.6 If the animal health problem was serious, it was matched only by a growing concern about the risks that this new bovine disease posed for human health. On 16 February 1988, Mr Cruickshank of the Animal Health Group in the UK’s Ministry of Agriculture, Fisheries and Food (MAFF) gave expression to this concern when he wrote ‘we do not know whether [this disease] can be passed to humans. The last point seems to me the most worrying aspect of the problem. There is no evidence that people can be infected but we cannot say there is no risk’ (BSE Inquiry Report, Volume 1: 44). During this same period, stories about this new bovine disease began to appear in the broadcast and print media. The Daily Telegraph (25.10.1987), The Times (29.12.1987) and the BBC News (30.10.1987) all picked up on the announcement of this new disease in the ‘Short Communications’ section of the British Veterinary Association’s journal the Veterinary Record (Reilly and Miller 1997: 240). This was the slow start7 to what was to become an unprecedented level of media coverage of the BSE affair, coverage that generated public anxiety and public understanding in roughly equal measures. Against this backdrop of human and animal health concern, scientists were to undertake deliberations that would lead to the two most significant disease control measures during the BSE crisis.8 Those measures were the introduction of the ruminant feed ban on 14 June 1988 (which took effect on 18 July 1988) and the human SBO ban in November 1989. The ruminant feed ban was enacted through Article 7 of the Bovine Spongiform Encephalopathy Order 1988 which stated that ‘No person shall knowingly sell or supply for feeding to animals any feedingstuff in which he knows or has reason to suspect any animal protein has been incorporated. No person shall feed to an animal any feedingstuff in which he knows or has reason to suspect that any animal protein has been incorporated’. The introduction of this ban was directly motivated by the findings of John Wilesmith’s early epidemiological investigation of BSE cases and specifically his claim that cattle had developed BSE as a result of consuming scrapie-infected sheep tissues in feedstuffs.9 The introduction of the human SBO ban was an altogether more haphazard affair. Following the publication of the Southwood Report, a number of influences came together to encourage MAFF to introduce a ban on the use in human food of those types of offal that were most likely to contain BSE infectivity. (It should be noted that the Southwood Report itself stated that beyond the ban on offal in baby food, no other measures were justified to prevent others from eating offal from sub-clinical animals). These influences included the public reaction to the report (particularly the recommendation banning offal in baby food only), newspaper stories that urged a

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more widespread ban on offal and concerns expressed by the pet food industry about the use of bovine raw materials in pet food. In this emergent phase of the BSE inquiry, we can make a number of statements about the reasoning strategies that scientists are likely to employ. The primary concern of scientists will be to embark on inquiry, regardless of the risks – principally, the risk of error – that may be incurred by investigators at this stage. To the extent that just ‘getting started’ on inquiry is a more pressing concern to scientists than ‘being right’, we can expect a corresponding adjustment in the burden of proof at this initial stage of inquiry. Specifically, this burden must be lowered to allow investigators to forge ahead tentatively on the basis of rather limited evidence. It is in this context that presumptive reasoning strategies come to the fore. These reasoning strategies give investigators an early epistemic foothold on inquiry when a requirement for knowledge and certainty would serve only to foreclose inquiry. But these strategies must do more than merely launch investigators into inquiry. They must also work at closing the knowledge gaps that confront scientists and at resolving the uncertainty that these gaps create for investigators. Such closure and resolution may be achieved in a variety of ways. Some of these ways concern direct knowledge generation, as when investigators concluded that scrapie had not transmitted to humans because there was no evidence in 250 years of the disease that transmission had occurred. The use of the argument from ignorance in this case generated a proposition (scrapie is not a zoonosis10 ) that was then used by BSE scientists in their further deliberations. Other ways involve putting in place the conditions that make knowledge generation possible. We will see subsequently how the argument from ignorance was also used by BSE scientists to remove questions from inquiry that could not be addressed in the short or longer term, thus ensuring most effective use of cognitive and practical resources during the investigation into this disease. Through a combination of these reasoning strategies, scientists achieved a robust means (at least initially) of confronting uncertainty during inquiry into BSE.

4.2.1 Argument from Analogy In Chapter 2, we examined the evidential basis of an aetiological claim that was advanced by John Wilesmith and his colleagues at the Central Veterinary Laboratory. That claim sought to relate BSE to scrapie, a TSE in sheep, in the sense that the former disease was caused by the latter disease. Although the proponents of this claim could not have been aware of it at the time, this claim was to have a profound influence on the subsequent development of scientific inquiry into BSE. The effect of this claim was felt in two ways in inquiry. The first of these ways was that it had an early impact on the emerging argumentative strategy that was to shape risk assessments and official health pronouncements for most of the duration of the BSE crisis. The claim that BSE was similar to scrapie in sheep led investigators to believe that this new bovine disease would have few, if any, implications for human health. It achieved this reassuring conclusion by means of the following argument from analogy:11

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BSE is similar to scrapie in sheep. Scrapie is not a zoonosis. Therefore, BSE will not be a zoonosis.

We described in Chapter 2 how the major (analogical) premise of this argument had the status of a presumption. We saw in that chapter how it derived some tentative warrant from the histopathological, molecular and epidemiological evidence that was adduced in support of it. Yet, this evidence still fell some way short of the evidence that could establish if BSE had been caused by transmission of scrapie to cattle. The only evidence that could address this question was the results of straintyping studies, which were not available when Wilesmith and his colleagues were undertaking their early epidemiological investigations. Lacking the validation of this altogether stronger evidence, this major premise, it could be argued, was something of a faulty analogy12 or at least not a particularly strongly warranted one. (It was established in 1987, before Wilesmith et al. produced their aetiological claim in 1988, that scrapie was not a zoonotic condition. So the minor premise of the above argument is essentially warranted13 ). To the extent that the proposed similarity between BSE and scrapie could not be conclusively established, a charge of fallaciousness could quite legitimately be levelled against this analogical argument. But to do so would have had the effect of foreclosing inquiry and with it any prospect of definitively addressing the question of the relationship of BSE to scrapie. By holding this analogical premise as a weakly warranted presumption, investigators were at least able to move forward in inquiry on a rational basis. During the course of inquiry, this particular presumption may be found to be wanting (as indeed it was). Once discovered to be problematic, investigators are obliged to remove this presumption from further inquiry. But until such times as this rejection becomes necessary, the analogical premise of the above argument and the particular conclusion that this premise warrants served to legitimate an emerging argumentative strategy that would see investigators consistently arguing that BSE would not transmit to humans. There was a second way in which Wilesmith et al.’s aetiological claim influenced early inquiry into BSE. As well as serving to establish the argumentative strategy that spanned most of the duration of the BSE crisis, Wilesmith et al.’s claim was also the basis of several other analogical arguments that were used by scientists to warrant a range of decisions. Most of these decisions related to measures intended to protect human health. The introduction of the human SBO ban in November 1989 was one such measure. Considerable deliberation preceded the introduction of this ban, as scientists attempted to establish a rational basis for including some bovine tissues in the ban, while excluding other tissues. Analogical argument based on scrapie was used extensively during this deliberative process. For example, the decision to exclude tissues from calves less than 6 months old from the ban was motivated by an analogical argument based on scrapie as was the decision by Dr Richard Kimberlin14 to seek the exclusion of thymus from the ban: Analogy with scrapie research suggested that infectivity would not reach the brain or spinal cord of cattle in the first six months of life (BSE Inquiry Report, Volume 1: 116).

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MAJOR PREMISE: MINOR PREMISE: CONCLUSION:

BSE is similar to scrapie in sheep. In scrapie, infectivity does not reach the brain or spinal cord in the first 6 months of life. In BSE, infectivity will not reach the brain or spinal cord in the first 6 months of life.

[Dr Kimberlin]. . .said that he was not overly concerned about the thymus because scrapie research indicated that thymus was lower risk than other LRS [lymphoreticular system] tissues (BSE Inquiry Report, Volume 1: 117).

MAJOR PREMISE: MINOR PREMISE: CONCLUSION:

BSE is similar to scrapie in sheep. In scrapie, the thymus is lower risk than other LRS tissues. In BSE, the thymus will be lower risk than other LRS tissues.

The protection of the food chain was not the only concern to scientists whose task was to assess the risk of BSE to humans. Bovine tissues were used in an extensive range of human medicinal and surgical products, including vaccines and catgut sutures. An assessment of the risk that some of these products posed to human health was made by one of the Section 4 committees, the Committee on the Safety of Medicines (CSM).15 The CSM was chaired by Professor Sir William Asscher, who presented the following justification to Lord Phillips and his team of the committee’s decision not to take licensing action against oral medicinal products in which bovine material had been used. An argument from analogy based on scrapie was again integral to the reasoning of this committee: The CSM was . . . aware of the issues involving CJD and human growth hormone at this time and of the occurrence of CJD following dura mater implants. They had come to our attention in the course of considering product licenses for dura mater. These experiences made us particularly wary of parenteral, as compared to oral, medicinal products. At the time, the fact that scrapie had not transmitted to man also gave us reassurance that BSE was unlikely to be acquired by the oral route (BSE Inquiry Report, Volume 7: 73).

MAJOR PREMISE: MINOR PREMISE: CONCLUSION:

BSE is similar to scrapie in sheep. Scrapie has not transmitted to humans via the oral route. BSE will not transmit to humans via the oral route.

As well as warranting decisions relating to the human SBO ban and human medicines, analogical argument was the basis of early research into BSE. In December 1988, Mr Bradley of the Central Veterinary Laboratory produced an updated paper on the CVL’s research and development programme, in which he outlined the aims of the CVL programme, the work that was already taking place and proposed work. Five experiments were already in progress, addressing questions in the areas of epidemiology, clinico-pathological studies, transmission, molecular biology and molecular genetics. In all five areas, research was predicated upon similar investigations that had been conducted into scrapie. Epidemiological studies, for example, sought to establish the natural transmission routes of BSE, both from dam to offspring (vertical or maternal transmission) and from animal to animal (horizontal or lateral transmission). Both routes of transmission were known to occur in scrapie, which became a primary motivation for similar transmission studies in cattle:

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The possibility that maternal transmission played a role in transmission was considered early in the epidemic. There was evidence of maternal transmission of scrapie in sheep but not in other TSEs such as kuru, non-familial CJD and transmissible mink encephalopathy (TME). It was therefore essential to determine if it occurred in cattle, as procedures put in hand for arresting the epidemic depended on maternal transmission not being an important factor. Lateral transmission was also considered since this, too, had been identified as a transmission route for scrapie (BSE Inquiry Report, Volume 2: 95).

MAJOR PREMISE: MINOR PREMISE: CONCLUSION:

BSE is similar to scrapie in sheep. There is maternal and lateral transmission of scrapie in sheep. There will be maternal and lateral transmission of BSE in cattle.

Mr Bradley also discussed in his paper the BSE transmission studies to other species that were in progress by December 1988. Hamsters (and calves) had been inoculated at the Central Veterinary Laboratory; marmosets had been inoculated at the Medical Research Council/Clinical Research Centre laboratory; mice, sheep and goats had been inoculated at the Neuropathogenesis Unit and plans to inoculate mink at the CVL were at a fairly advanced stage. By 1988, these species were known to be susceptible to scrapie, as had been shown in a series of experiments that commenced in 1965 and terminated in the demonstration of transmission of scrapie to marmosets in February 1988 (see Section 1.2.4). That these same species were first to be investigated by scientists in relation to BSE was evidence, once again, of the force of the analogy with scrapie. That analogy can be captured as follows: MAJOR PREMISE: MINOR PREMISE: CONCLUSION:

BSE is similar to scrapie in sheep. Scrapie has been transmitted to marmosets, mink, goats, mice, sheep and hamsters. BSE will be transmitted to marmosets, mink, goats, mice, sheep and hamsters.

The analogical arguments examined above are by no means exhaustive of the use of this argument form in the early phase of the BSE inquiry. But they do demonstrate the significant contribution of analogical reasoning to the deliberations of scientists on a number of issues relating to BSE. These arguments provided essential presumptive warrant for many of the decisions that were taken to protect public health. These decisions required scientists to engage with issues at the cutting edge of science,16 to address questions before experiments could produce the evidence that would provide answers. Indeed, scientists could not even await the results of these experiments, many of which would take years to complete on account of the long incubation periods of TSEs. At the same time, public health decision-making had to proceed apace to address the risk that this new bovine disease may pose to human health through the food chain and medicinal and surgical products. A policy of inaction was not an option for investigators and, indeed, represented a potentially dangerous stance in the face of uncertainty about this disease. Analogical argument, even weakly warranted analogical argument (as these arguments were), represented scientists’ best and only prospect of addressing the difficult public health decisions

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that confronted them. This was reasoning based on faute de mieux considerations,17 in which scientists acknowledged that if they rejected analogical argument, there would be nothing to replace it. Yet, in saying there was nothing better than analogical argument, we are not saying that this argument was not somehow good enough. For through analogical reasoning, scientists were able to initiate a number of measures that were to prove vital in containing the transmission of BSE to humans. This reasoning strategy was thus an important cognitive instrumentality that warranted decisions in the practical sphere when pervasive uncertainty otherwise threatened an effective, early scientific response to BSE.18 If the protection of human health was a pressing early concern of scientists, it was matched only by the need to establish a programme of research into BSE. Even if implemented with the greatest of urgency, experimental studies of BSE could take many months and possibly years to complete. So a framework for research was an early priority for scientific investigators. The generation of research questions about any newly emerging infectious disease is by its nature a protracted and difficult affair. A large range of possibilities could be considered within an explanation of the origin, transmission properties and pathological features of such a disease. Some means needs to be found of reducing this large number of possibilities to those that can be practically investigated by scientists using the resources available to them in inquiry. A rational strategy for limiting the possibilities that scientists need to investigate is to establish an analogy between the new disease and a pre-existing (and better known) disease. Such a strategy was achieved by BSE scientists when they forged an analogy between BSE and scrapie. The experience of scrapie told scientists that certain lines of inquiry could be productively pursued. In this way, the diagnostic significance of scrapie-associated fibrils and prion proteins was already established by the time Mr Bradley was devising his BSE research and development paper. Through Patricia Merz’s early electron microscopy work, it had been established that scrapie-associated fibrils (SAFs) were to be found in all combinations of strain of scrapie agent and strain or species of host examined (Merz et al. 1981). Prusiner et al. (1983) subsequently identified that the aggregation of prion proteins was responsible for the abnormal structures that Merz had been attempting to characterise. Later work by Kascsak et al. (1986) revealed distinct Western blot profiles for SAFs isolated from animals that had been infected with different strains of the scrapie agent. Here was a well-established research framework which made it eminently reasonable for investigators to pursue the type of studies that Mr Bradley summarised within the molecular biology component of his research and development paper: Work in progress, which was aimed at determining whether the BSE agent was identical to the natural scrapie agent or a modified scrapie agent, and whether there were multiple BSE strains, included assembling a lesion/SAF/PrP profile for brains, which might correlate with the agent strain (BSE Inquiry Report, Volume 2: 187).

Earlier scrapie studies provided scientists with a ready-made template for research into BSE. This had the effect of priming certain research areas for BSE scientists. The identification of SAFs in bovine brain tissue was one such area. The

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experience of scrapie had taught scientists that distinct SAF profiles occurred in specific strains of the scrapie agent. If one or more of these profiles could be established in bovine brain tissue, then this was an indication that the agent causing BSE was related to the scrapie agent. The question of the origin of BSE subsumed a large range of investigative possibilities for scientists,19 one of which (the identification of SAFs) assumed epistemic prominence20 on the basis of an analogy with scrapie. The discovery of SAFs in bovine brain tissue would be a discovery of considerable significance for investigators. These abnormal structures were not only known to be unique to TSEs (thus confirming the classification of this new bovine disease as a TSE), but they also had the potential to address the question of the origin of the causative agent of BSE (if a SAF profile, that was recognisable from work on scrapie, was observed to occur in bovine brain tissue, here was evidence in support of a scrapie origin for BSE). The identification of SAFs was therefore a productive line of investigation for scientists who could use the presence of these structures to address significant questions relating to the nosology and origin of BSE. Analogical reasoning based on the findings of prior scrapie studies thus had the effect of directing cognitive and practical resources during inquiry to those questions that held most significance for BSE scientists. This reasoning provided scientists with an effective means of determining areas of research priority for BSE and, in so doing, reducing the number of investigative possibilities that needed to be actively pursued during inquiry.

4.2.2 Argument from Ignorance The argument from ignorance was used extensively during the BSE crisis. The ‘no evidence’ claims upon which this argument is based became the mantra of the BSE story, as everyone from scientists, government ministers, industry representatives and health officials sought to reassure an alarmed public about the human health risks of BSE. The most common manifestation of the argument had a ‘no evidence’ claim21 as its premise. This premise is evident in the question-answer exchange below: On 15 October [1987] Mr. Suich circulated information in Question and Answer form to enable press officers and others to answer queries about BSE. This included: Q. Can it be transmitted to humans? A. There is no evidence that it is transmissible to humans. (BSE Inquiry Report, Volume 3: 123).

The conclusion of the argument, that BSE is not transmissible to humans, was more often implied than directly stated. However, this was an implication that the proponents of this ‘no evidence’ claim understood would be drawn by the public. Moreover, they were content to let this implication stand, despite repeated opportunities to correct it22 : PREMISE: CONCLUSION:

There is no evidence that BSE is transmissible to humans. BSE is not transmissible to humans.

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According to the standard account of this argument, its fallaciousness consists in the attempt to prove that a proposition is true (false) on the grounds that it has not been proved (there is no evidence) that it is false (true). Lack of proof, evidence or knowledge of the truth (falsity) of a proposition, it is argued, is a weak basis indeed for concluding that a proposition is false (true). A proposition may well be true but we may be unable to establish that this is so and any inference to this proposition’s falsity simply prejudges the matter: ‘If some proposition has not yet been proved true, we are not entitled to conclude that it is false. Many true propositions have not yet been proved true, of course, just as many false propositions have not yet been proved false. The fact that we cannot now be confident rarely serves as a good reason to assert knowledge of falsity, or of truth. Such an inference is defective; the fallacy is called the argument from ignorance, or the argument ad ignorantiam’ (Copi and Cohen 2009: 142; italics in original). It would seem that the charge of fallacy is even more strongly levelled in a scientific context, where various factors militate against investigators obtaining the evidence they require to establish the truth of a proposition. As Copi and Cohen (2009: 142) remark: The fallacious appeal to ignorance crops up in science when plausible claims are held to be false because evidence of their truth cannot be provided. There may be good reason for its absence: In archaeology or in paleontology, for instance, that evidence may have been destroyed over time. In astronomy or in physics, the evidence desired may be so distant in space or in time that it is physically unobtainable. The fact that some desired evidence has not been gathered does not justify the conclusion that an otherwise plausible claim is false.

Copi and Cohen’s caution about drawing conclusions in science on the basis of a lack of evidence is particularly pertinent in the case of the above argument from ignorance. In that argument, a lack of evidence of BSE’s transmissibility to humans is taken as grounds for the claim that BSE is not transmissible to humans. But when Mr. Suich of MAFF’s Animal Health Division prepared this question and answer brief in October 1987, scientists had only known about the existence of BSE for some 11 months. Given the lack of knowledge that surrounded BSE at this time and what was known about the lengthy incubation periods of TSEs in general (see Chapter 1), no evidence of BSE’s transmissibility to humans could possibly have been obtained by investigators by this date. A claim of ‘no evidence’ thus carried little, if any, evidential weight under these circumstances. To this extent, it would appear incontestable that Mr Suich had made use of a fallacious argument from ignorance. However, as I will argue below, not every occurrence of this argument form was fallacious in the context of early scientific inquiry into BSE. To demonstrate this claim, I will examine how scientists used this argument to achieve certain epistemic gains during the early phase of this inquiry. One use of this argument permitted scientists to derive a conclusion about the non-transmissibility of scrapie to humans. This conclusion was then used as a minor premise in an analogical argument to derive the conclusion that BSE would not transmit to humans. Although the capacity to generate propositions for use in subsequent reasoning was an important gain for scientists, it was by no means the only beneficial employment of this argument in the early phase of BSE inquiry. We will also see that the argument from

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ignorance played a significant role in prioritising research questions during inquiry by removing those questions that could not be addressed in the short or longer term. Between 1986 and 1989, scientists made various pronouncements about the lack of risk that BSE posed to human health based on the absence of an epidemiological link between scrapie and CJD. In this way, Richard Kimberlin, an independent TSE consultant, submitted a paper in June 1989 to the Canadian Journal of Veterinary Research in which he stated ‘the absence of an epidemiological link between scrapie and CJD suggests that even if scrapie could infect humans, usually it does not. For this reason alone, BSE is unlikely to be a major threat to humans’ (Kimberlin 1990: 35). In a letter dated 13 March 1989 to Dr Helen Grant, a neuropathologist at the Middlesex and Charing Cross hospitals, Sir Richard Southwood, the Chairman of the Southwood Working Party, remarked: ‘The evidence to date seems to indicate that the BSE agent is very similar to scrapie and of course we have lived with scrapie for 200 years, and most of us have at some time or other eaten sheep offal – though the incidence of CJD remains low’ (BSE Inquiry Report, Volume 4: 56). A reconstruction of the reasoning of these extracts results in the following argument sequence, in which the conclusion of an argument from ignorance (scrapie is not transmissible to humans) forms the minor premise in a subsequent analogical argument: Argument from ignorance: PREMISE: CONCLUSION:

There is no evidence in 200 years that scrapie has transmitted to humans. Scrapie is not transmissible to humans.

Analogical argument: MAJOR PREMISE: MINOR PREMISE: CONCLUSION:

BSE is similar to scrapie in sheep. Scrapie is not transmissible to humans. BSE will not be transmissible to humans.

The warrant that attends the conclusion of the above analogical argument rests on the strength of this argument’s minor premise. However, in order to establish the strength of this premise, we must first conduct a rational appraisal of the argument from ignorance that generated this particular proposition. To the extent that any argument from ignorance is based on a lack of evidence or knowledge, such an argument is always going to fall short of a deductive proof.23 But even as we admit the tentative, presumptive nature of the conclusion of an ignorance argument, it is clear that this conclusion can be more or less strongly warranted. The key factors in a determination of this warrant are (i) the completeness of the knowledge base upon which the ‘no evidence’ claim of the argument is based and (ii) an exhaustive search of that base. The first of these factors amounts to a requirement for epistemic closure (see note 43, Chapter 3). In the argument from ignorance at the start of this section, such closure could not be assumed – in October 1987, scientists had little or no knowledge of this new bovine disease and studies to establish this knowledge had yet to be initiated. The conclusion of this ignorance argument, that BSE

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was not transmissible to humans, was thus largely unwarranted. However, a quite different level of warrant is present in the above argument from ignorance. Here, scientists operated on the assumption that the epidemiological knowledge base that could address the question of a link between scrapie and CJD in humans was indeed closed. To the extent that this knowledge base lacked evidence of an epidemiological link between scrapie and CJD, scientists could quite legitimately conclude that scrapie was not transmissible to humans. We consider this argument further below. Scientists who argued from a lack of evidence that scrapie transmits to humans to the conclusion that scrapie does not transmit to humans did so non-fallaciously, I am claiming. Some consideration of the different components of this argument reveals why this is the case. A claim of ‘no evidence’ only carries evidential weight if the knowledge base to which that claim belongs can be fully circumscribed and if an exhaustive search of that base can be undertaken. In the case of the present argument from ignorance, these two requirements amount to a complete collation of all the evidence relating to the epidemiology of scrapie and CJD (a complete knowledge base) and a thoroughgoing review of this evidence by scientists who are qualified to assess its significance (an exhaustive search). Clearly, these requirements were satisfied by scientists who addressed the question of the transmissibility of scrapie to humans. Brown et al.’s (1987) review of world literature considered all studies that had examined if there was an epidemiological link between scrapie and CJD in humans.24 To the extent that these studies failed to reveal such a link, scientists were justified in claiming that scrapie is not transmissible to humans. This claim then acted as a premise in further reasoning (in this case, a minor premise in an analogical argument) from which a range of additional propositions were derived. It was therefore directly facilitative of other processes of reasoning during the BSE inquiry. One such process involved decision-making relating to measures to protect human health. The recommendations of the Southwood Working Party, for example, were based in large part on the thesis that scrapie was not transmissible to humans.25 The deliberations of Southwood scientists, amongst others, were thus possible because of presumptive claims that issued from ignorance arguments. Through its generation of presumptive theses, the argument from ignorance made a significant contribution to the early phase of the inquiry into BSE. This argument transformed a lack of knowledge into a positive epistemic resource from which presumptive claims emerged. It was thus less a fallacy of reasoning than a rational strategy for managing uncertainty at the outset of inquiry. But something more needs to be said about the logical and epistemic features of this argument that underpin its capacity to generate presumptive theses. Specifically, these features involve the combined operation of a complete knowledge base and an exhaustive search process. A complete knowledge base contains all the evidence in a particular domain or relating to a specific topic or question. While this sounds like an unattainable requirement for evidence, we have already seen how this requirement can be met in mundane as well as in expert contexts (see notes 44 and 45, Chapter 3). The claim that a knowledge base is complete or closed is the basis of the major premise in the following modus tollens inference:

4.2

The Early Years: 1986–1989

MAJOR PREMISE: MINOR PREMISE: CONCLUSION:

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If p were true (where p is a proposition), then p would be in the knowledge base. But p is not in the knowledge base. So p is not true.

The minor premise of this inference is established by means of an exhaustive search of the knowledge base in question. Applied to the current case, this inference allows scientists to reason as follows: if it were true that scrapie is transmissible to humans, then the proposition ‘scrapie is transmissible to humans’ would be in the epidemiological knowledge base; but this proposition is not in the epidemiological knowledge base, so it is not true that scrapie is transmissible to humans. The logical features of the argument from ignorance are none other than the logical features of modus tollens inference. But the argument from ignorance contributes a unique epistemic twist to this deductively valid inference pattern. For the content of the premises of this argument relates to a knowledge base and not to an external state of affairs. The reasoner who argues from ignorance is thus turning his epistemic resources into a productive source of presumptions for use in inquiry. It emerges that BSE scientists made non-fallacious use of the argument from ignorance when they addressed the question of scrapie’s transmissibility to humans. However, this was not the only non-fallacious use of this argument during the early phase of inquiry into BSE. To examine a second, and quite distinct, use of this argument, we must return to the argument from ignorance presented at the start of this section and repeated below: PREMISE: CONCLUSION:

There is no evidence that BSE is transmissible to humans. BSE is not transmissible to humans.

This argument was repeatedly used by government officials and ministers, particularly during media briefings, to reassure the public that BSE presented little or no risk to human health. Like analogical argument (see Section 4.2.1), argument from ignorance was an integral part of the argumentative strategy that saw key protagonists during the BSE crisis consistently arguing that BSE was unlikely to transmit to humans. While the contribution to that strategy from analogical argument had certain rational merits, it is less clear that the same can be said of the role of the argument from ignorance in that strategy. The latter argument was intended to create an understanding on the part of the public that BSE was not transmissible to humans on the grounds that there was no evidence that BSE was transmissible to humans. But we have already seen that this ‘no evidence’ premise carried little, if any, evidential weight given that an inadequate period of time had elapsed in which to gather evidence about this new bovine disease. The BSE knowledge base was anything but complete and any attempt to base a conclusion on this incomplete base was inevitably problematic. As an argument that was designed to inform the public about the human health implications of BSE, the argument from ignorance was an inherently weak, fallacious form of reasoning. But this same argument assumed quite different rational properties when it was used by scientists during the early stage of the BSE inquiry.26 In that context, the argument from ignorance served the important epistemic function of prioritising questions during inquiry. One question

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in particular, the question of the transmission of BSE to humans, was effectively removed from inquiry through the use of ignorance argument. We consider how and why this occurred further below. The question of BSE’s transmissibility to humans presented scientists with certain insurmountable barriers to direct investigation. Ethical constraints on the use of human subjects in scientific experiments obviously precluded the use of inoculation and oral transmission studies that had previously established susceptibility to specific TSEs in other species. In the absence of a direct attempt to address the question of BSE transmission to humans, scientists could investigate the occurrence of natural transmission of BSE to humans. This was, in effect, the purpose of the CJD Surveillance Unit which was established in May 1990.27 But even natural transmission would only likely manifest itself after a number of years, given what was known about the lengthy incubation periods of TSEs. For ethical and other reasons, the single most important question of the BSE crisis was effectively beyond the investigative reach of BSE scientists in the short and possibly longer term. Under these circumstances, scientists had to find some means of removing this question from inquiry in order to give priority to other questions that could be addressed. A question can only be removed from further consideration in inquiry if it has been definitively addressed, that is, the proposition at issue in the question (in this case, that BSE is transmissible to humans) has either been confirmed or disconfirmed. If the proposition remains unconfirmed,28 it must continue to be actively tested and investigated by scientists until such times as its confirmation or disconfirmation can be achieved. The argument from ignorance made it possible for scientists to characterize the proposition ‘BSE is transmissible to humans’ as disconfirmed (i.e. BSE is not transmissible to humans), thereby excluding this proposition from further deliberation during inquiry. With the question of transmission effectively isolated from inquiry, scientists could then direct their cognitive and practical resources to matters that could be addressed through experimental investigation. This use of the argument from ignorance is examined further in Cummings (2002b). In this section, we have seen a number of ways in which the argument from ignorance was put to work by scientists and others during the early stage of the BSE inquiry. At least one of these ways involved the fallacious use of this argument – in various media briefings about the risk that BSE posed to human health, government officials and ministers fallaciously argued that BSE was not transmissible to humans on the grounds that there was no evidence that it was transmissible to humans. We will examine fallacious uses of ad ignorantiam further in Chapter 5. But by far the most interesting uses of this argument for our present purposes are those that found scientists employing the argument from ignorance to secure various epistemic and other gains in a context that was characterized by pervasive uncertainty. This argument was used to generate presumptive claims which could then participate in other processes of reasoning (e.g. decision-making). This use of the argument from ignorance saw specific, appropriately constrained knowledge bases active in the generation of presumptions during inquiry. As well as generating propositions for use in inquiry, the argument from ignorance also served

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to remove certain propositions from consideration during inquiry. Not every question that BSE scientists wished to address was directly amenable to experimental investigation. By virtue of ethical prohibition and practical limitations, some questions had to be set aside by scientists in preference for other questions for which there was a realistic prospect of obtaining answers. The argument from ignorance became the mechanism by means of which these questions were excluded from ongoing, active consideration during inquiry. Where the former use of ad ignorantiam concerned the generation of propositions in BSE inquiry, the latter use achieved the regulation of propositions in this inquiry. The argument from ignorance was thus an important instrumentality of cognitive rationality in the initial phase of inquiry into this new bovine disease.

4.2.3 Question-Begging Argument Also known as petitio principii or circular argument, question-begging argument has had a long history in philosophical discussions of the fallacies. Typically, this argument is taken to consist in the attempt to use as a premise in an argument the very conclusion that the argument is intended to prove or a premise that otherwise depends on the conclusion for its proof. It thus represents, it is claimed, a subversion of normal probative ground rules in which we argue from premises that are better known than, or more established than, the conclusion to be proved (premises cannot possibly fulfil this condition29 if they depend on the conclusion, or if they are the conclusion in a somewhat different guise). Almost without exception,30 theorists have sought to characterize this argument as an inherently weak, fallacious form of reasoning. Thus, in the contemporary literature31 on question-begging argument, we find Sanford (1972: 198) characterizing this argument as a failure ‘to increase the degree of reasonable confidence which one has in the truth of the conclusion’. According to Biro (1984: 239), the problem with question-begging argument is that it is ‘epistemically non-serious’, where epistemic seriousness describes an argument in which the premises are more knowable than the conclusion. For Rescher (1977: 11), circular sequences in disputation must be blocked since they ‘frustrate the aim of the [dialectical] enterprise’ which is ‘to deepen the grounding of the contentions at issue’.32 Regardless of the particular conception of question-begging argument at work in these various views of the fallacy, the same message emerges from each – petitio principii is an essentially unproductive form of argument that attempts to bypass the task of grounding the conclusion or question-at-issue. However, as I will argue below, this is not the full story about question-begging argument. As question-begging argument began to be submitted to a more systematic treatment in a post-Hamblin era of fallacy analysis, it soon became apparent to analysts that arguments with a distinctly circular form were not all inherently fallacious. Indeed, many such arguments were merely reflecting certain natural cyclical processes at work in fields such as economics, mathematics,33 geology, paleontology and even epistemology (Walton 1985; Cummings 2000). The decisive factor in an evaluation of question-begging argument was now less the structure of these

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arguments than the purpose(s) for which they had been advanced. If that purpose included a requirement to argue from better known, or more established, propositions to less well known, or less established, propositions, then the circular structure of question-begging argument is clearly problematic. If there is no such requirement for evidential or epistemic priority in a particular context of argument, an accusation of fallacy against the proponent of a circular argument is altogether less tenable.34 At the outset of scientific inquiry, particularly inquiry into a newly emerging infectious disease, there are few well known, established theses at the disposal of investigators. To insist that scientists fulfil a priority requirement at this stage of scientific inquiry is to misrepresent the epistemic standing of the propositions that are available to scientists in this context. A more sensible epistemic policy is to suspend this priority requirement until such times as a knowledge base of well established propositions is available to investigators. In the interim period, it is quite legitimate for scientists to use a proposition as a premise in argument that is no better established than the conclusion to be proved. We will examine the basis of this claim by considering how question-begging argument was used by scientists in the early stage of inquiry into BSE. On the recommendation of the Southwood Working Party, it was announced in February 1989 that a committee had been established to advise on research in relation to BSE.35 Known as the Tyrrell Committee, it was chaired by Dr David Tyrrell (a virologist who was the Director of the Medical Research Council Common Cold Unit) and had a membership consisting of Dr Watson (Director of the CVL), Professor John Bourne (Director of the Institute for Animal Health), Dr Robert Will (a clinical neurologist and expert in CJD) and Dr Richard Kimberlin (an independent TSE consultant). One of the areas recommended for research by Sir Richard Southwood and his team was an oral transmission experiment in which scrapieinfected meal would be fed to cattle. This study, it was argued, would serve to test the hypothesis that scrapie was the origin of BSE. Its importance was such that it was one of the recommendations made by Southwood scientists following their first meeting on 20 June 1988: We believe that tests should be undertaken on cattle and appropriate laboratory animals with meal known to be infective with scrapie to test the current hypothesis that this is the origin of the disease (BSE Inquiry Report, Volume 4: 9).

It is clear from an Interim Report produced by the Tyrrell Committee and presented to the government on 10 June 1989 that David Tyrrell and his committee members treated the question of the origin of BSE as something that was yet to be definitively established. The scrapie hypothesis of the origin of BSE was thus something to be investigated and established rather than simply assumed from the outset. This is evident from the following comments in the Interim Report: We need to be sure that the disease really came from sheep and to know whether it is likely to establish itself long-term in bovines (BSE Inquiry Report, Volume 1: 56).

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However, even though the scrapie origin of BSE was one of the Southwood priorities for research, the scrapie transmission experiment to cattle was not recommended by the Tyrrell Committee.36 Indeed, this action as well as views expressed by members of the Tyrrell Committee suggested that these scientists had already accepted that scrapie was the origin of BSE, even though this was a thesis that they were charged with attempting to establish. For example, Professor John Bourne reported to Lord Phillips and his team that the task of the Tyrrell Committee was ‘to go forward specifically on two major research fronts, one to increase the epidemiological work, and the other, to put in a much stronger science base relating to an understanding of the pathogenesis of the disease based upon the mouse and sheep model’.37 For Professor Bourne at least, scientific research into BSE was to proceed on the basis that scrapie was the origin of this new bovine disease. The thesis to be proved – that scrapie is the origin of BSE – was something assumed at the outset of the committee’s deliberations rather than something that was established by means of those deliberations. But to establish that the Tyrrell Committee was arguing in a circle, it is necessary to go beyond merely relating what should have been a research priority for Tyrrell and his colleagues – the confirmation or disconfirmation of the scrapie origin of BSE – with an assumption on the part of these scientists at the outset of their work. For these components must be shown to be propositions in an (extended) argument in which the thesis that scrapie is the origin of BSE functions as both a premise and a conclusion. Just such a demonstration can be given, I believe. The two major research fronts that Professor Bourne expected the Tyrrell Committee to develop were premised upon an understanding that the pathogenesis of BSE would be similar to that of scrapie. The thesis that ‘the pathogenesis of BSE is similar to the pathogenesis of scrapie’ is only rationally warranted on the assumption that BSE is bovine scrapie (i.e. scrapie is the origin of BSE). The dependency relation between this scrapie origin claim and the pathogenesis claim is shown in Diagram 4.1 as a logical relation between propositions (1) and (2), in which (1) provides a rational basis for the thesis in (2). The similarities in pathogenesis of BSE and scrapie were to be used, according to Professor Bourne, ‘to increase the epidemiological work’ and ‘to put in a much stronger science base’ on BSE. Yet, an examination of the research priorities recommended by the Tyrrell Committee to achieve these aims reveals that the thesis that ‘scrapie is the origin of BSE’ is held as something which is contested and subject to proof. One of the epidemiological research priorities proposed by Tyrrell and his colleagues included a ‘more detailed examination of the source of meat and bone meal associated with high BSE infection rates’ (BSE Inquiry Report, Volume 11: 23). This particular priority was nothing other than the attempt to establish if scrapie had been orally transmitted to cattle via feedstuffs. In other words, this epidemiological research priority was an attempt to address the question if scrapie was the origin of BSE. To the extent that this research priority is treating as problematic the very scrapie origin thesis that is assumed at (1), Tyrrell scientists may be seen to be arguing in a circle. The circular dependency relations in this argument can be clearly demonstrated in the following diagram:

106 Diagram 4.1 Circle in the reasoning of the Tyrrell Consultative Committee on research

4 Good Arguments During the BSE Inquiry (1) BSE is bovine scrapie (IMPLICIT THESIS: scrapie is the origin of BSE)

(2) Pathogenesis of BSE is similar to pathogenesis of scrapie

(3) To establish source of meat and bone meal associated with high BSE infection rates (TREATS AS PROBLEMATIC THESIS: scrapie is the origin of BSE)

CIRCLE: The epidemiological research question at (3) treats as problematic the thesis which is implicit in (1)

So we have seen that in assuming the very thesis that the Tyrrell scientists were to treat as problematic and hence subject to investigation, these scientists have effectively argued in a circle. But such circular argument need not be fallacious and, in this particular case, almost certainly is not. The Tyrrell Committee was tasked with investigating the scrapie model of BSE. This model, which had hitherto been the dominant analogy in scientific reasoning, was itself to be treated as the subject of investigation.38 However, at this early stage of inquiry into BSE, there was no independent knowledge base on BSE that scientists could use to test the validity of the scrapie analogy (indeed, if there had been such a knowledge base, there would have been no need for the scrapie analogy in the first place). For example, there were no results available from pathogenesis studies on BSE to show which bovine tissues carried infectivity, the titres of infectivity in these tissues, etc. Scientists had little option but to proceed to test the validity of the scrapie model from within the model itself. This required that investigators first assume that scrapie was the origin of BSE. This assumption allowed scientists to generate theses about the behaviour of BSE, theses which could then be tested using experimental studies of the type recommended by the Tyrrell Committee. To the extent that the scrapie analogy was the only rational basis available to scientists for generating research priorities for BSE at this early stage of inquiry, circularity was an inevitable feature of the reasoning of Tyrrell scientists. Circular argument in this case was not a feature of flawed or defective reasoning on the part of scientists. Rather, it was a consequence of the need to develop research priorities for BSE when the only available rational basis for doing so was the scrapie analogy that was itself to be investigated as part of these priorities. The reasoning of Tyrrell scientists took the form of a circle in which scientists assumed that scrapie was the origin of BSE even as they were attempting to prove this proposition by means of the establishment of research priorities. However,

4.3

Summary

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the circular reasoning of these scientists was anything but fallacious, it is argued, because these scientists were compelled to develop research priorities for BSE upon a rational basis and the only rational basis available to scientists at this initial stage of inquiry was the scrapie model of BSE (a knowledge base that was independent of this model was not available to investigators at this time). The circularity at issue in this case was thus an inevitable consequence of the requirement to validate the scrapie model of BSE when this model was the only framework available to scientists for posing research questions about BSE. The inevitability of this pattern of circular reasoning, however, does not in itself make this reasoning rationally acceptable. Certain merits must attend this type of reasoning for scientific inquiry in order for circular reasoning to have any rational standing in this inquiry. By engaging in circular reasoning, Tyrrell scientists were effectively pulling themselves up in inquiry by their own bootstraps.39 Lacking evidence that was independent of the conclusion-to-be-proved at the outset of inquiry, scientists subscribed to the view that scrapie was the origin of BSE. This view allowed scientists to generate multiple presumptive theses about the behaviour of BSE. The epistemic fate of these theses in inquiry was to determine the wisdom of the decision to adopt scrapie as a model of BSE. But even in those cases where theses were shown ultimately to be problematic, their generation nonetheless permitted scientists to forge ahead in inquiry until such times as independent lines of evidence became available to investigators. Circular reasoning thus facilitated inquiry into BSE by licensing progression in inquiry until such times as scientists were able to develop an independent knowledge base on BSE.

4.3 Summary In this chapter, we have described a number of ways in which scientists used traditionally fallacious modes of reasoning to achieve certain epistemic gains in the early stage of scientific inquiry into BSE. What these forms of reasoning had in common was their capacity to circumvent the uncertainty and lack of knowledge that characterized early inquiry into this new bovine disease. Their means of achieving this circumvention, however, differed with each form of argument used. Some reasoning strategies served to generate plausible theses for consideration during inquiry. They were thus a productive source of theses at a time in inquiry when little was known about BSE. Other strategies had a regulative function in that they achieved a prioritisation of the questions that could be addressed through inquiry. Cognitive and practical resources could then be appropriately assigned to those questions which had the best prospect of being addressed by scientists. Still other strategies facilitated inquiry by enabling it to progress in the absence of evidence that is independent of the conclusion-to-be-proved. Such a strategy allowed scientists to embark on inquiry in the expectation that as independent lines of evidence emerged, they would supersede the conclusion-dependent evidence that had carried investigators to a particular point in their deliberations. Each of these reasoning strategies

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represented a considerable divergence from traditionally dominant, deductive forms of argument and embodied instead a type of reasoning based on presumption. In this concluding section, we summarize the features of each of these reasoning strategies as they were employed by BSE scientists at the outset of inquiry. The stage will then be set to develop this model of scientific reasoning further in order to accommodate the unique epistemic circumstances of, and reasoning strategies employed in, later stages of inquiry into BSE. Argument from Analogy: Analogical argument was used extensively by scientists in the early weeks and months of the inquiry into BSE. Its influence was particularly keenly felt in the developing argumentative strategy that was to span the entire duration of the inquiry. This strategy represented the ‘public face’ of the scientific and other deliberations that were taking place about BSE. It was therefore less a vehicle for the transmission of objective scientific information about BSE than it was a tool for the political presentation of this information through various media outlets. When analogical argument was being used to construct this strategy in the initial months following the emergence of BSE, this argument reflected the type of reasoning that was increasingly evident in scientific deliberations about BSE. To this extent, the argumentative strategy at this initial stage of inquiry into BSE was rationally warranted (we will see in Chapter 5 that this was not always the case). The scientific arguments that motivated this strategy were based in large part on a somewhat tentative analogy with scrapie in sheep. As well as licensing decisions relating to the protection of human health, analogical reasoning based on scrapie generated several productive lines of inquiry for investigators. This reasoning strategy thus bridged the lack of knowledge and uncertainty in early inquiry into BSE by (1) warranting decisions in the practical sphere when there was an inadequate evidential base for these decisions and (2) generating research questions for investigation that represented the best prospect for scientists of addressing gaps in scientific knowledge. Analogical reasoning emerged as a productive epistemic resource for scientists who were confronted with the uncertainty that pervaded early inquiry into BSE. Argument from Ignorance: Like analogical argument, the argument from ignorance operated at two related levels during the BSE crisis. This argument was also instrumental in establishing the argumentative strategy that was to find scientists, politicians and others consistently arguing throughout the course of the BSE affair that this bovine disease presented little or no risk to humans. And like analogical argument, the contribution of ignorance argument to this argumentative strategy was rationally motivated at least at the outset of inquiry. This is because ignorance argument was shown to perform a couple of important epistemic functions in the absence of knowledge of BSE. Firstly, this argument served to generate plausible theses for use in inquiry at a time when little was known about BSE and most experimental studies into this disease had yet to be initiated. Secondly, ignorance argument served to exclude from ongoing consideration during inquiry those questions for which there was little prospect of obtaining answers in the short and longer term. With such questions effectively excluded from inquiry, scientists were able to direct scarce cognitive and practical resources towards those questions that were

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amenable to experimental investigation. It thus emerged that as well as generating theses for use in inquiry, ignorance argument achieved the regulation of theses through its prioritisation of the questions to be addressed in inquiry. This reasoning strategy demonstrated how when certain knowledge bases were appropriately constrained during inquiry into BSE, even an absence of knowledge could be used to derive tentative (presumptive) conclusions about this bovine disease. Once again, a traditionally fallacious mode of reasoning had demonstrable epistemic benefits for inquirers who were confronting uncertainty at the outset of scientific inquiry. Question-Begging Argument: It is perhaps a sign of the resourcefulness of presumptive frameworks that even a circular pattern of argument had demonstrable benefits for inquirers in the early stage of inquiry into BSE. Almost universally rejected as an unproductive form of argument, circular reasoning enabled Tyrrell scientists to progress in inquiry using evidence that was dependent on the conclusion-to-be-proved until such times as independent lines of evidence could be established. Even if this conclusion-dependent evidence was shown during the course of inquiry to be lacking in some respect, circular reasoning had nevertheless succeeded in opening inquiry up to investigators in ways that were capable of yielding useful evidence. The objector who demands that inquiry set out only on the basis of conclusion-independent evidence is not only asking investigators to incur an unacceptable delay in the initiation of inquiry (an imprudent course of action when investigators are dealing with an infectious disease), but is also seeking to institute the evidential standards of a later phase of inquiry at the very outset of inquiry. This misapplication of evidential standards is tantamount to the attempt to apply deductive standards to the evaluation of non-deductive forms of argument, a tendency in argument evaluation that finds the circular and other forms of argument examined in this chapter condemned as fallacious.40 The purpose of this chapter has been to demonstrate that when examined within the contexts in which they are advanced, these various forms of argument are not only non-fallacious, but they can also serve to facilitate inquiry that proceeds under conditions of uncertainty. It remains to be seen how these same forms of argument fare within later stages of inquiry into BSE.

Notes 1. The expression ‘argumentative strategy’ has been used by many argumentation theorists, although with somewhat different meanings from the meaning employed in the present context. For example, Joviˇci´c (2006: 29) states that ‘[a] person displays an argumentative strategy when he with or without awareness avails himself both of the reasoning and the social aspects in an argumentative activity with the aim of persuading an audience to accept the claims advanced’ (italics in original). For Godden and Walton (2004: 219), the expression ‘argumentative strategy’ refers to an altogether more circumscribed unit of argument than that envisaged by Joviˇci´c: ‘In this paper, we argue that denying the antecedent is not always a fallacious argumentative strategy’. 2. This standard list includes the fallacies that Woods et al. (2004) have described as the gang of eighteen. These fallacies include ad baculum, ad hominem, ad misericordiam, ad populum, ad verecundiam, ad ignorantiam, post hoc, ergo propter hoc, affirming the consequent, denying

110

3.

4.

5.

6.

7.

8.

9.

10. 11.

12.

4 Good Arguments During the BSE Inquiry the antecedent, begging the question, equivocation, amphiboly, hasty generalization, biased statistics, composition and division, faulty analogy, gambler’s fallacy and ignoratio elenchi. I am not taking the position of Finocchiaro’s ‘thoroughgoing rationalist’. Rather, my stance is much closer to that of the realist in that I acknowledge that fallacies exist: ‘a thoroughgoing rationalist may be inclined to go to the absurd extreme of claiming that no actual argument is ever fallacious. . .the rationalist might in his quest try to find evidence that [logic textbook] accounts are not arguments, and hence not logically incorrect for categorial reasons. He may find rationality in them by categorizing them differently. I personally don’t know what this category would be, but I doubt very much that the rationality involved would be pedagogic or rhetorical rationality. The realist in me prevails here and parts company with the rationalist’ (Finocchiaro 1981: 17). Of course, two very significant civil servants in the BSE affair, the Chief Medical Officer and the Chief Veterinary Officer, were also scientists. Their roles were to present government policy on matters relating to human and animal health, respectively. Section 4 Committees were established under Section 4 of The Medicines Act 1968. Four of these committees were involved in matters relating to BSE: the Veterinary Products Committee; the Committee on Dental and Surgical Materials; the Committee on the Review of Medicines; the Committee on Safety of Medicines. The following figures reveal the extent of the escalating animal health problem. In May 1987, BSE had been confirmed in four herds. By 15 December 1987, there were 95 confirmed cases on 80 farms. On 19 February 1988, there were 264 cases from 223 farms. A total of 2,296 cases on 1,742 farms had been confirmed by 13 January 1989 (BSE Inquiry Report, Volume 1: 13–15). Reilly and Miller (1997: 241) explain the rather slow emergence of reports on BSE as follows: ‘[M]edia coverage of BSE developed slowly, and did not enter mainstream public debate until 1990. There was already a well-developed interest in food safety because of salmonella and listeria, and the government was in the process of introducing a new Food Safety Act. Food had been in the media throughout 1988 and 1989, but BSE had been hidden behind the other so-called ‘food scares’, coming to prominence only when political actors engaged with the issue’. One distinguished epidemiologist described the ruminant feed ban to Lord Phillips and his inquiry team as ‘a spectacularly successful control measure. . .one of the notable success stories of global disease control’ (BSE Inquiry Report, Volume 1: 39). This is evident in a submission that Mr Rees (Chief Veterinary Officer, 1980–1988) made to the Minister on 6 May 1988. John Wilesmith is amongst the ‘investigating teams’ that Mr Rees makes reference to: ‘The Chief Veterinary Officer is satisfied from the information produced by the investigating teams that the source of the transmissible agent which has caused BSE is through meat and bone meal derived from sheep material in which the rendering process has failed to inactivate the scrapie agent. Affected sheep material is continuing to be processed and it must be assumed therefore that cattle continue to be exposed to infection’ (BSE Inquiry Report, Volume 3: 72). A zoonosis is any infection or disease that is transmitted to man from lower vertebrates. We can see this argument at work in the following extract from the BSE Inquiry Report, in which Lord Phillips and his team are reconstructing the reasoning that led the Southwood Working Party to conclude that BSE was unlikely to have implications for human health: ‘On 9 February 1989 they [the Southwood Working Party] submitted a report to the Government in the knowledge that it would be published. The report concluded that the risk of transmission of BSE to humans appeared remote and that “it was most unlikely that BSE would have any implications for human health.” This assessment of risk was made on the following basis: BSE was probably derived from scrapie and could be expected to behave like scrapie. Scrapie had not transmitted to humans in over 200 years and so BSE was not likely to transmit either’ (BSE Inquiry Report, Volume 1: xx). Walton (2008: 314) states that there are three critical questions that can be asked of any argument from analogy. The second of these questions relates to the analogy premise: ‘The

Notes

13.

14.

15.

16.

17.

18.

19.

20.

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second criticism would be to argue that the analogy premise fails. This means questioning whether the analogy is faulty because the two situations compared are not similar in the relevant respect’. ‘Extensive retrospective studies together with a review of world literature led to the conclusion, published in 1987, that scrapie had never passed to humans despite opportunities to do so over the 250 years during which the disease had contaminated sheepmeat entering the human food chain’ (BSE Inquiry Report, Volume 2: 67). The paper to which Lord Phillips and his team makes reference is Brown et al. (1987), an article that falls outside of those considered in Chapter 1 of this volume. Dr Richard Kimberlin was a TSE research scientist at the Neuropathogenesis Unit in Edinburgh between 1981 and 1988. Since 1988, he was an independent TSE consultant. During the BSE crisis, he was a member of the Tyrrell Committee (an expert committee that was set up to recommend research priorities for BSE) and the Spongiform Encephalopathy Advisory Committee. The Committee on the Safety of Medicine provided advice to government on questions relating to the safety, quality and efficacy of human medicines that fell outside of the remit of the Committee on the Review of Medicines and the Committee on Dental and Surgical Materials. Two sub-committees that reported to the CSM on matters related to BSE were the Biologicals Sub-Committee (BSC) and, after its establishment in 1989, the BSE Working Group. Dr Jeffreys (Principal Medical Officer, Department of Health) remarked of the period during which the policy implications of the CSM recommendations were assessed as follows: ‘All of [the] issues needed to be debated and required considerable technical expertise. They were not questions which admitted of simple straightforward answers; indeed this was leading edge science’ (BSE Inquiry Report, Volume 7: 75). To the extent that analogical argument is based on presumption, the same faute de mieux considerations may be seen to be at work in this concept. Rescher (2001: 31) remarks that ‘[p]resumptions arise in contexts in which we have questions and need answers. And when sufficient evidence for a conclusive answer is lacking, we must, in the circumstances, settle for a more or less plausible one. It is a matter of faute de mieux, of this or nothing (or at any rate nothing better). Presumption is a thought instrumentality that so functions as to make it possible for us to do the best we can in circumstances in which something must be done’ (italics in original). In Cummings (2004c), I demonstrate how analogical reasoning fulfilled a similar function in early scientific work on HIV/AIDS. Also, Plant (2008: 49) describes how analogical reasoning shaped early actions in the management of SARS: ‘we considered that the SARS organism was most likely a virus and spread predominantly via the respiratory route. Hence we acted as though that was true, meaning that infection control, patient management, patient isolation and so on were all treated as though the (assumed) virus causing SARS was similar to other viruses’ (italics added). Even apart from scrapie as the origin of BSE, a number of other possibilities were considered within an explanation of the origin of the disease. Some of these possibilities were actively considered by Mr Wilesmith during his early epidemiological investigations of the disease. They included the use of organophosphates, an autoimmune reaction, endocrine poisoning and methyl bromide poisoning. An objector could argue that talk of research areas being ‘primed’ and some investigative possibilities being ‘prominent’ is unnecessarily psychological in nature and that this is symptomatic of psychologism in this study of scientific reasoning. The charge is justified and it is not one that I would even wish to overturn. In admitting cognitive agency into the account of fallacies that I am pursuing, I am quite prepared to adopt the approach to psychologism that is advocated by Gabbay and Woods (to appear) in their study of empirically sensitive logic: ‘Investigators who make room for context and agency are drawn to a form of what used to be called the Laws of Thought approach and, accordingly, are committed to an element of psychologism in logic. This psychologism is not inadvertent. Since human agents come

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with psychologies as standard equipment, once you re-admit them to logic, you admit their psychological make-ups as well, warts and all. . . Psychologism is once again an open question in the research programme of logical theory. Its re-emergence should not be prejudged. Better to wait and see how, once it is up and running, a psychologically real, agent-based logic fares as a theory of reasoning’. 21. Two other variants of this argument involve claims of ‘no reason’ and ‘no (scientific) justification’. See Cummings (2002b) for discussion of these variants. 22. A notable exception was the following statement from Dr. Kenneth Calman (Chief Medical Officer, 1991–1998) in a press release in October 1995 to mark the release of the fourth annual report of the CJD surveillance unit. Dr. Calman stated: ‘I continue to be satisfied that there is currently no scientific evidence of a link between meat eating and development of CJD and that beef and other meats are safe to eat. However, in view of the long incubation period of CJD, it is important that the Unit continues its surveillance of CJD for some years to come’ (BSE Inquiry Report, Volume 1: 149). The first sentence of this statement establishes the basis of an argument from ignorance – there is no scientific evidence of a link between meat eating and the development of CJD, therefore there is not a link between meat eating and the development of CJD. That this is the intended implication of these remarks is indicated by Dr. Calman’s further claim that ‘beef and other meats are safe to eat’. The force of the argument from ignorance is substantially weakened, however, by Dr. Calman’s further remark about the long incubation period of CJD. This additional claim serves to highlight the fact that the absence of evidence of a link between meat eating and CJD should not be taken to indicate that such a link does not exist. 23. Where an exhaustive search of a closed knowledge base has been undertaken, the argument from ignorance is deductively valid. Walton (1992: 385–386) captures the deductive form of this argument as follows: ‘To the extent we know a knowledge-based K is closed, i.e., complete, in the sense of containing all the relevant information, we can infer that if a proposition A is not in it, then A is false. This argumentation scheme for the argumentum ad ignorantiam has the following form: All the true propositions in domain D of knowledge are contained in K. A is in D. A is not in K. For all A in D, A is either true or false. Therefore, A is false. This form of inference is deductively valid.’ 24. See note 33 in Chapter 2 for a summary of the epidemiological findings of Brown et al. (1987). 25. In a letter to a medical correspondent in August 1988, Sir Richard Southwood stated: ‘My colleagues and I have made various recommendations based, I have to admit, largely on guesswork and drawing parallels from the existing knowledge of scrapie and CJD’ (BSE Inquiry Report, Volume 4: 45). Within the General Conclusions of the Southwood Report, Sir Richard remarked: ‘scrapie has been widespread in sheep flocks in Britain and in other countries for at least two centuries, while CJD, a human encephalopathy with a worldwide distribution, has remained rare. From the present evidence, it is likely that cattle will prove to be a “dead-end host” for the disease agent and most unlikely that BSE will have any implications for human health’ (BSE Inquiry Report, Volume 4: 36). 26. At all stages of the BSE inquiry, scientists produced the ‘no evidence’ statements that are the basis of the argument from ignorance. On 5 June 1987, the Chief Veterinary Officer, Mr William Rees, wrote in a submission to MAFF’s Parliamentary Secretary, Mr Donald Thompson, that ‘[t]here is no evidence that the bovine disorder is transmissible to humans’ (BSE Inquiry Report, Volume 3: 25). In June 1992, the Spongiform Encephalopathy Advisory Committee (SEAC) published an Interim Report on research, in which it was stated that ‘[t]here remains no evidence to suggest that the human disorders are causally associated with those in animals’ (BSE Inquiry Report, Volume 6: 512). By implication, this statement is

Notes

27.

28.

29.

30.

31. 32.

33.

34.

35.

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saying that there is no evidence that the human disorders are causally associated with BSE. The (intended) conclusion is that the human disorders are not causally associated with BSE, i.e. BSE is not transmissible to humans. The CJD Surveillance Unit was established under the direction of Dr Robert Will at the Western General Hospital in Edinburgh. Its main objectives were ‘to identify any change in the epidemiological characteristics of CJD and to assess the extent to which any such changes were linked to the occurrence of BSE’ (BSE Inquiry Report, Volume 8: 13). Woods and Walton (1978: 91) use the language of confirmation theory to characterize the argument from ignorance. This characterization makes clear how the argument suppresses the possibility that a proposition can be unconfirmed: ‘the fallacy. . .consists in suppression of the possibility that H [the hypothesis] may be unconfirmed, i.e., the live possibility that there are no known data for H is omitted’ (italics in original). The same suppression that is presented by these theorists as a fallacy was, I am claiming, a highly desirable attribute of this argument in the context of the BSE inquiry. Walton and Batten (1984: 154) call this condition ‘evidential priority’: ‘The assumption is that the evidentiary wellknownness of A, in order to make A of utility as a premiss, must be prior to that of B. Once the deduction is granted however, the value of B should be adjusted upwards to a plausibility value equal to (and not greater than) A. Once A has been so utilized as a premiss for B however, B could never be used as a premiss in an argument that has A as a conclusion. Reason: to be useful as a premiss, the value of B must be greater than that of A. But. . .the value of B should not be greater than that of A, if A has been used as a premiss for B in a previous deduction. Thus arguing in a circle, from A to B, and then subsequently from B to A, violates some requirement of evidential priority’. Three such exceptions are Cummings (2000), Sorensen (1991) and Walton (1985). Sorensen (1991: 245) states that ‘a variety of arguments having the form “P, therefore, P” do not beg the question’, where question-begging form is defined as the propositional identity of premise and conclusion. It will not have escaped the reader’s attention that the argument form ‘P, therefore, P’ is deductively valid. This led some philosophers (e.g. Sextus Empiricus, Mill) to claim that all deductively valid arguments commit the fallacy of begging the question. Walton (1991) provides an excellent overview of contemporary and historical literature on question-begging argument. Rescher’s prohibition of circular sequences in disputation has particular significance in the present context, given his aim to develop a model of formal disputation that can capture the rational methodology of scientific inquiry: ‘We shall explore this particular sector of dialectics (formal disputation) to see what epistemological lessons can be drawn from it in order to exhibit the utility of such “dialectics” for the theory of knowledge. The goal of this exploration is the development of a dialectical model for the rationalization of cognitive methodology – scientific inquiry specifically included’ (Rescher 1977: xii). Walton (1985: 263) remarks that ‘[i]n mathematics, it is common practice to start at proposition A and then prove B, then start again at B and prove that A follows. An equivalence proof in mathematics, of the if and only if type, often takes this form. Although the form of proof is circular, in many instances such a proof is rightly thought non-fallacious’. Walton (1985: 272) remarks that ‘in the majority of circular arguments we looked at, the circularity cannot be condemned as wrong or fallacious precisely because the context of dialogue fails to indicate decisively that a priority condition is a procedural requirement. The economist’s argument we began with, for example, should not be declared fallacious or viciously circular by a reasonable critic unless the critic can cite evidence of an agreement, or at least a clearly agreed upon context or background requirement to argue only in one direction or the other. Similarly for the mathematician. If the objective (the problem) is to prove from A to B, and also from B to A, there need be no fallacy in solving the problem by arguing in a circle’. The committee’s terms of reference were ‘[t]o advise the Ministry of Agriculture, Fisheries and Food and Department of Health on research on transmissible spongiform encephalopathies including: (a) work already in progress or proposed; (b) any additional work

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36.

37.

38.

39.

40.

4 Good Arguments During the BSE Inquiry required; (c) priorities for future relevant research. In the context of these terms of reference, transmissible spongiform encephalopathies include those affecting both domestic and wild ruminants and man’ (BSE Inquiry Report, Volume 1: 55–56). One of the propositions for research into TSEs omitted from the final report of the Tyrrell Committee was the following: ‘Of meat and bone meal made from scrapie-sheep. Orally to cattle, to confirm the current hypothesis of the origin of BSE’ (BSE Inquiry Report, Volume 11: 26). Professor Bourne’s remarks are taken from the transcript of oral evidence that was given to Lord Phillips and his team on 19 March 1998. The full exchange reads as follows: ‘MR WALKER: . . .It is very helpful to have the indication of how you saw the task at the outset. Perhaps I could turn to Professor Bourne? PROFESSOR BOURNE: Clearly, we saw BSE as a very serious issue, and we were aware at that time that BSE was a TSE, that it had only a few months previously been shown by the work of Fraser et al. We recognised that an understanding of the basics of this disease was going to come through continuing work on scrapie. That was the model that one would work on, scrapie with work in sheep and in lambs. We also recognised that the facilities available for this work were fragile, there were not many facilities available for this work. I saw it as a need to really put in place a much stronger fundamental science programme to understand the pathogenesis nature of the disease. We were also aware at that time of the epidemiological evidence coming from the Ministry work, particularly John Wilesmith’s group. I think the importance of that work was very evident to us. So my view was that we had to go forward specifically on two major research fronts, one to increase the epidemiological work, and the other, to put in a much stronger science base relating to an understanding of the pathogenesis of the disease based upon the mouse and scrapie model’ (10–11). That the analogy with scrapie was itself the focus of investigation by the Tyrrell Committee is evident from the following comments in the Tyrrell Report: ‘Many of the practical measures taken have been based on shrewd judgements of the analogy between BSE and scrapie of sheep. Specific studies on BSE itself are now needed to establish whether those conclusions were sound’ (BSE Inquiry Report, Volume 11: 208); ‘If the preliminary studies and arguments-by-analogy used to determine our present control policies turn out to be incorrect, it will be essential to have well-documented facts available so that current policies can be effectively revised’ (BSE Inquiry Report, Volume 1: 56). The issues of circularity and bootstrapping are a constant preoccupation of theorists in epistemology. In this context, circularity emanates from the need to make use of one’s rational methods in order to validate those methods: ‘As one probes backward to substantiate the substantiating considerations that one uses in justificatory reasoning, either one continues to have recourse to ever newer materials (in which case there is an unending and thereby vitiating regress) or one eventually has justificatory recourse to previously employed materials (in which case there is a vicious circularity)’ (Rescher 2001: 140). Bootstrapping through the use of presumptions is an antidote to vicious circularity: ‘The point of this line of thought is precisely that this would be viciously circular, since we have no independent access to “the truth” as such. What we must do in rational inquiry is pull ourselves up by our own bootstraps, relying on our principles of presumption but critically reappraising them as well. We begin by provisionally accepting certain theses whose initial status is not that of certified truths at all, but merely that of plausible postulations, whose role in inquiry is (at this stage) one of regulative facilitation’ (Rescher 2006: 67–68). This tendency is aptly captured by Finocchiaro (1981: 15–16) as follows: ‘[L]et us examine the second element of textbook accounts of fallacies, the description of various devices which I wish to call by the neutral term of “disputed practices”. One problem with these descriptions is that they are usually prejudicial in the sense that their fallaciousness is built right into their description. . .There is a pattern in these biased descriptions, and it is the following. If the disputed practice is a type of inductive argument, namely one claiming that the conclusion is only strongly, but not conclusively, supported by the premises, then the practice will

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be described as a type of deductive argument, namely one claiming that the conclusion is conclusively supported by the premises. If the disputed practice is a type of what might be called a partial argument, namely one claiming that the conclusion is only partly, but not too strongly supported by the premises, then the practice will be described as a type of allegedly inductively strong argument. . .the pattern (or shall I say the fallacy?) is that of exaggerating the strength of the connection claimed between various assertions. . .’.

Chapter 5

The Unravelling of an Argumentative Strategy

5.1 Introduction The early years of the BSE inquiry marked out a period of considerable scientific and political activity in relation to public health in the UK. The emergence of a new brain disease in cattle mounted a significant challenge to scientists who were required to form judgements and make decisions about BSE in a context of pervasive uncertainty. At the same time, government ministers and officials struggled to develop policies and legislation that would adequately address the perceived risk that BSE presented to human and animal health. Against the backdrop of an escalating public health crisis, scientists secured a rational basis for their approach to the management of BSE in a group of reasoning strategies that have traditionally been characterized as informal fallacies. These strategies, which included question-begging argument and the argument from ignorance, conferred a number of gains upon inquiry and placed several new modes of reasoning1 at the disposal of scientific investigators. The analysis of these arguments presented challenges to traditional positions both in logic and in public health science. The almost complete dominance of deductive and inductive reasoning in the philosophical study of argument and reasoning on the one hand and fields like epidemiology on the other hand is very directly challenged through the presumptive nature of these argument forms. A number of other orthodoxies are also subject to revision through the analysis pursued here – amongst others, that some forms of argument are inherently weak or fallacious, that scientific inquiry should give priority to deductive modes of reasoning and linear directions of argument, that only deductive forms of argument are capable of generating knowledge, and that scientific inquiry is a uniform intellectual activity across each of its phases and notwithstanding its varying goals. Reconsideration of each of these positions is an inevitable consequence (or precondition) of the view of reasoning that is being presented in these chapters. In the last chapter, we drew a distinction between the argumentative strategy that spanned the duration of a scientific inquiry and the various arguments that formed a type of sub-structure to this strategy. These arguments, it was contended, could serve to rationally legitimate the particular views that were propounded as part of the argumentative strategy. Alternatively, the argumentative strategy may become L. Cummings, Rethinking the BSE Crisis, DOI 10.1007/978-90-481-9504-6_5,  C Springer Science+Business Media B.V. 2010

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detached from these arguments, it may receive little in the way of rational validation from them and may even be usurped by political and commercial interests that are contrary to the aims of scientific inquiry. The argumentative strategy that spanned the BSE inquiry found scientists and others consistently arguing that BSE presented little or no risk to human health and that British beef was safe to eat. And in the early years of this inquiry, there was a certain rational force to these claims. We saw in the last chapter how these claims received validation from the analogical, questionbegging and ignorance arguments that were employed by scientists at the outset of inquiry. This phase of inquiry was marked by considerable uncertainty, by an overriding requirement to initiate inquiry even at the expense of incurring error and by a concomitant shift in standards of evidence and proof. However, it cannot be assumed that these same considerations applied at later stages of inquiry when the results of experiments began to emerge and more became known about the transmission and other properties of this new bovine disease. How these same arguments fared under these changing epistemic conditions will be the subject of this chapter and the next chapter. Specifically, I will argue that the middle phase of the BSE inquiry marked a significant departure of the argumentative strategy from the arguments that had formerly provided this strategy with rational legitimacy. This departure continued in an even more pronounced form into the late phase of inquiry. It manifested itself in the ongoing reassurances by scientists and government ministers that BSE presented little or no risk to human health and that beef was safe to eat in the absence of rational validation from the arguments that had previously served to substantiate these claims. In effect, the same arguments that had served to launch inquiry into BSE began to look decidedly weak in the much changed epistemic conditions of the middle and later phases of inquiry. Other argument forms, which were not examined in the last chapter, were also advanced by scientists during these phases of inquiry. They too will be shown to have provided a weak rational basis for the continuing reassurances and pronouncements by scientists and others regarding the lack of risk of BSE to human health. The marked separation of the argumentative strategy of the BSE inquiry from the arguments that had at one time provided this strategy with rational legitimacy is the sense in which the argumentative strategy may be described as ‘unravelling’ in the later stages of inquiry. Certainly, dissenting scientific voices found it increasingly difficult to be heard in these later stages as political and commercial interests began to dominate the argumentative strategy of the BSE inquiry. If, as I am claiming here, there is a separation of the argumentative strategy of the BSE inquiry from the arguments that had previously given this strategy rational support, then it should be possible to discern this separation in quite specific features of the argumentative structure of the inquiry during the period in question. This should go beyond pronouncements that particular arguments are weak or fallacious to include statements that base this fallaciousness in various distortions of the inquiry process itself. We will see, for example, that certain arguments in the middle and final stages of the BSE inquiry are deemed fallacious because the normally defeasible conclusions of these arguments appeared irrefutable in the face of

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contrary evidence. The burden of proof that would typically be discharged to defeat such conclusions was raised to an extent that did not befit the presumptive status of these arguments. The conclusions of these arguments effectively became lodged or ‘fossilized’ in inquiry. A distortion in the dialectical structure of BSE inquiry, manifesting as aberrant standards of evidence and burdens of proof, thus finds a direct correlate in various weaknesses in the arguments that were advanced by scientists during the middle and final stages of inquiry. Before we can address the rational merits or otherwise of these arguments, though, we must first examine the key scientific developments that took place during the middle and late phases of the BSE inquiry. It is to an examination of these developments in the middle phase of inquiry that I now turn.

5.2 The Middle Years: 1989–1994 The years between the introduction of the human SBO ban in November 1989 and the emergence of results of the CVL’s pathogenesis experiment in June 1994 (‘the middle years’) was a period of considerable scientific developments in the BSE inquiry. These developments took the form of the establishment of scientific committees and surveillance bodies on the one hand and scientific findings relating to the transmission properties and host range of BSE on the other hand. In April 1990, the Spongiform Encephalopathy Advisory Committee (SEAC) was established. SEAC’s terms of reference were ‘[t]o advise the Ministry of Agriculture, Fisheries and Food and the Department of Health on matters relating to spongiform encephalopathies’ (BSE Inquiry Report, Volume 11: 40). It was chaired by Dr David Tyrrell and contained many of the members of the Tyrrell Committee along with several additional experts.2 Following a successful research grant application to the Department of Health by Dr Robert Will, a consultant neurologist, the CJD Surveillance Unit (CJDSU) was established in May 1990 at the Western General Hospital in Edinburgh. The role of this unit was to identify changes in the epidemiological characteristics of CJD and to determine if such changes were linked to the presence of BSE. In the same month that the CJDSU was established, officials at MAFF and the Department of Health reported to their respective ministers that Bristol University had diagnosed a ‘scrapie-like’ encephalopathy in a domestic cat. This event sparked considerable media interest and public anxiety,3 as domestic cats were not within the host range of scrapie. It also prompted the Agriculture Committee of the House of Commons to institute an inquiry into BSE in May 1990. The Committee reported in July 1990 with the reassuring conclusion that beef was safe to eat.4 In March 1991, the first of 300 BABs that year (cattle born after the ruminant feed ban came into force in July 1988) was reported to Mr John Gummer, the Minister of Agriculture, Fisheries and Food. The emergence of BABs provoked considerable concern, as it was unclear at the time if they were caused by maternal transmission of BSE or if these animals had become infected by feed containing ruminant protein which was in the distribution pipeline or unused on

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farms when the ban came into force. The whole area of feed was considered by an Expert Group on Animal Feedingstuffs which was established by MAFF in February 1991. The group was chaired by Professor Eric Lamming and it reported in June 1992. One of the group’s conclusions was that the controls in place relating to animal feed were working well, despite the emergence of BABs.5 Against the backdrop of these various developments, the BSE epidemic raged on. By the end of 1989, 10,091 cases of BSE had been confirmed in the UK. One year later, this figure had risen to 24,396 confirmed cases (BSE Inquiry Report, Volume 1: 15–16). The scientific developments in this middle phase of the BSE inquiry must be viewed within the context of this significant burden of animal disease.

5.2.1 Argument from Analogy We described in Chapter 4 how the argument from analogy was a dominant form of argument in the early years of the BSE inquiry. Decisions relating to the bovine tissues to include in the human SBO ban and the safety of human medicinal and surgical products were very directly justified in terms of an analogy between BSE and scrapie disease in sheep. The dominance of this argument form extended into the middle phase of inquiry. Thus, we find analogical arguments being used extensively as a means of justifying important public health pronouncements issued by SEAC in July 1990 and again in February 1992. In July 1990, SEAC provided the Chief Medical Officer with advice on the safety of beef. This advice – that ‘British beef can be safely eaten’ – was issued in the form of a letter and accompanying annex6 and reflected an understanding of the dose that would be required to transmit BSE and the efficiency of the oral route of transmission that was based upon knowledge of scrapie.7 SEAC’s use of analogical reasoning is evident in the following extracts from the annex to the letter. The reconstructed analogical arguments appear below each extract: Parallels with scrapie and other spongiform encephalopathies suggest the ‘dose’ of BSE agent if it is indeed present in food as consumed will be so small as to be undetectable by the most sensitive known method for these agents, namely bioassay by intracerebral inoculation into mice. . .It is concluded that the occasional low doses of BSE agent in human food are well below those capable of infecting humans, even if humans were specially susceptible to the agent (BSE Inquiry Report, Volume 11: 59, 61).

MAJOR PREMISE: MINOR PREMISE: CONCLUSION:

BSE is similar to scrapie in sheep. Low doses of scrapie agent are insufficient to transmit disease. Low doses of BSE agent will be insufficient to transmit disease.

[W]e consider that the oral route of transmission is so inefficient that there is a huge safety margin. . .Experimental studies. . .show ingestion to be very inefficient, at least 5 orders of magnitude less efficient than intracerebral injection [Kimberlin and Walker (1989) Virus Res 12: 201–212]. (BSE Inquiry Report, Volume 11: 59, 60).8

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The Middle Years: 1989–1994

MAJOR PREMISE: MINOR PREMISE: CONCLUSION:

121

BSE is similar to scrapie in sheep. In scrapie, the oral route of transmission is inefficient. In BSE, the oral route of transmission will be inefficient.

In February 1992, SEAC was once again called upon to pronounce on the human health implications of BSE. The Medical Research Council advised MAFF and the Department of Health on 14 February 1992 that BSE had been experimentally transmitted by inoculation to marmosets. SEAC considered the transmission of BSE to marmosets at an informal meeting held on 27 February 1992. The advice to issue from this meeting drew on an analogy with scrapie to provide reassurance that the marmoset results presented no new risk to human health from BSE. Where other analogical arguments concluded with predictions about the likely future behaviour of BSE, the analogical argument in this case sought to rationalize an experimental finding about BSE: Although marmosets have not previously been infected with BSE, they have been infected with S.E’s including scrapie using similar methods so the results of this experiment are not surprising. We conclude that the measures at present in place provide adequate safeguards for human and animal health (SEAC 1992a: 5).

MAJOR PREMISE: MINOR PREMISE: CONCLUSION:

BSE is similar to scrapie in sheep. Scrapie is transmissible to marmosets by inoculation. BSE is transmissible to marmosets by inoculation.

These analogical arguments relating to the dose, efficiency of transmission and host range of BSE played a significant role in forming the scientific advice issued by SEAC during the middle phase of the BSE inquiry. In using these arguments, scientists extended this dominant form of reasoning from the early stage of the inquiry. But while the analogical arguments of this early stage were warranted by the adverse epistemic conditions in which scientists were compelled to operate – scientists had to initiate inquiry in the absence of direct evidence relating to BSE – it is less clear that the above analogical arguments are warranted within the quite different evidential context of the middle phase of the BSE inquiry. It will be recalled that the major (analogical) premise of these arguments was established by the early investigations of BSE undertaken by John Wilesmith and his colleagues at the CVL. On the basis of epidemiological, molecular and histopathological evidence, Wilesmith et al. concluded that BSE was similar to scrapie disease in sheep in the sense that the former disease was caused by the latter disease. This conclusion, it was argued, was rationally warranted. But it could only be tentatively advanced given certain identified weaknesses in the evidence upon which it was based. In effect, this conclusion had the status of a presumptive thesis. In the absence of experimental and other findings relating to BSE in the early phase of inquiry, this presumptive thesis persisted by default and was used by scientists to licence a range of decisions relating to the containment of BSE. But the inherent defeasibility of this presumptive thesis meant it would always be vulnerable to the emergence of new evidence. In the middle phase of the BSE inquiry, this vulnerability should have been dramatically exposed. It is a sign of the dominance of the analogy with scrapie that this exposure for the most part did not occur.

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Several developments during the middle phase of the BSE inquiry should have led scientists to question this dominant pattern of analogical reasoning. One of the first of these was the discovery in May 1990 of a spongiform encephalopathy in a domestic cat. This discovery was potentially explosive – Lord Phillips and his team described it as a ‘bombshell’. Not only had a spongiform encephalopathy never before been diagnosed in a domestic cat, but (and most importantly) domestic cats were not susceptible to scrapie. Here was evidence that BSE may have a different host range to that of scrapie. SEAC discussed this case of spongiform encephalopathy in a cat at its second and third meetings, which were held on 17 May 1990 and 13 June 1990, respectively. While the minutes of these meetings revealed that SEAC members believed they had insufficient evidence to come to any judgement about the significance of this case,9 it is clear that the emergence of feline spongiform encephalopathy (FSE) did little to undermine the committee’s confidence in the dominant scrapie analogy of the day. This analogy, we described above, was the basis of SEAC’s advice to the Chief Medical Officer in July 1990 that British beef was safe to eat. Even more worrying was SEAC’s continuing adherence to this analogical strategy nearly 2 years later in February 1992, when SEAC scientists were called upon to discuss the human health implications of the finding that BSE had been experimentally transmitted to marmosets. For by that stage, further cases of FSE had been diagnosed – there were 23 confirmed cases by the end of 1991 (BSE Inquiry Report, Volume 6: 410). It could no longer be plausibly argued that there had always been the occasional case of FSE which had simply gone unrecognized.10 Despite growing evidence that the dominant analogy with scrapie may not be warranted, SEAC members continued to make this analogy the basis of their advice about the human health implications of BSE. The problems for this analogy did not end with the discovery of cases of FSE. A growing number of exotic ungulate species went on to develop spongiform encephalopathies during the middle phase of the BSE inquiry.11 These animals had most likely become infected through ingestion of feed containing bovine derived meat and bone meal. These natural transmissions through the oral route were of concern, because if BSE were to transmit to humans, it would most likely do so through oral transmission. Of even greater significance was the fact that these exotic ungulate species, like domestic cats, had not previously been susceptible to scrapie. Also, the Neuropathogenesis Unit confirmed in November 1990 that it had succeeded in orally transmitting BSE to ‘negative’ line sheep which were not susceptible to scrapie.12 Here, again, was evidence that BSE and scrapie were sufficiently dissimilar to warrant a more thoroughgoing scepticism towards the dominant scrapie analogy. SEAC’s apparent indifference to the growing weakness of the scrapie analogy was nowhere more evident than in their response to the finding that BSE was experimentally transmissible to marmosets. As far as SEAC scientists were concerned, this finding provided confirmation of the dominant scrapie analogy and with it the conclusion that existing measures were adequate to protect human health. But this finding could also be used to support a quite different conclusion about the potential risks that BSE posed to humans. This was the first case of transmission of BSE to an animal species that was genetically close to humans. And if BSE had

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crossed one species barrier to infect a marmoset, it could do the same again to infect humans. Yet, as the notes of an informal meeting of SEAC held on 27 February 1992 reveal, this possibility was not even considered by the committee’s scientists. So complete was the dominance of analogical reasoning during this period that it had become an overarching framework through which experimental findings were interpreted. SEAC’s reasoning leading to the public health pronouncements of July 1990 and February 1992 is revealing in terms of what it can tell us about how SEAC scientists viewed the analogy between BSE and scrapie disease in sheep. This analogy had served scientists well in the early phase of the BSE inquiry. It provided rational warrant for their decisions to remove certain bovine tissues from the human food chain (the human SBO ban), for example, and generated a number of specific, and potentially productive, directions of research for investigators. In the absence of contrary evidence at this initial stage of inquiry, the analogy became a rational and effective response on the part of scientists to the pervasive uncertainty that characterized the BSE problem. But the presumptive status of this analogy meant it could be readily overturned by the emergence of contrary evidence. The defeasibility of this analogy was put to the test in the middle phase of inquiry when certain developments and findings suggested that any similarity between BSE and scrapie could no longer be presumed to hold. But what followed indicated that this analogy was already assuming a quite different status for the scientific investigators of the middle phase of inquiry. Far from being treated as a defeasible proposition that could be overturned by contrary evidence, the scrapie analogy was viewed by SEAC scientists as a certain, almost irrefutable thesis. As such, it continued to shape the reasoning of these scientists far beyond the point at which existing evidence indicated that it was appropriate for it to do so. The persistence of this analogy in the absence of any justificatory evidential base was symptomatic of a wider malaise within the inquiry process. It is to an examination of this claim that I now turn. The analogical reasoning of SEAC scientists, I am claiming, represents a point in the BSE inquiry where the analogy with scrapie no longer received support from the developing evidential base of this inquiry. Separated from this base, this analogy became detached from the types of evidential considerations that would normally secure the defeat of presumptions in inquiry. The question of how this separation was achieved is interesting for what it can tell us about the operation of the wider process of inquiry. As a presumptive thesis, the scrapie analogy should have been overthrown by the evidence that emerged during the middle phase of the BSE inquiry. However, the burden of proof that would typically need to be discharged to displace a presumption was raised to such an extent that evidential considerations could not be brought to bear against the scrapie analogy. The operation of the normal dialectical process of presumption and burden of proof became distorted during the middle phase of inquiry with the result that the scrapie analogy persisted in inquiry when it was clear that it no longer had sufficient evidential support for doing so. The separation of this analogy from the evidential base that had once sustained it mirrored a similar departure of the argumentative strategy of the BSE inquiry from the arguments that had provided this strategy with rational warrant. Such was the

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concern of scientists to continue basing their assessments of risk on the reassuring conclusions of the scrapie analogy that this analogy eventually came to be upheld at the expense of any rational grounds for the thesis it contained. It was at this point in inquiry that we witness a marked divergence between an argumentative strategy that aimed to pursue certain conclusions about BSE and arguments which, as we have shown, were progressively incapable of supporting these conclusions. Our discussion of SEAC’s analogical reasoning would not be complete if we did not conclude this section with some consideration of a further occasion on which this committee was asked to consider the human health implications of BSE. The occasion in question falls at the end of the middle phase of inquiry and concerns the release of results of a pathogenesis study that had been initiated at the CVL in December 1991. In Section 4.2.1 in Chapter 4, we described the extensive deliberations of scientists who were charged with providing advice to ministers on the extent of the human SBO ban. An issue of particular concern for these scientists was whether tissues from calves less than 6 months old should be included in the ban. Although some scientists initially expressed concerns that these tissues may be infective, it was eventually decided that an exemption for offal from calves was justified. The decision to exclude offal from calves from the human SBO ban was reversed in June 1994 when it became apparent that the pathogenesis of BSE was dissimilar in significant respects from that of scrapie (BSE Inquiry Report, Volume 1: 137–138). Specifically, the CVL’s pathogenesis study revealed infectivity in bovine tissues (e.g. distal ileum) earlier than had been expected using the scrapie model (BSE Inquiry Report, Volume 2: 121). As soon as health officials became aware of the findings of this study, an ‘exceptional meeting’ of SEAC was called. This meeting took place on 25 June 1994 and concluded that ‘[t]here is a theoretical risk and Government could respond by a limited SBO ban for calves to exclude the intestines’ (SEAC 1994a: 4). The Chief Medical Officer, Dr Calman, said that he would be advising ministers that the distal ileum and thymus of calves should be proscribed as SBO. MAFF immediately wrote to the operators of all slaughterhouses, telling them of the proposed extension of the SBO ban (BSE Inquiry Report, Volume 1: 137–138). The scientific and government response to the results of the pathogenesis study was so prompt and thoroughgoing that Lord Phillips and his team described it as ‘a model of how government ought to handle such an issue’ (BSE Inquiry Report, Volume 1: 138). But this episode is remarkable in one further respect. It represented the first acknowledgement by SEAC that an experimental finding could not be explained by the hitherto dominant scrapie analogy.13 Moreover, the minutes of the SEAC meeting recorded that ‘had these findings been available when the SBO ban was drawn up and there was still clear evidence of substantial exposure of calves through contaminated feed they [the Committee] would undoubtedly have taken a different view on the 6 months exemption from the SBO ban’ (SEAC 1994a: 3). But although the findings of the pathogenesis study were not available at the time an exemption from the ban for calves was being considered, SEAC scientists could have arrived at the same conclusion – that an exemption for calves was not justified – much earlier in the inquiry process, and certainly well before this exceptional

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meeting of SEAC took place in June 1994. For the first indications that the analogy with scrapie was problematic were already evident some 4 years earlier in July 1990 when SEAC provided advice to the Chief Medical Officer on the safety of beef. By June 1994, the force of evidence against the scrapie analogy was so overwhelming that SEAC scientists could no longer adhere to this analogy with confidence (but see Section 6.2.1 in Chapter 6). Yet, a more rigorous examination of the rational standing of the scrapie analogy by SEAC scientists could have resulted in the rejection of this analogy long before the results of the pathogenesis study forced health officials to seek an extension of the human SBO ban.

5.2.2 Argument from Ignorance Like analogical argument, the argument from ignorance was a prominent reasoning strategy in the middle phase of the BSE inquiry. Statements from scientific committees during this period abounded in claims of ‘no scientific justification’ and ‘no scientific evidence’. Some of these claims were challenges to courses of action that had already been implemented in response to BSE such as the practice of not breeding from the offspring of BSE cows and the slaughterhouse practice of head splitting. In this way, in advice to agriculture and health ministers on 17 May 1990, SEAC stated that ‘there is no scientific evidence currently available to support official advice against the use for breeding of the offspring of cows suffering from BSE’ (SEAC 1990c: 1; italics added). A note of the third meeting of the Tyrrell Committee held on 13 June 1990 recorded that ‘[t]he committee could see no scientific justification for allowing the continued practice of head splitting and brain removal prior to removal of head meat’ (Tyrrell Committee 1990: 1; italics added). In a letter to the Chief Medical Officer dated 24 July 1990, SEAC concluded that ‘we believe there is no scientific justification for not eating British beef and that it can be eaten by everyone’ (SEAC 1990d: 2; italics added). Dr Calman (Chief Medical Officer, 1991–1998) released a statement on 26 January 1994 in which he stated that ‘on the basis of the work done so far, there was no evidence whatever that BSE caused CJD and, similarly, not the slightest evidence that eating beef or hamburgers caused CJD’ (BSE Inquiry Report, Volume 1: 143; italics added). These repeated ‘no evidence’ claims formed the premise in a classic argument from ignorance, which can be reconstructed as follows: PREMISE: CONCLUSION:

There is no evidence that BSE in cattle causes CJD in humans. BSE in cattle does not cause CJD in humans.

In Section 4.2.2 in Chapter 4, we described how the argument from ignorance had a largely facilitative function in the early stage of the BSE inquiry. In specific terms, this argument served to remove questions from inquiry when there was little prospect of scientists being able to address those questions and generated a number of propositions which could then serve as premises in further arguments about BSE. To this extent, the argument from ignorance was a rational and effective strategy of reasoning on the part of scientists who were confronted with pervasive uncertainty

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at the outset of the BSE inquiry. The question that we must now address is whether or not this remained the case in the epistemic conditions that obtained in the middle phase of inquiry. This phase was characterized by the emergence of findings about BSE from experimental studies (e.g. the CVL’s pathogenesis and attack rate studies) and natural transmissions (e.g. cases of feline spongiform encephalopathy). An evidential base on BSE thus began to develop at this time. If it can be demonstrated that this base contained information that weakened the ‘no evidence’ claims that form the premise of ignorance arguments, then there is a case for saying that ignorance reasoning was no longer warranted during the middle phase of inquiry. Alternatively, if it can be demonstrated that the information in this base had few, if any, implications for the ‘no evidence’ premise of these arguments, then there are clear grounds for maintaining that the argument from ignorance was still a rationally warranted strategy of reasoning in the middle phase of inquiry. I believe it can be shown, and will argue subsequently, that the developing knowledge of BSE in the middle phase of inquiry made it increasingly difficult for scientists to deploy the type of ignorance arguments that had served them well in an earlier stage of inquiry. We described in Chapter 4 how a claim of ‘no evidence’ could provide varying degrees of warrant for the conclusion of an ignorance argument. In cases where a knowledge base is closed or complete and an exhaustive search of that base has been undertaken, a ‘no evidence’ claim could provide deductive warrant for the conclusion of this argument. The assumption of epistemic closure or completeness combined with an exhaustive search, it was argued, could be realized in mundane and expert reasoning contexts. It was realized in the context of the question of the transmissibility of scrapie to humans, where no evidence of scrapie transmission to humans in 200 years despite extensive epidemiological investigations of the disease provided strong grounds for the conclusion that scrapie is not transmissible to humans. However, in the study of a newly emerging infectious disease like BSE, where an assumption of complete knowledge about the disease (or aspect thereof) cannot be made, the warrant that a ‘no evidence’ claim can provide for the conclusion of an ignorance argument inevitably falls short of deductive proof. Such arguments are invariably presumptive in nature. But even these presumptive arguments can be more or less warranted. In order to consider what, if any, presumptive warrant attended the ignorance arguments of the middle phase of inquiry, we shall discuss the following argument that was used by SEAC scientists during this phase. The argument turned on the proposition that British beef can be safely eaten (proposition p) and had the form ‘there is no scientific justification for not-p, therefore p’: PREMISE: CONCLUSION:

There is no scientific justification for the claim that British beef cannot be safely eaten. British beef can be safely eaten.

During the middle phase of the BSE inquiry, evidence emerged that had a more or less direct bearing on the question of the safety of beef for human consumption. Firstly, it became apparent to investigators that the oral route, through which humans

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would most likely be exposed to BSE, was a particularly efficient means of transmission of the disease. Previously unidentified spongiform encephalopathies had appeared in exotic ungulates and domestic cats by the time SEAC issued its advice about the safety of beef. Although these cases could not be definitively linked to BSE at the time,14 a food-borne source was considered the most likely route through which these animals were exposed to BSE infection. Also, a range of species which had been experimentally challenged through the oral route to BSE had been shown to be susceptible to the disease.15 Combined with the finding that the dose which was required to achieve transmission of BSE was considerably smaller than had been expected on the basis of scrapie studies (see Section 5.2.1), these natural and experimental transmissions of BSE through the oral route should have been a cause of significant concern for investigators. Secondly, it became apparent to investigators during the middle phase of inquiry that the various measures which had been taken to remove sources of BSE infection both from animal feed and from the human food chain were not doing so effectively. A sizeable number of cattle who were born after the ruminant feed ban still went on to develop BSE. Known as BABs, these animals could pass in a subclinical condition into the human food chain. Also, slaughterhouse practices were such that they were unable to achieve full compliance with the terms of the human SBO ban. In 1995, for example, it was discovered that there had been a number of occasions on which meat inspectors had applied a health stamp to carcasses to which fragments of spinal cord were attached (BSE Inquiry Report, Volume 1: 19). It took until December 1995 before the practice of extracting mechanically recovered meat (MRM) from the spinal column of cattle was banned. Through this practice, fragments of infective spinal cord that remained in the spinal column made their way into MRM.16 Furthermore, the human SBO ban had permitted an exemption in respect of tissues from calves less than 6 months old. But the CVL’s pathogenesis study produced results in 1994 which clearly indicated that these tissues carried infectivity. In short, there was every reason to believe that BSE infected beef was still making its way onto the plates of consumers. If humans were susceptible to BSE, they were certainly receiving exposure to the BSE agent in beef and beef products. Thirdly, in addressing the issue of the safety of beef, investigators inevitably had to consider the related issue of the susceptibility of humans to BSE. If it was known, for example, that humans were particularly resistant to BSE, an assessment of beef safety might not need to be so exacting about the level of infectivity to which people were exposed in beef. Short of actual transmission occurring, scientists resorted to the analogy with scrapie in determining human susceptibility to BSE. On the basis of this analogy, it could be argued that because humans were not susceptible to scrapie, they too would not be susceptible to BSE. However, most of the previous section was devoted to examining the weaknesses of this particular analogy. Certainly, these weaknesses precluded the making of any statements about the likely susceptibility of humans to BSE which might be based on this analogy. With scrapie analogy providing no evident support for the claim that beef is safe to eat and other evidence in the middle phase of inquiry pointing clearly in the direction that beef could not

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be safely eaten, the premise in SEAC’s ignorance argument above looks decidedly weak – there was, in fact, every justification for claiming that British beef could not be safely eaten. To the extent that the developing evidential base of the BSE inquiry fails to support the ‘no scientific justification’ premise of SEAC’s ignorance argument, the conclusion of this argument – British beef can be safely eaten – lacks even presumptive warrant. The changed epistemic conditions of the middle phase of inquiry, specifically the emergence of evidence that served to weaken claims regarding the safety of beef, found the use of the argument from ignorance by scientists could no longer be defended as a rationally warranted strategy of reasoning. Of course, it may be argued that other uses of the argument from ignorance during this period were warranted and that this single instance of the fallacious use of ignorance reasoning fails to undermine the rational standing of this argument form in the middle phase of inquiry. It is certainly the case that different evidential considerations apply to the question of whether the offspring of BSE cows should be used for breeding than apply to the question of the safety of beef. And it is possible that these different considerations may find certain ignorance arguments warranted where SEAC’s use of ignorance argument was clearly not warranted. But this objection misses the main thrust of the above discussion, which is that more advanced stages of a scientific inquiry often present difficult terrain for ignorance arguments. As a presumptive reasoning strategy, ignorance argument can be readily overturned by the emergence of contrary evidence. In the early stage of inquiry, where evidence relating to a particular question is limited in extent or lacking altogether, ignorance argument is afforded a degree of protection. If little or no evidence is available to investigators at the outset of inquiry, then there can be little or no contrary evidence on the basis of which an ignorance argument may be defeated. During later stages of inquiry, when evidence from experimental studies and other sources is forthcoming, ignorance arguments may find themselves vulnerable to rejection. However, if ignorance argument can survive the challenge of emerging evidence during these more advanced stages of inquiry, it can grow in epistemic stature. For at these stages, an evidential base relating to a particular question may be especially well developed. Such a base is thus more likely to satisfy the requirement in ignorance argument that a knowledge base be closed or complete. It remains to be seen if this situation obtains in the final stage of the BSE inquiry.

5.2.3 False Attribution of a Part to a Whole One of the most disconcerting discoveries during the middle phase of the BSE inquiry was the finding that the oral route was a considerably more efficient means of transmission of BSE than investigators had come to expect using the analogy with scrapie. This had implications not only for the transmission of BSE to humans through the consumption of beef but also through the ingestion of bovine-derived oral medicines. The range of these medicines was considerable at the time BSE emerged.17 An assessment of the risk, if any, that BSE posed to human health through the ingestion of these medicines fell to certain of the Section 4 committees

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(see note 5, Chapter 4). One of these committees, the Committee on the Safety of Medicines (CSM), received advice on BSE from two sub-committees, the BSE Working Group and the Biologicals Sub-Committee (BSC). The implications of BSE for human medicines were first discussed at a CSM/BSC meeting on 6 January 1988 and were still being addressed in March 1996, the end of the period we are considering in this book.18 Throughout this time, scientific advice repeatedly stated that no action needed to be taken in relation to oral products. The minutes of a meeting of the Biologicals Sub-Committee held on 2 November 1988 recorded that ‘[n]o immediate licensing action should be taken against oral products, in which bovine material has been used’ (BSC 1988: 2). Motivating this decision in relation to oral medicines was the view that the bovine material in oral medicines was so minimal in amount compared to that which is ingested in food that it was unlikely to pose any additional risk to human health.19 And to the extent that it could be argued that beef was safe to eat, then the minimal amount of bovine material in oral medicines would present no risk to human health. This reasoning is evident in a paper on BSE discussed at the November 1988 meeting of the Biologicals Sub-Committee. This paper was prepared by Drs Purves and Rotblat, a pharmaceutical officer and medical officer in the Department of Health, respectively: No action should be taken with regard to [oral] products in view of the widespread consumption of beef by the population at large (Purves and Rotblat 1988: 8).

In evidence to Lord Phillips and his inquiry team, Professor Collee (Chair of the Biologicals Sub-Committee) remarked of the decision by the CSM/BSC not to legislate against oral medicinal products: ‘we felt that it would be alarmist to take the view that BSE could be transmitted by the oral route, particularly in the case of orally administered medicinal products where the dose involved would be much smaller than in food’ (BSE Inquiry Report, Volume 7: 123). The issue of the safety of oral medicines was raised again in 1992 when concerns about gelatine20 were brought to the attention of SEAC.21 SEAC considered gelatine for the first time at its meeting in October 1992. In a letter to Professor Collee in advance of this meeting, Dr Kimberlin expressed the view that existing controls were sufficient to minimize any risk from gelatine and that it was still tenable to argue that gelatine presented a ‘very low risk with regard to BSE contamination’.22 In the event, the advice to emerge from SEAC’s meeting was that given existing regulations in relation to SBOs, gelatine posed a ‘negligible’ risk of BSE transmission to humans.23 It can be seen that scientific advice on the safety of oral medicines remained unchanged in the period between January 1988, when BSE was first discussed at a CSM/BSC meeting, and October 1992, when SEAC considered gelatine for the first time. The question which we must now address is whether that advice was rationally warranted and, if not, what features of the argument that was used to justify this advice can be shown to be problematic. For Lord Phillips and his colleagues, the decision by CSM/BSC not to take action on oral medicinal products and the grounds for this decision were essentially sound. In consideration of this episode in the BSE affair, the inquiry team concluded:

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It seems to us that careful consideration was given to the question of oral transmission via medicinal products by the experts who sat on the Section 4 committees and by the HVMBG (BSE Inquiry Report, Volume 7: 123).24 We felt that it was not unreasonable for the Section 4 committees to assume that if it was safe to eat meat, it must be safe for humans to eat the minimal amount of bovine material contained in oral medicines such as gelatine in capsules (BSE Inquiry Report, Volume 1: 178).

The second of the above extracts captures succinctly the line of reasoning that consistently led scientists to the view that bovine-derived oral medicines presented little or no risk to human health and, as such, required no legislative action. A reconstruction of the reasoning of this extract produces the following two-premise argument: MAJOR PREMISE: MINOR PREMISE: CONCLUSION:

If it is safe to eat meat, then it is safe to consume bovinederived oral medicines. It is safe to eat meat. It is safe to consume bovine-derived oral medicines.

The deductive validity of this argument is not in question. It is an example of modus ponens, a valid inference of the form if p then q, p, therefore q. But while the validity of the argument is assured, what can be questioned is the rational warrant that attends each of the premises. We have already seen how the minor premise, ‘It is safe to eat meat’, received some degree of presumptive warrant from the analogy with scrapie that shaped many of the early risk assessments relating to BSE. If scrapie had failed to transmit orally to humans through the ingestion of sheep meat, then it was unlikely, scientists argued, that BSE would transmit orally to humans through the ingestion of beef. The scientists of the Section 4 committees also drew upon this analogy when considering the risks that medicinal products presented to human health.25 Notwithstanding its initial presumptive warrant, this analogy appeared increasingly problematic during the middle phase of inquiry, when scientific findings and developments meant that scientists could no longer plausibly argue that BSE would behave like scrapie. With its analogical basis now in question, the minor premise lacked the rational warrant it had at an earlier stage of inquiry. But of greater interest in the present context than the changing fortunes of the minor premise is the rational standing of the argument’s major premise. The grounds of this premise can be formulated as follows: If meat is safe to eat, then any part of meat is safe to eat.

As stated here, these grounds are entirely reasonable – the property ‘is safe’ is divisible between the whole (meat) and its parts (parts of meat). Despite their reasonableness, these grounds support the major premise of the above argument in appearance only. The oral medicines that are mentioned in that premise contain the bovine product gelatine, a product that is not properly a ‘part of meat’ (‘meat’ was taken to mean ‘skeletal muscle’ by the Section 4 committees). Moreover, while it was believed that meat (beef) posed little or no risk to humans, there was every reason to believe that gelatine could present an altogether greater level of risk.

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A potential route of BSE contamination, for example, was from CNS material (brain and spinal cord) in skulls and vertebrae used in the preparation of gelatine, as Mr Bradley (Head of Pathology Department, CVL) remarked in a letter to Mr Lowson (Head of Animal Health (Disease Control) Division, MAFF) on 25 September 1992: Skulls and vertebrae especially of old UK dairy cows, as a source of tallow or gelatin may increase the risk that some infectivity could be present in the raw material. Thus it is essential we are satisfied that in all cases where tallow or gelatin is used in medical or cosmetic products, it is safe (Bradley 1992: 1–2).

and as Dr Kimberlin also remarked in a letter to Professor Collee on 31 July 1992: Potentially, vertebrae are a much greater source of contamination because of the associated spinal cord, with a far lower contribution, in terms of weight and infectivity titre, from spinal nerves. However, the greatest potential source of BSE contamination would be from whole skulls containing brain (Kimberlin 1992: 2).

If the raw material used to produce gelatine contained the BSE agent, then scientists needed to be confident that the manufacturing processes26 used in gelatine production would be effective in eliminating it. But here, again, there was reason to believe that such elimination might not occur. The BSE agent could be expected to display the same extraordinary resistance to physical and chemical challenge that is exhibited by the agents that cause other prion diseases (see Section 1.2.5 and note 2 in Chapter 1). In such a case, even very robust manufacturing processes might be found to be incapable of destroying this agent. As it happened, concern was expressed that the manufacturing processes used to produce gelatine might prove to be inadequate in eliminating the infectious agent in BSE: [S]ome manufacturers do include vertebrae and skulls, and it is only in this context that I might have some doubts about the ability of the subsequent processing to remove and inactivate BSE contamination (Kimberlin 1992: 2).

or at best represented something of an unknown and should be further investigated: It is possible that gelatin is of low risk with regard to BSE contamination, but there are justifiable anxieties when the source material includes brain and spinal cord of cattle (or sheep) from countries with known cases of BSE or at risk of having BSE cases. Validation studies to demonstrate the safety of processing and extraction procedures in this context would be commendable. . . (Collee 1992: 1).

In short, investigators were on the shakiest of grounds in claiming that gelatine (and, by implication, the oral medicines that contain gelatine) presented a negligible risk of BSE to humans. From contaminated source material to deficiencies in manufacturing processes, there was every reason to believe that gelatine carried a risk of BSE infection. Even more problematic was the attempt by scientists to argue that if meat was safe to eat, then bovine-derived oral medicines would also be safe to eat. For, as we have seen, an important ingredient within these medicines, gelatine, was derived from bovine tissues that could harbour considerable BSE infectivity in the form of CNS material. Gelatine was not in any sense a ‘part’ of meat and could not therefore assume the properties, including the property of ‘being safe’, that could

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be attributed to meat. In arguing that oral medicines were safe to eat on the grounds that meat was safe to eat, scientists had made a false attribution of a part (gelatine) to a whole (meat). To the extent that this attribution was not warranted given what was known about bovine ingredients in oral medicines, scientists in the Section 4 committees who considered the issue of the safety of these medicines may be said to have argued fallaciously. This point warrants further consideration. The argument of the Section 4 committees in support of the safety of medicines fails in the final analysis, not through any lack of logical warrant between the premises and conclusion – this argument has a deductively valid form27 – but because the content of the major premise could not be substantiated given what was known at the time about bovine products in oral medicines. Specifically, it could not be reasonably argued that if meat was safe to eat, then oral medicines would also be safe to eat. Meat and gelatine in oral medicines were derived from distinct types of bovine tissue and, if the experience of scrapie had taught investigators anything, it was that different types of tissue carried quite different levels of infectivity. So, in effect, no conclusion could be drawn about the level of BSE infectivity in gelatine in oral medicines on the basis of the level of BSE infectivity in meat.28 Meanwhile, other evidence tended to suggest that the infectious agent of BSE could be present to a significant extent in gelatine – the source material used in the production of gelatine could not be guaranteed to be free off the BSE agent, while manufacturing processes were unlikely to effectively eliminate the agent. It emerges that yet another argument during the middle phase of the BSE inquiry failed to support the dominant view that BSE would have few, if any, implications for human health. That this view continued to hold, notwithstanding its lack of supporting arguments, is an indication of the extent to which the argumentative structure of the BSE inquiry had departed from any logical base. It was no longer the rationally motivated structure that had characterized the early phase of the inquiry into BSE. Indeed, this structure was now entirely dependent on a number of fallacious argument forms which, at best, provided it with the appearance29 of rational warrant. Before examining the arguments that were advanced by scientists during the final stage of the BSE inquiry, one further comment is in order about the fallacious argument that we have been calling false attribution of a part to a whole. In Chapter 4, we described how the notion of a standard list of fallacies, which contained an invariant set of members, was something of a fallacy theorist’s fiction. In support of this claim, we argued that traditional fallacies could be shown to have non-fallacious variants in certain contexts of use. Also, other argument forms not included in the standard list could nevertheless be shown to be weak or fallacious arguments. In Chapter 4, we examined several examples of how traditional fallacies were anything but fallacious in the context of early scientific inquiry into BSE. In this chapter, we have now seen an example of a novel fallacy, an argument that is evidently fallacious but which is not part of the fallacy theorist’s standard list. These examples clearly demonstrate that there is no such thing as an inherently weak form of argument, as is assumed by the notion of a standard list of fallacies. Rather, arguments assume quite different rational attributes within the various contexts in which they occur and it is to an examination of those contexts that we must turn to establish those attributes.

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5.3 Summary The discussion of Chapters 4 and 5 has served to demonstrate the varied epistemic conditions that attend different stages of a scientific inquiry into an emerging infectious disease. At the outset of inquiry, when few, if any, experimental studies have been conducted, scientists are often confronted with an extensive lack of knowledge and uncertainty. This is particularly true in the case of a transmissible spongiform encephalopathy such as BSE, where the long incubation period of these diseases ensured that it would be some months and even years before the most rapidly initiated experimental studies would begin to yield results. During the adverse epistemic conditions of early inquiry, scientists were shown to use reasoning strategies which, it was argued, are adapted to contexts of uncertainty. In the last chapter, we described several such strategies and examined how these arguments served to facilitate inquiry when little was known about BSE. The purpose of this chapter has been to demonstrate that the epistemic conditions of the early stage of BSE inquiry were not replicated in the middle phase of this inquiry and that the reasoning strategies used by scientists during the early months and years of the BSE crisis were poorly adapted to the quite different epistemic conditions that obtained during the middle years of this crisis. The emergence of experimental results and other findings about BSE during the middle stage of inquiry substantially altered the evidential base that scientists used to formulate their risk assessments. It is against this developing base that previously warranted ignorance and analogical reasoning strategies began to appear less able to support scientific assessments that BSE posed little risk to human health. To characterize the impact of changing epistemic conditions and a developing evidential base on the reasoning of scientists during the middle phase of inquiry, a distinction was drawn between the argumentative strategy of this inquiry and the arguments that may or may not provide this strategy with rational warrant. In the early phase of the BSE inquiry, these two argumentative levels of inquiry operated in tandem, with the argumentative strategy receiving rational validation from the arguments that scientists used to justify their risk assessments. As evidence relating to BSE started to emerge in the middle phase of inquiry, the argumentative strategy of inquiry began to depart from the analogical and other arguments that had previously validated this strategy. Although scientists continued to produce claims to the effect that BSE posed little risk to humans and that beef was safe to eat as part of the overarching argumentative strategy of inquiry, it was shown that these claims no longer received rational validation from the arguments that scientists advanced during the middle stage of inquiry. These arguments were essentially fallacious and provided the argumentative strategy with rational warrant in appearance only. The fallaciousness of these arguments, it was argued, was not an inherent property of the structures concerned. After all, many of the same logical structures had functioned non-fallaciously in the early phase of inquiry and some of these structures were even deductively valid. Rather, the fallaciousness of these arguments only became apparent when they were examined within the epistemic contexts in which they were advanced. It was only by examining these contexts that we were able to reveal the

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evidential and dialectical features of inquiry against which these arguments were found to be lacking. We will have more to say about these features, particularly dialectical aspects of inquiry, in the next chapter. In summary, the contribution of the current chapter to the model of scientific reasoning being developed in this book can be captured in logical terms on the one hand, and in scientific terms on the other hand. In logical terms, the main lesson to emerge is that one and the same argument form can exhibit significant merits in one epistemic context and attract substantial criticism in another epistemic context. Logicians need to dispense with the idea that there are inherently good or rationally warranted arguments (as well as bad or rationally unwarranted arguments) and that these can somehow be determined in advance of an examination of the contexts in which these arguments are advanced. It is only by rejecting this idea that logicians can begin to develop new modes of reasoning which can address uncertainty and other epistemic challenges. In scientific terms, the main lesson to emerge is that inquiry is an evolving process that pursues a course through distinct phases characterized by different evidential standards and epistemic conditions. The scientist cannot afford to operate with a fixed set of cognitive strategies, principally reasoning strategies, which are applied in a uniform fashion throughout an inquiry. Scientific investigators must be attune to the evidential standards and epistemic conditions that operate at different stages of inquiry and be capable of responding to these standards and conditions with appropriately adapted reasoning strategies. Deductive modes of reasoning will almost certainly be amongst these strategies. But equally, there must be a place for non-deductive reasoning strategies within the scientist’s cognitive toolkit. This toolkit contains, in particular, the various argument forms discussed in these chapters. This is despite the fact that these arguments failed to support scientific assessments of risk during the much altered epistemic conditions of the middle phase of the BSE inquiry.

Notes 1. None of these argument forms are ‘new’ in a historical sense. As the discussion of Chapter 3 demonstrated, informal fallacies such as question-begging argument and the argument from ignorance have a very long history in philosophical thought. These arguments are not even ‘new’ in the sense that BSE scientists were the first group of investigators to use them – I discuss in Cummings (2004c), for example, how analogical reasoning was employed by scientists during early work in relation to HIV/AIDS. The sense in which these arguments are ‘new’ is that this is the first attempt to give these arguments prominence within an account of scientific reasoning in contexts of uncertainty. 2. These members were Professor Fred Brown (a virologist), Professor Ingrid Allen (a neuropathologist), Professor Richard Barlow (a pathologist and veterinarian), Mr David Pepper (a veterinary surgeon), Professor John Pattison (SEAC Chairman from November 1995), Professor John Collinge (Head of the Neurogenetics Unit at St Mary’s Imperial College School of Medicine), Dr Michael Painter (a consultant in communicable disease control with a public health background), Professor Peter Smith (an expert on human epidemiology and statistics of the London School of Hygiene and Tropical Medicine), Professor Jeff Almond (an expert in virology and immunology from the School of Animal and Microbial Sciences at the University of Reading) and Mr Ray Bradley (a MAFF observer since SEAC’s inception

Notes

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4.

5.

6. 7.

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and later member of SEAC). Dr William Hueston, an American scientist trained in veterinary medicine and epidemiology, replaced Professor Barlow in 1994 following his resignation. Based on an examination of British national press coverage of BSE between 1988 and 1996, Miller (1999: 1247–1248) states that BSE ‘became a significant public issue on two occasions. . .when “Max” the cat was revealed to be infected in May 1990. . .and in March 1996 when the government stated that BSE was the “most likely” cause of new variant CJD’. We discuss the latter event subsequently in the main text. The Committee concluded that ‘[t]he Government has already acted to cut off the presumed source of the disease in cattle and has banned the sale of all specified cattle offals for human consumption. We believe these measures should reassure people that eating beef is safe’ (BSE Inquiry Report, Volume 1: 131). Professor Lamming’s group concluded that ‘[t]he evidence suggests that in the majority of cases, the controls are working, despite the fact that the ruminant protein ban and the specified bovine offals ban are to a considerable extent dependent on self-regulation by the industry. However, there are indications that some cattle may have had access to ruminant meat and bone meal since the 1988 ban and it is thought that this may account for most of the 69 confirmed cases of BSE in cattle which, up to 5 June 1992, have been born after the ruminant feed ban was introduced. The majority were born shortly after the statutory intervention. This number is small compared with the earlier incidence, but it suggests that the integrity of the ban is not complete’ (BSE Inquiry Report, Volume 5: 36). This letter and annex were entitled ‘The epidemic of BSE and the public health implications of eating beef’. SEAC’s claim that the oral route would prove to be a particularly inefficient route of BSE transmission was also based on what was known about the efficiency of different routes of transmission of BSE to mice. The annex to SEAC’s letter stated that ‘[i]n the transmission work done to date with BSE, the incubation period in mice was longer after a large oral dose of BSE-infected cattle brain than after much smaller parenteral injections [Fraser et al. (1988) Vet Rec 123:472 and Barlow and Middleton (1990) Vet Rec. 126:111–112].’ (BSE Inquiry Report, Volume 11: 60). Of course, an analogical argument is at work here also. It can be reconstructed as follows: MAJOR PREMISE: MINOR PREMISE: CONCLUSION:

Transmission efficiency of BSE in humans is similar to transmission efficiency of BSE in mice. In mice, the oral route of transmission of BSE is inefficient. In humans, the oral route of transmission of BSE will be inefficient.

8. Kimberlin and Walker’s paper is entitled ‘The role of the spleen in the neuroinvasion of scrapie in mice’. 9. The minutes of the second SEAC meeting held on 17 May 1990 state in relation to spongiform encephalopathy in cats: ‘It would be premature to draw conclusions at this stage’ (SEAC 1990a: 3). The minutes of the third SEAC meeting held on 13 June 1990 record that ‘[t]he Committee was in no position to offer advice on the implications for human health until more was known about the condition’ (SEAC 1990b: 2). 10. This is a response to a possibility raised by SEAC when it first considered cat spongiform encephalopathy at its second meeting on 17 May 1990. The Committee felt that one possible explanation of this disease in cats was that it was a pre-existing disorder which had not ‘been recognised previously in view of the rarity of cat neuropathological studies’. 11. Several reports of novel spongiform encephalopathies in exotic ungulates emerged between November 1989 and June 1994. The exotic ungulates in question were an eland (Fleetwood and Furley 1990), an Arabian oryx (Kirkwood et al. 1990) and a greater kudu (Cunningham et al. 1993; Kirkwood et al. 1990, 1992, 1994). Additionally, reports emerged in the same period of spongiform encephalopathies in non-domestic cats including a puma (Willoughby et al. 1992) and a cheetah (Peet and Curran 1992). Like exotic ungulates, these species had not been shown to be susceptible to scrapie through natural transmission.

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12. Lord Phillips and his inquiry team remarked of this finding: ‘One of the strangest features of the BSE story is the fact that nobody appears to have attached significance to the results of the NPU BSE into sheep experiment. The first point of significance was that BSE transmitted into negative line sheep, which were not susceptible to scrapie. This was one of a number of factors which threw doubt on Mr Wilesmith’s theory as to the nature of the agent’ (BSE Inquiry Report, Volume 6: 521). 13. The minutes of the meeting record that ‘[w]hat was somewhat unexpected was the fact that infectivity was present by 6 months and could not be ruled out at any time between 2 and 6 months. In natural sheep scrapie there is no infectivity in any tissue at 8 months though infectivity is found at 10–16 months’ (SEAC 1994a: 2). 14. It wasn’t until 1994 that strain-typing studies revealed that cases of spongiform encephalopathy in domestic cats were linked to BSE. In a study of transmission of FSE to mice, Fraser et al. (1994: 449) concluded ‘[t]he ranking of incubation periods between the mouse strains inoculated with FSE is similar to that for BSE and differs from scrapie. . .The lesion profile in mice inoculated with FSE also resembles that observed in mice inoculated with BSE, rather than scrapie. . .Furthermore, material from all three cats transmitted the condition to all the inoculated mice, comparable to the consistent transmissions from BSE, whereas not all cases of scrapie transmit to mice. . .Thus the similarities indicate that BSE and FSE probably arose from a common source’. Kirkwood and Cunningham (1994: 300–301) advance similar findings in relation to exotic ungulates to support their claim that spongiform encephalopathy in these species is caused by the BSE agent: ‘Four pieces of evidence support this hypothesis. . .the similarity of the pattern of variation in the incubation period in six strains of mice inoculated with brain homogenates from a kudu and a nyala, to the pattern observed when mice have been inoculated with brain homogenates from BSE-affected cattle and brain homogenates from sheep, goats and pigs that had been experimentally infected with BSE. . .there were no significant differences in the character or distribution of the histological and ultrastructural lesions between the mice inoculated with the kudu and nyala brain homogenates and the mice inoculated with brain homogenates from BSE-affected cows’. 15. During the middle phase of inquiry, the species that had been shown to be susceptible to BSE by being experimentally challenged through the oral route included sheep and goats (Foster et al. 1993), mice (Middleton and Barlow 1993), mink (Robinson et al. 1994) and cattle (Wells et al. 1994). 16. In a generally critical assessment of the handling of the MRM problem, Lord Phillips and his inquiry team remarked that ‘[t]he potential risk posed by MRM called. . .for consideration by those in the Meat Hygiene Division with knowledge of slaughterhouse conditions and practices and of the extent to which the spinal column was likely to contain portions of spinal cord, or to be contaminated with this as a result of the process of carcass-splitting. This does not appear to have received vigorous consideration’ (BSE Inquiry Report, Volume 6: 240). 17. Richard Kimberlin (1993) prepared a report for The Wellcome Foundation Ltd. in which he examined the risk of several ingredients of bovine origin (gelatin, casein, lactose, magnesium stearate) for a number of oral medicines that were manufactured by the company. The drugs in question were Semprex capsules, Pro-Actidil tablets and Zyloric tablets. 18. In a paper on 8 March 1996, Dr Eileen Rubery of Health Aspects of Environment and Food Division wrote: ‘Other routes of exposure need to be considered. Cat-gut and vaccinations are invasive activities that a large proportion of the population are exposed to. Could either of these routes be the actual route of exposure? What about gelatine capsules for pharmaceuticals, and gelatine capsules for health foods? Do we need to take any further action to control potential exposure via these routes?’ (BSE Inquiry Report, Volume 7: 320). 19. Following the first meeting of the Southwood Working Party on 20 June 1988, Dr Pickles (DoH Principal Medical Officer) wrote in a letter to Dr Jones (Medicines Division): ‘For oral products, there would only be a trivially increased load on top of that taken in food in omnivores/carnivores including man’ (BSE Inquiry Report, Volume 7: 64).

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20. At the time of the BSE crisis, gelatine was used in various medicinal products including capsules, pastes, pastilles, tablets and suppositories. It was also used as a blood volume expander. Gelatine was produced from bovine bones and hide using a process of acid/alkaline hydrolysis which produces very harsh chemical and physical conditions. 21. Concerns were expressed to Professor Collee by two attendees at a meeting on TSEs which was held in Heidelberg. Dr Minor (Head of Virology at the National Institute for Biological Standards and Control) described how ‘[a]t a recent meeting in Heidelberg a gentleman from a gelatin manufacturing concern presented an account of the process which was very worrying. As you know, the assumption has been that gelatin is produced under such vigorous conditions that it gives no cause for concern, but the process he described was, to me, shockingly mild. Moreover he claimed that any old cow bone went into the production vat, including spine and skull. . .’ (BSE Inquiry Report, Volume 7: 184). Dr Taylor (Principal Research Scientist, Neuropathogenesis Unit) remarked that ‘[l]ike Philip [Minor], I was not impressed by the reassuring noises made. . .at the Heidelberg meeting. However, I am not really familiar with gelatin manufacturing processes in the UK. . .I would certainly be concerned if it is produced by a similar procedure to the German process described at the meeting’ (BSE Inquiry Report, Volume 7: 184–185). 22. ‘My experience of the manufacture of gelatin leaves me uncertain about the NEED to take any actions other than those already put into effect with regard to countries known to have BSE. After all, the potential risks from brain and spinal cord are automatically dealt with in those countries (e.g. U.K., Switzerland) which have instituted a specified bovine offals ban. . .The general assumption that gelatin is of very low risk with regard to BSE contamination is still tenable’ (Kimberlin 1992: 2–3). 23. The minutes of SEAC’s meeting in October 1992 record that: ‘So long as brains were excluded from the manufacturing process, the risk that agent might be present in gelatin was negligible. . .Bovine material used in the manufacture of gelatin for [injection or implantation, or taken by mouth] should exclude specified offals, as well as skulls and vertebrae’ (SEAC 1992b: 7). 24. The Human and Veterinary Medicines Briefing Group (HVMBG) reviewed papers that were prepared for the CSM and formulated advice to the CSM on BSE in general. It was not one of the Section 4 committees or one of the sub-committees that provided advice to the Section 4 committees. It had a diverse membership including Dr Jefferys, Dr Adams, Dr Purves and Dr Rotblat from Medicines Division; Dr Minor and Dr Schild from the National Institute for Biological Standards and Control; Professor Collee from the CSM/BSC; Dr Pickles on behalf of the Southwood Working Party; and Mr Kidd, Mr Bradley, Mr Taylor, Mr Scollen and Dr Little on behalf of MAFF. 25. In evidence to Lord Phillips and the inquiry team, Professor Asscher (Chair, Committee on Safety of Medicines) remarked: ‘The CSM was, however, aware of the issues involving CJD and human growth hormone at this time and of the occurrence of CJD following dura mater implants. They had come to our attention in the course of considering product licences for dura mater. These experiences made us particularly wary of parenteral, as compared to oral, medicinal products. At the time, the fact that scrapie had not transmitted to man also gave us reassurance that BSE was unlikely to be acquired by the oral route’ (BSE Inquiry Report, Volume 7: 73). 26. A detailed account of these processes is given on pages 122–124 in Volume 13 Industry Processes and Controls of the BSE Inquiry Report. 27. It is not uncommon for arguments to have a deductively valid form but still be fallacious. The most prominent example of a fallacy that is deductively valid is question-begging argument (see note 30 in Chapter 4). 28. In fact, for most of the period in which the Section 4 committees based their assessment of the BSE risk of oral medicines on the safety of meat, these scientists did not have specific experimental findings relating to the infectivity of bovine muscle. The infectivity of different bovine tissues was investigated in a study undertaken by the Neuropathogenesis Unit in

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Edinburgh. This study produced preliminary results in 1992. Fraser et al. (1992) reported that bioassays of spleen, lymph nodes, semen, buffy coat (a laboratory term for white blood cells) and muscle from a BSE affected cow failed to produce disease in RIII mice (a Sinc s7 homozygous strain) in an observation period of over 800 days. 29. By definition, fallacies must at least create the appearance of being rationally warranted arguments: ‘A fallacy is committed when an argument that is not good nonetheless appears good’ (Powers 1995: 287; italics in original); ‘we can define a fallacy as any error or weakness that detracts from the soundness of an argument, yet somehow manages to disguise this weakness so as to give the argument the appearance of being better than it really is’ (Hughes and Lavery 2004: 108). In the same way, the fallacious arguments advanced in support of the argumentative structure of the BSE inquiry conferred only the appearance of rational warrant on this structure, at least in the middle phase of that inquiry.

Chapter 6

An Unchallengeable Scientific Consensus

6.1 Introduction It was described in the last chapter how during the middle years of the BSE inquiry, the adverse epistemic conditions of the early stage of inquiry were replaced by findings from experimental studies into BSE and from natural transmissions of the disease to a number of other species. The emergence of these findings changed in a significant way the evidential base that scientists used in their risk assessments and other deliberations relating to BSE. The expansion of this base found many of the reasoning strategies that scientists had used at the outset of inquiry lacking the rational warrant they had enjoyed in this early phase of inquiry. In the period between June 1994 and March 1996 (the ‘final years’), this lack of rational warrant persisted in an even more pronounced form. During this time, scientists continued to use many of the same arguments that had dominated the early and middle phases of the BSE inquiry. But in the absence of any rational warrant, these arguments supported scientific pronouncements about risk in appearance only. In short, by the time scientists were assessing the implications of the CVL’s pathogenesis study in June 1994, an unassailable scientific consensus had formed to the effect that beef was safe to eat and that BSE posed little, if any, risk to human health. So widespread was this consensus that few scientists even attempted to challenge it. Where such challenge did occur, it was often ignored, dismissed or otherwise invalidated. What had started in the middle phase of inquiry as a separation of the argumentative strategy of inquiry from the arguments that were advanced as its rational base was effectively complete in the period between June 1994 and March 1996. The result was the persistence of claims which attempted to reassure the public that BSE posed little risk to human health, but which did so in the absence of their own rational warrant. The period between June 1994 and March 1996 was marked by a number of key developments in the reasoning of scientists. The dominant scrapie analogy, which was already weakened by the emergence of scientific findings in the middle phase of inquiry, was dealt a number of serious blows during this period. Although it could no longer be plausibly argued that BSE would behave like scrapie – the evidence by this stage indicated that BSE behaved very differently from scrapie – scientists continued to use this analogy in their risk assessments and other deliberations. Even more surprising is the fact that this analogy was still dominating scientific thinking L. Cummings, Rethinking the BSE Crisis, DOI 10.1007/978-90-481-9504-6_6,  C Springer Science+Business Media B.V. 2010

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at a time when scientists were beginning to revise earlier decisions and judgements that had been based on it. The ‘no evidence’ claims that are integral to the argument from ignorance occurred with predictable frequency during the months between June 1994 and March 1996. These claims were already beginning to lose rational warrant during the middle phase of inquiry when scientific findings about BSE started to emerge. In the final phase of inquiry, this loss was all but complete when investigators began to uncover evidence of a novel form of CJD in young people. Other forms of fallacious reasoning were also evident during the final phase of inquiry. We will see, for example, that SEAC scientists committed the fallacy of arguing to the wrong conclusion during their assessment of the risks that blood and blood products may pose for the transmission of CJD. The failure of each of these forms of argument to provide rational warrant for the conclusions they purport to justify is an indication of the extent to which scientific pronouncements of risk had strayed beyond any evidential base by the final stage of the BSE inquiry. We will return to these points subsequently.

6.2 The Final Years: 1994–1996 Although the shortest of the three periods that we will consider, the time between the release of results of the CVL’s pathogenesis experiment in June 1994 and the announcement in March 1996 to British Parliament that BSE was the most likely cause of cases of CJD in young people was anything but an uneventful time in the BSE crisis. These final years of the BSE inquiry commenced with an event of huge significance. The discovery of infectivity in the distal ileum (small intestine) of a calf which had been orally infected with BSE less than 6 months earlier in a pathogenesis experiment at the CVL caused considerable consternation. Previously, only the brain and spinal cord of BSE cattle had been found to be infective. Moreover, calves less than 6 months had been excluded from the human SBO ban on the grounds that lambs of a similar age did not display infectivity. MAFF responded by seeking an immediate extension of the human SBO ban to include the distal ileum of calves. Also in June 1994, the ELISA test,1 which had been developed in order to detect ruminant protein in animal feed, was first used to conduct on-farm testing. The farms that were selected for testing were those on which BABs had occurred. By September 1994, an attack rate experiment initiated at the CVL in January 1992 was beginning to reveal that even 1 g of brain homogenate administered orally to cattle was sufficient to cause BSE. This finding was confirmed by histopathological examination in February 1996. It was a surprise to investigators who had expected, based on the experience of scrapie, that the oral route would not be a particularly efficient route for the transmission of BSE to cattle.2 Further attempts were made in 1995 to reduce the risk of transmission of BSE to humans. In December 1995, MAFF introduced a ban on mechanically recovered meat (MRM) from the spinal column of cattle following a recommendation from SEAC. Even at this stage, however, there were indications that such a ban was too late to prevent the very event it was designed to avert. Deaths among dairy farmers

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who had had cases of BSE in their herds continued in this period. In December 1994, a third dairy farmer died of CJD (the first two farmers died in October 1992 and August 1993). The Chief Medical Officer was made aware of a fourth case of CJD in a dairy farmer on 29 September 1995. Although these cases were not thought at the time to be linked to BSE – and this is still the case today3 – their emergence generated public anxiety and considerable media interest. Of much greater significance in this period was the growing number of young people who had developed CJD. At an emergency meeting of SEAC held on 16 March 1996, Dr Will of the CJDSU reported that there had been nine confirmed cases and three suspect cases of CJD in young patients. These cases constituted ‘a distinct entity unlike any previously seen in CJD’ according to three independent neuropathologists (BSE Inquiry Report, Volume 1: 157). In a statement to Ministers, SEAC stated that ‘[t]his is cause for great concern. On current data the most likely explanation at present is that these cases are linked to exposure to BSE before the introduction of the SBO ban in 1989’ (BSE Inquiry Report, Volume 1: 158). On the afternoon of 20 March 1996, Mr Stephen Dorrell, the Secretary of State for Health, made an announcement to this effect to the House of Commons. This announcement takes us up to the end of the period we are considering in this study, a period which had seen some 160,000 cattle slaughtered as a result of BSE and the beginnings of a related human health crisis (BSE Inquiry Report, Volume 1: 19).

6.2.1 Argument from Analogy The reader of Section 5.2.1 might be forgiven for thinking that the final phase of the BSE inquiry would see scientists engaging quite differently with the type of analogical reasoning based on scrapie that had dominated the middle phase of inquiry. After all, during the middle years of the inquiry, evidence from scientific experiments and natural transmissions had clearly indicated that the pathogenesis and host range of BSE differed in significant ways from these same disease characteristics in scrapie. In particular, the finding of BSE infectivity in the distal ileum of calves in the CVL’s pathogenesis study had forced SEAC scientists to seek an extension to the human SBO ban. This move constituted a revision of an earlier decision in which the scrapie analogy had been used to justify an exemption for certain bovine tissues. It might be thought that these developments would be enough to lead scientists in the final phase of inquiry to overturn the scrapie analogy or at least to question its validity as a rational basis for scientific risk assessments. In the event, neither scenario occurred in the months between June 1994 and March 1996. What we find instead is an analogy that had relinquished its defeasible, presumptive character and that had assumed the status of an irrefutable thesis. In the discussion to follow, we will examine the pernicious consequences that this unassailable thesis had on the conduct of inquiry. These consequences stem from the suspension of the normal operation of dialectical presumption and burden of proof in inquiry. Amongst other things, this suspension required dissenting scientists who opposed the scrapie analogy to discharge an excessive burden of proof in order to overturn this analogy.

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However, we begin by considering some of the questions that were addressed by scientists through use of the scrapie analogy during the final phase of inquiry. Scientists continued to undertake risk assessments during the final years of the BSE inquiry. In September 1994, SEAC published a report entitled ‘Transmissible Spongiform Encephalopathies: A Summary of Present Knowledge and Research’. In Chapter 5 on transmission in this report, SEAC scientists reaffirmed their longstanding view that BSE posed little risk to human health: ‘our scientific assessment is that the risk to man and other species from BSE is remote’ (SEAC 1994b: 72). This risk assessment was based in large part on the dominant analogy between BSE and scrapie, as is evident from the following extract from the report: The risk to man from BSE depends on the inherent risk that the BSE agent is a human pathogen, which cannot yet be evaluated, and on the level of exposure to the pathogen, which can. Since scrapie was first clearly described in the literature of the 18th century there has been no epidemiological linkage of the disease, or indeed any animal TSE, with human disease, or vice versa. This does not prove there is no risk, but it suggests that any risk is probably small (SEAC 1994b: 71–72).

We described in Section 4.2.1 how the scrapie analogy generated early research studies into BSE. This function of the analogy was again evident during the final stage of the BSE inquiry. In February 1995, the Chief Veterinary Officer Mr Keith Meldrum sent a research findings update to MAFF’s Permanent Secretary. These findings had emerged during a recent review of MAFF research and development on TSEs.4 An embryo transfer experiment in sheep, which had been undertaken at the Neuropathogenesis Unit, had produced ‘some disturbing results’. This experiment was expected to demonstrate that properly washed embryos from scrapie infected sheep would not transmit infection. In the event, some of the offspring from this experiment went on to develop scrapie. This result raised the possibility that scrapie could be spread through semen.5 Mr Meldrum was concerned that the implications of this finding for BSE should be examined through the institution of relevant experimental research.6 To this end, the role of semen in BSE transmission was added to MAFF’s existing research on BSE epidemiology.7 The rational standing of the scrapie analogy was considerably weakened by developments in knowledge of BSE in the middle and final stages of inquiry. Notwithstanding this fact, this analogy – as the current example demonstrates – still continued to exert considerable influence on the research priorities of this inquiry. Such was the power of the scrapie model over the BSE inquiry that it also spawned a number of other analogies which were used in risk assessments between June 1994 and March 1996. An analogy between scrapie and CJD in humans8 was integral to deliberations concerning the safety of blood and blood products. SEAC scientists considered the risk of person-to-person transmission of CJD through blood transfusions and the use of plasma at its 22nd and 23rd meetings, which were held in November 1995 and January 1996, respectively. These scientists judged that blood transfusions and blood products posed a ‘very small risk’ of CJD transmission and that no new measures were required to address this risk.9 This risk assessment was consistent with the scientific view that human blood was safe as blood and plasma

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had not been found to contain scrapie infectivity. This view was expressed in a briefing note prepared by Mr John Sloggem, a Department of Health Pharmaceutical Officer, for a meeting of the Biologicals Sub-Committee on 1 November 1995:10 There is no experimental evidence in animals to suggest that CJD is transmitted by whole blood or plasma. Plasma being cell free is thought safer because scrapie infectivity is tissue associated and sheep plasma – cell free – appears clear of scrapie infectivity (Sloggem 1995: 1; bold in original).

From shaping risk assessments to setting research priorities, scrapie analogy continued to influence scientific deliberations about BSE in the final stage of inquiry into this disease. However, this analogy was so extensively weakened by the final phase of this inquiry that it was not able to confer rational warrant on these deliberations. By the time SEAC scientists undertook their risk assessment of BSE in September 1994, substantial evidence about BSE from experimental studies and natural transmissions had already been amassed by investigators. And that evidence increasingly indicated that BSE and scrapie differed in significant ways. Notwithstanding this fact, scientists continued to accede to this analogy, even to the point of countering possible presentational difficulties that experimental results may pose for this analogy.11 Of course, not all scientists were equally eager to defend this analogy. A small number of scientists did attempt to challenge this analogy. Chief amongst them were Professor Richard Lacey (Professor of Clinical Microbiology, University of Leeds) and Dr Stephen Dealler (Consultant Microbiologist, Burnley General Hospital). However, the challenges of these scientists were often to no avail in a context in which the normal operation of dialectical presumption and burden of proof in inquiry was suspended. In effect, the claims of dissenting scientists appeared to be incapable of discharging the burden of proof that was required to overturn this analogy. In the rest of this section, we examine how this excessive burden manifested itself in inquiry. In Chapter 7, we consider how a further argumentative tactic – ad hominem argument – was used to deny these dissenting scientists the dialectical right to raise counter-claims during inquiry. In Chapter 2, we described how early epidemiological evidence provided at least some initial warrant for the aetiological claim that scrapie was the cause of BSE in cattle. This claim was significant in that it provided a rational basis for the analogy between BSE and scrapie that was to shape much subsequent reasoning about this new bovine disease. In the months between June 1994 and March 1996, the scrapie origin of BSE was to come under direct challenge from a small number of scientists. One of these scientists, Professor Richard Lacey, wrote in an article in the Journal of Nutritional and Environmental Medicine: [T]here is virtually no epidemiological data, and certainly no experimental data, to support the assertion that the infective agent of BSE was derived from sheep scrapie. Until proved otherwise, with cattle remains having comprised the major component of meat and bonemeal, should not BSE be considered as an inherent cattle disease, unless evidence is provided to the contrary? (Lacey 1995: 402–3).

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A former colleague12 of Professor Lacey’s, Dr Stephen Dealler, was equally sceptical that scrapie was the origin of BSE. In an article in the British Food Journal, Dr Dealler stated that: The original idea was that BSE was derived from the transfer of scrapie to cattle through feed, but various problems have appeared with this hypothesis during the past year (Dealler and Kent 1995: 10).

In their attempt to challenge the scrapie origin of BSE, scientists like Lacey and Dealler were seeking to overturn a presumption in favour of the dominant analogy between BSE and scrapie. For this presumption to be overturned, these investigators had to discharge a burden of proof by advancing evidence against those scientists who argued that BSE had originated from scrapie in sheep. To the extent that dialectical rules governing the making of claims and the use of evidence are being observed by scientists involved in the BSE inquiry, we can expect these scientists to fulfil certain obligations. Firstly, both parties to the dispute about the scrapie origin of BSE must have equal opportunities to advance claims and to bring forth evidence in support of those claims. Secondly, both parties are also obliged to give due consideration to the claims advanced by others as well as to the evidence that is used to support those claims. Thirdly, both parties are obliged to accept the force of the better argument and relinquish their commitment to a particular claim when sufficient evidence is adduced against that claim. In the case of the question of the origin of BSE, it can be shown that none of the above obligations were observed by scientists who attempted to defend the claim that scrapie was the origin of BSE in cattle. In failing to fulfil their dialectical obligations, these scientists had distorted the normal operation of presumption and burden of proof in inquiry. The upshot of this distortion was that claims which sought to relate BSE to scrapie assumed the status of unassailable theses. With no amount of evidence able to discharge the burden of proof that was required to overturn these claims, they persisted in inquiry as ‘fossilized’ presumptions. We will examine this point further below. Before doing so, we demonstrate how scientists who supported the dominant scrapie analogy failed to fulfil their dialectical obligations to other, dissenting scientists in inquiry. We described above how participants in inquiry should have equal opportunities to advance claims and support those claims by bringing forth evidence. There is clear evidence that this dialectical right was not afforded to scientists who did not subscribe to the dominant view that scrapie was the origin of BSE in cattle. On several occasions, dissenting scientists were denied opportunities to present their claims and research to scientific peers and others. When, in July 1994, Dr Dealler was refused his request of a meeting with the recently appointed Minister of Agriculture, Mr William Waldegrave,13 this marked another episode in a long-running series of attempts by Dr Dealler to discuss his views on BSE with SEAC scientists and MAFF. The first of these unsuccessful attempts occurred in August 1993. At their meeting on 7 October 1993, SEAC scientists were to discuss a paper by Dr Dealler. In a letter to SEAC’s Chairman, Dr Tyrrell, in August 1993 giving permission for the paper to be discussed, Dr Dealler stated ‘I would expect that the MAFF would criticise many of the findings of the work and I would be very unhappy for this

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criticism to take place on the committee without my being given an opportunity to answer at that time’ (Dealler 1993: 1). In the event, Dr Dealler was not given this opportunity, receiving instead a written correspondence about his paper from Dr Tyrrell on 26 October 1993. The communications that followed Dr Dealler’s request to attend SEAC’s meeting are interesting in what they reveal about MAFF’s view of those scientists who challenged the scientific consensus on BSE. In a letter dated 1 September 1993, Mr Bradley of the CVL communicated his unease at the idea of Dr Dealler attending SEAC’s meeting. He did so in terms which were dismissive of those scientists who failed to adhere to the then dominant views on BSE: If we accede to this request it will create a precedent, provide an opportunity for Professor Lacey to build upon and it may be difficult to restrict attendance in future to the likes of these two, Dr Narang or indeed anyone else who is inclined to make a point (Bradley 1993: 1).

The second failed attempt by Dr Dealler to present his views to SEAC scientists occurred in February 1994. Following two telephone conversations with Mr Lister (Department of Health Environment and Food Division), in which Dr Dealler expressed frustration that his views were not receiving due consideration by SEAC members, Mr Lister recommended that Dr Dealler be invited to a full SEAC meeting.14 Mr Bradley was again quick to recommend that such an invitation should not occur. On this occasion, his objection appeared to be based on a desire to shield SEAC from any possible criticism or negative scrutiny that might result from an encounter with Dr Dealler: If things backfired the SEAC could be brought into disrepute. Of course I could be wrong and they might clear the matter up once and for all. That is to my mind wishful thinking and the risks to the SEAC as a whole if they fail to deliver are not inconsiderable (Bradley 1994a: 2).

Mr Bradley’s overriding concern was clearly the protection of SEAC at all costs. This concern might have some basis in what appears to be doubt on Mr Bradley’s part that SEAC would be able to defend itself adequately in an interaction with Dr Dealler. As well as being denied opportunities in which to advance their claims, there is evidence that the views of dissenting scientists were not given due consideration by SEAC scientists. This evidence goes beyond reports from the dissenting scientists concerned15 and includes practical and other restrictions that were placed on the assessment of the work of these scientists. In this way, even as Mr Lister was recommending that a meeting should take place between Dr Dealler and SEAC, he was concerned to ensure that this meeting was time-limited.16 As well as limiting the time in which dissenting scientists could present their views, there is evidence that SEAC scientists did not subject the work of these scientists to an objective scientific review. In May 1993, Mr Wilesmith of SEAC’s Epidemiology Subgroup conducted a critique of Professor Lacey’s paper ‘BSE – The Gathering Crisis’. This critique was as much a series of ad hominem attacks against the paper’s author as it was an attempt to challenge what Mr Wilesmith perceived to be scientific misconceptions on the part of Professor Lacey. Although we will return to this point in

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Chapter 7, comments from the beginning of Mr Wilesmith’s critique are typical of those that occur throughout his review: Thank you for. . .the copy of Professor Lacey’s latest exposure of his ignorance on this topic. As you are aware, I feel that we have two basic options for dealing with this tendentious individual who has failed to apply any scientific scholarship to his so-called critique of BSE (Wilesmith 1993: 1).

Mr Wilesmith undertook several reviews of the work of dissenting scientists on behalf of SEAC. Each of these reviews contained a large component of ad hominem argument, which compromised the scientific objectivity of Mr Wilesmith’s response. Mr Wilesmith also conceded in a private correspondence that certain claims by one dissenting scientist were accurate, but that he was unable to communicate this assessment to the scientist concerned.17 This admission compromised the impartiality of the scientific reviews that Mr Wilesmith was able to undertake. Furthermore, there is clear evidence that SEAC members lacked requisite expertise to assess some of the work of dissenting scientists. One such piece of work was a paper by Dr Dealler in the British Food Journal. The minutes of SEAC’s 22nd meeting held on 23 November 1995 record that SEAC’s new chairman, Professor Pattison, thought that ‘the Committee may need help in interpreting Dealler’s mathematical calculations’.18 Notwithstanding this lack of internal expertise, on only one occasion did SEAC scientists ask for a paper to be reviewed by outside experts.19 It emerges that a number of factors, ranging from time constraints to a lack of adequate scientific review, limited the extent and rigour of the appraisal undertaken by SEAC and MAFF scientists of dissenting scientists’ work. We described above how dissenting scientists were denied the dialectical opportunity to advance claims and to bring forth evidence in support of those claims. We can now see that these same scientists were not afforded the dialectical right to have those claims properly considered by scientists who formed a particular consensus view on BSE. It remains to be seen if the third of our dialectical requirements was any more successfully addressed by scientists who were part of this consensus during the BSE epidemic. The third dialectical requirement described above required scientists to accept the force of the better argument and relinquish their commitment to a claim when sufficient evidence is adduced against that claim. There is every indication that this requirement was not fulfilled by scientists who defended the dominant analogy between BSE and scrapie. We have already seen, for example, how this analogy continued to motivate risk assessments even after it became apparent that BSE and scrapie differed in important respects. By June 1994, it was clear to scientists that the dose of infective agent that could transmit BSE was much smaller than had been anticipated on the basis of scrapie studies. Also, the oral route was a more efficient means of transmission of BSE than experience with scrapie had led investigators to expect. Furthermore, a greater number of species were susceptible to BSE than had previously been demonstrated in scrapie. Along with this extended host range, BSE displayed a different pattern of pathogenesis, with certain bovine tissues infective earlier in the course of the disease than experience with scrapie had led investigators to believe would be the case. Any one of these items of contrary evidence should

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have been enough to cause scientists to question the validity of scrapie as the origin of BSE and with it the rational acceptability of the dominant scrapie analogy – this analogy, after all, only had a tentative epistemic standing in inquiry, a standing that was reflected in its presumptive status. Certainly, the combination of this contrary evidence should have effectively overturned this presumptively warranted analogy. The fact that it failed to do so and that scientists continued to base their risk assessments upon this analogy into the late phase of inquiry is evidence that this third dialectical requirement was no more successfully observed by scientists than the previous two dialectical requirements. That scrapie analogy persisted in inquiry beyond the point where it was appropriate for it to do so was made possible by certain dialectical features of late inquiry. Firstly, the critical reflection that had attended the use of this analogy in early inquiry was noticeably lacking in the period between June 1994 and March 1996 among scientists who supported the consensus view of the origin of BSE. Whereas the Southwood Working Party was concerned to emphasise the largely conjectural basis of the analogy with scrapie,20 the scientific committees of late inquiry treated this analogy as an unchallengeable thesis. At none of SEAC’s meetings between June 1994 and March 1996 was the rational standing of the scrapie analogy explicitly considered much less openly challenged. Secondly, where such challenge was forthcoming from dissenting scientists, it was effectively dismissed through the actions of SEAC scientists. Dissenting scientists were denied opportunities in which to present their views. Moreover, when those views were considered by SEAC scientists, they often received inadequate scientific review. The combined effect of these features of late inquiry was to shelter the scrapie analogy from critical scrutiny and to ensure its persistence in the face of contrary evidence. The normally defeasible nature of presumption was subverted by investigators with the result that the scrapie analogy persisted in inquiry as an unassailable thesis. To the extent that no degree of critical challenge or contrary evidence would effect the removal of this analogy from inquiry, it had become a fossilised thesis within inquiry – a thesis which harked back to an earlier stage of inquiry but which had long since ceased to function in any rationally warranted capacity within that inquiry. It remains to be seen if other reasoning strategies continued to enjoy rational warrant in the much changed evidential conditions of late inquiry.

6.2.2 Argument from Ignorance By June 1994, the argument from ignorance was a long established feature of the reasoning of BSE scientists. The evolution of this argument through successive stages of inquiry had revealed it to be an adaptive strategy to the epistemic conditions that confronted investigators during inquiry. At the outset of inquiry, when evidence was lacking and knowledge of BSE was limited, the argument from ignorance served to facilitate scientific inquiry by generating propositions for use in inquiry and excluding other propositions from further consideration in inquiry. In the changed epistemic conditions of the middle phase of inquiry, this same

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argument assumed a quite different rational status. As the results of experimental studies began to emerge in the middle phase of inquiry, it became apparent that this argument did not enjoy the same rational standing that had characterised its use in early inquiry. The argument from ignorance was also employed extensively by scientists during the late phase of inquiry. The ‘no evidence’ statements, which form the premise of ignorance arguments, were advanced by the Chief Medical and Veterinary Officers during this period.21 These same statements were also evident in the Fourth Annual Report of the CJD Surveillance Unit where they were used to dismiss any increased risk of CJD according to occupational group.22 SEAC scientists continued to use ‘no evidence’ statements in their risk assessments with decisions from the safety of blood to optic nerve infectivity premised on these statements. The question that will concern us in this section is whether these ‘no evidence’ statements, and the arguments of which they are a part, are any more or less warranted in the epistemic conditions of late inquiry than in the conditions that obtained at earlier stages of inquiry. By the late phase of inquiry into BSE, two types of ignorance argument predominated. There were those arguments that had survived the emergence of evidence during the middle phase of inquiry and had gone on to improve their epistemic standing as a result of doing so. The presumptively warranted conclusions of these arguments had grown in epistemic stature and were for the first time the basis of knowledge claims. At the same time as the presumptively warranted conclusions of some ignorance arguments were experiencing an improved epistemic standing in inquiry, other ignorance arguments were being used by investigators for the first time. The merits of these particular arguments are to be assessed against the evidential base which had developed by this late stage of inquiry. In this section, we will examine both types of ignorance argument. The first type of ignorance argument is exemplified by SEAC’s deliberations concerning the safety of blood. SEAC addressed the question of the safety of blood at its 22nd meeting held on 23 November 1995. The Department of Health wished to receive SEAC’s response to the question ‘Is there any new evidence to suggest blood, and particularly blood products, pose a risk of [CJD] transmission?’ (SEAC 1995a: 9). The minutes of SEAC’s meeting recorded that ‘[t]he Committee concluded that there is no new evidence of risk from blood’ (SEAC 1995a: 12). SEAC’s further assessment of the risk of BSE transmission through bovine eyeballs is an example of the second type of ignorance argument described above. The infectivity of bovine eyeballs, including the retina and optic nerve, was discussed at several SEAC meetings. These tissues were of concern to SEAC scientists because of the potential risks that they posed to individuals undertaking dissections in schools. The minutes of SEAC’s 20th meeting held on 8 September 1995 recorded that ‘[t]here is still no evidence of transmission with optic nerve’ (SEAC 1995b: 5). These ‘no evidence’ statements may be reconstructed as premises within the following arguments: PREMISE: CONCLUSION:

There is no new evidence of risk of CJD transmission from blood. Blood does not pose a risk of CJD transmission.

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There is still no evidence of BSE transmission via the optic nerve. The optic nerve does not transmit BSE.

These arguments have the logical features of classic arguments from ignorance in which the absence of evidence in support of the proposition p is used as grounds for the conclusion that p is false. Additionally, however, the premises of these arguments contain certain words (‘no new evidence’ and ‘still no evidence’) which have a bearing on how these arguments are to be evaluated.23 The issue of the safety of blood and blood products had been addressed by a number of bodies by the time SEAC scientists considered the risk of CJD transmission through blood at its 22nd meeting on 23 November 1995. An argument from ignorance was also the basis of this earlier risk assessment, as the minutes of SEAC’s meeting record:24 On 22 November 1995 the Committee for Proprietary Medical Products was advised by its Biotechnology group that there is no justification for recalling blood products as there is a lack of evidence on transmission via blood and blood products (SEAC 1995a: 10).

When the Department of Health asked SEAC to consider the CJD risks associated with blood, it was thus asking these scientists to revisit an earlier risk assessment that had been based on ignorance argument.25 To the extent that this earlier assessment survived SEAC’s further consideration of blood safety – SEAC scientists concluded that there was ‘no new evidence’ of risk from blood – the presumptively warranted conclusion of the first ignorance argument above increased its epistemic standing within inquiry. In effect, the thesis ‘blood does not pose a risk of CJD transmission’ moved closer to becoming a knowledge claim in inquiry where formerly it had the status of a presumption. To explain how this occurred, we need to consider what happened to the ‘no evidence’ thesis that constitutes the premise of this argument. This thesis increased its epistemic standing through the operation of presumption and burden of proof in inquiry. By withstanding successive attempts to bring forth evidence that called into question the safety of blood, the claim that ‘there is no (new) evidence of risk of CJD transmission from blood’ achieved increasing epistemic credibility in inquiry. As such, it was likely to persist in inquiry for at least some time to come. It should be noted, however, that the persistence of this claim is quite unlike the persistence that we witnessed in relation to the scrapie analogy. The former is a result of epistemic strengthening in which a presumptively warranted thesis grows in stature as it demonstrates its capacity to withstand successive dialectical challenges in inquiry. The latter is persistence as a result of suspension of the normal operation of dialectical presumption and burden of proof through which unwarranted theses are rejected from inquiry. What this example demonstrates is the capacity of presumptively warranted conclusions of ignorance arguments to improve their epistemic standing in inquiry. However, this improvement is not guaranteed in inquiry nor is it readily achieved. As inquiry proceeds, conclusions of ignorance arguments may be overturned by contrary evidence, as we observed in Section 5.2.2. Even when they are not directly defeated by contrary evidence, the presumptively warranted conclusions of these

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arguments may persist in inquiry with little in the way of additional evidential support. It is only when certain conditions are fulfilled that the conclusions of ignorance arguments can begin their epistemic ascent in inquiry. SEAC’s consideration of blood safety amply demonstrates at least one of those conditions. Where successive attempts are made by scientists in inquiry to consider evidence that relates to blood safety and, notwithstanding these attempts, there is no evidence to suggest that blood poses any risk of CJD transmission, then there are grounds for treating the ‘no evidence’ premise of ignorance argument as a more strongly warranted thesis than merely that of a presumption. To the extent that this premise provides grounds for the conclusion that blood does not pose a risk of CJD transmission, this conclusion is also elevated beyond its original presumptive status. Each time SEAC scientists tried, and failed, to demonstrate that blood and blood products posed a risk of CJD transmission, the thesis ‘there is no evidence of risk of CJD transmission from blood’ and any conclusions based on this thesis improved their epistemic standing in inquiry. By surviving successive dialectical challenges in inquiry, once presumptively warranted theses had begun an epistemic ascent that might eventually lead to them becoming knowledge claims in inquiry.26 SEAC’s assessment of the BSE risk presented by bovine eyeballs, including the retina and optic nerve, serves to demonstrate how certain ignorance arguments were also used for the first time by scientists in the late phase of inquiry. Bovine eyeballs were not only a potential risk to those who handled them during school dissections, but they were also likely to be included in certain human food products. On the specific question of the infectivity of the optic nerve, the minutes of SEAC’s meeting on the 8 September 1995 recorded that ‘there was still no evidence of BSE transmission via the optic nerve’. The word ‘still’ is significant in this statement as it attests to a passage of time during which investigations may be expected to have demonstrated BSE infectivity in the optic nerve, if the optic nerve did indeed harbour infectivity. The investigations that examined the infectivity of bovine eyeballs were part of a pathogenesis study that was being conducted by the Central Veterinary Laboratory. By the time SEAC was holding its 19th meeting on 21 June 1995, it was evident that the retina of bovine eyeballs carried infectivity – Mr Bradley used the occasion of this meeting to inform SEAC members that mice inoculated with retina from BSE cattle were showing clinical signs. That optic nerve infectivity had not been demonstrated in the time that it took scientists to demonstrate BSE infectivity of bovine retinas was grounds in support of the claim that the optic nerve does not transmit BSE. A modus tollens inference of the type that we have come to associate with the argument from ignorance (see Section 4.2.2) is in evidence: if proposition p were true – where p is the proposition that the optic nerve does transmit BSE – then we would know about it; but we do not know about it; therefore, p is not true. Although not part of the logical structure of ignorance argument, the word ‘still’ in the premise ‘there is still no evidence of BSE transmission via the optic nerve’ is nonetheless making a significant contribution to the rationality of this argument. The temporal meaning of this word serves to confer warrant on the ‘no evidence’ premise of this ignorance argument – if sufficient time had elapsed in which to demonstrate the infectivity of the optic nerve, and infectivity had still not been demonstrated,

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then the claim that ‘there is no evidence of BSE transmission via the optic nerve’ is rationally warranted. In earlier chapters, we described how the knowledge base upon which ‘no evidence’ claims in ignorance arguments are founded can provide these claims with more or less warrant in accordance with various factors. These claims are particularly strongly warranted when the knowledge base is complete. They are also strongly warranted when an exhaustive search of the base is undertaken. In discussing SEAC’s consideration of optic nerve infectivity, we are now able to identify a further factor that is integral to the rationality of ignorance argument. This factor is not only prior to the completeness of the knowledge base, and to an exhaustive search of this base, but is a precondition on the fulfilment of these other factors. The factor in question is time. A scientific knowledge base that is closed before adequate time has elapsed in which to conduct experiments and gather relevant evidence cannot possibly attain completeness. Similarly, a search process that is terminated prematurely is hardly exhaustive in nature. In short, the rationality of ignorance argument is as deeply rooted in temporal factors as it is in logical and epistemic factors. There can be no clearer demonstration of the need to examine scientific reasoning within a temporal context (see Section 2.2.4 for further discussion of this point).

6.2.3 Arguing to the Wrong Conclusion Like earlier stages in the BSE inquiry, scientific reasoning in the final phase of inquiry was not confined to analogical and ignorance argument. As the consensus view of BSE became increasingly difficult for scientists to defend in the months leading up to the emergence of new variant CJD in humans, it was unsurprising that a number of fallacious arguments should appear in the reasoning of scientists. One such argument, variously labelled in the fallacy literature as arguing to the wrong conclusion, ignoratio elenchi and missing the point, will be examined in this section. Although classifications and definitions of this fallacy vary considerably amongst theorists,27 we will consider below a characterisation of the fallacy which best captures the particular case that we will examine. The case in question relates to the discovery in May 1990 of feline spongiform encephalopathy (FSE) in a domestic cat. Although this event took place outside of the time period that we are considering in this chapter, its discussion and assessment by SEAC scientists in their report of September 1994 falls squarely within the final phase of the BSE inquiry. I will argue subsequently that SEAC scientists used this fallacy as a deceptive tactic in argumentation. In specific terms, it was in the interests of these scientists to draw an irrelevant conclusion from the discovery of FSE in a domestic cat rather than acknowledge the only relevant conclusion that could be drawn from this episode, the conclusion that BSE had probably transmitted to a species which was not susceptible to scrapie. This conclusion posed considerable difficulties for SEAC scientists who still subscribed to the scrapie analogy in the final phase of the BSE inquiry. Before we examine why SEAC members adopted this pattern of argument, we discuss how theorists have characterised the fallacy of arguing to the wrong conclusion.

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There are many ways in which the conclusion of an argument may be deemed irrelevant to the premises which are advanced in support of it. It is perhaps not surprising, therefore, that definitions of the fallacy of arguing to the wrong or irrelevant conclusion are equally numerous. Some definitions take the fallacy to result from a ‘disconnect’ between the premises and conclusion whereby the premises fail to connect in a coherent way to the conclusion.28 Other definitions state that the irrelevant conclusion appears or looks like the conclusion that is actually supported by the premises, but which the proponent of the argument fails to advance.29 To the extent that a fallacious argument can only be successful as a deceptive tactic in argumentation if it evades detection by an audience, and two conclusions which look or appear similar are likely to pass unnoticed by an audience, this characterisation of the fallacy would seem to account for how the argument serves to persuade listeners in practice. But this definition fails to apply to those arguments in which the irrelevance of the conclusion is so great that it bears no resemblance to the conclusion that the arguer should be attempting to establish. A definition that places less emphasis on conclusions appearing alike and more emphasis on the fact that the irrelevant conclusion strays from the point of the argument is better equipped to characterise the logical flaw in this type of argument. Such a definition is advanced by the prominent fallacy theorist Douglas Walton: The fallacy of ignoratio elenchi, also often called the fallacy of irrelevant conclusion or the fallacy of ignoring the issue, occurs where an argument is directed towards proving the wrong, or an irrelevant conclusion. Such an argument may be valid, but the problem is that it has strayed from the point (Walton 2008: 18; italics added).

Walton’s definition of this fallacy is particularly apt for our present purposes. For in considering SEAC’s assessment of the emergence of FSE in a domestic cat, we encounter a conclusion that is not only markedly dissimilar from the conclusion that SEAC should have drawn from the appearance of FSE, but is also, I contend, intended to serve as a distraction from this conclusion. In this sense, SEAC’s conclusion very much ‘strays from the point’ or ‘ignores the issue’ that is raised by the emergence of FSE. As described in Chapter 5, the development of FSE in a domestic cat caused considerable public and scientific concern. Domestic cats were not among the host range of scrapie. The fact that a cat had developed a spongiform encephalopathy for the first time was an indication that BSE – the presumed origin of FSE – might have a different host range to that of scrapie. In its report of September 1994, SEAC characterised the event in question in the following terms: When a cat was reported in 1990 to have succumbed to feline spongiform encephalopathy (FSE), some concern was expressed by the public and some scientists. But it was already known that this species was experimentally susceptible to CJD and had been used in the USA and Czechoslovakia for investigating human disease (SEAC 1994b: 28).

Whilst acknowledging the concern that was raised by the emergence of FSE, SEAC’s account misrepresents the only relevant conclusion that could be derived from this event. This conclusion – that BSE has a different host range from scrapie – can be shown to enter into a longer sequence of argument which terminates in a conclusion that is a direct challenge to the scrapie analogy. This fully reconstructed

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argument sequence is shown below with the conclusion of interest to the present analysis indicated by an asterisk: Argument sequence with ‘relevant’ conclusion: Argument 1: PREMISE 1:

PREMISE 2: PREMISE 3: PREMISE 4: CONCLUSION:

If species which are not susceptible to scrapie develop a BSErelated spongiform encephalopathy, then BSE has a different host range from scrapie. A domestic cat has developed feline spongiform encephalopathy. Domestic cats are not susceptible to scrapie. FSE is a BSE-related spongiform encephalopathy. BSE has a different host range from scrapie.∗

Argument 2: PREMISE 1: PREMISE 2: PREMISE 3: CONCLUSION:

If BSE and scrapie have different host ranges, then BSE is not bovine scrapie. If BSE is not bovine scrapie, then the scrapie analogy is untenable. BSE has a different host range from scrapie.∗ The scrapie analogy is untenable.

The difficulty for SEAC scientists is that this argument sequence is logically compelling. SEAC scientists could not reasonably deny the rational acceptability of premise 1 in argument 1. Premises 2, 3 and 4 in this same argument were strongly warranted theses, which had been established through histopathological examination, experimental inoculation and epidemiological investigation, respectively. To the extent that SEAC scientists subscribed to all four of these premises, they were logically compelled to derive the conclusion that BSE has a different host range from scrapie. But in so deriving this conclusion, these scientists became committed to certain of its logical consequences. One of these is developed in argument 2 above. In conceding that BSE has a different host range from scrapie, SEAC scientists would also be forced to concede that BSE could not simply be scrapie in cattle. And if BSE was not bovine scrapie, then there was no rational basis for the scrapie analogy that had dominated inquiry into BSE. To avoid the rejection of this analogy, an analogy that was still influencing BSE risk assessments in the late phase of inquiry, SEAC scientists sought to replace the conclusion of argument 1 above with the following thesis:30 The emergence of FSE has few, if any, implications for human health.

The above thesis blocked the derivation of conclusions that would expose the scrapie analogy to challenge. But it did so at the expense of instituting an irrelevant (or wrong) conclusion in place of one that received considerable support from the available histopathological, experimental and epidemiological evidence (represented by premises 2, 3 and 4, respectively, in argument 1). But SEAC’s conclusion was not merely irrelevant on the basis of the premises in argument 1 above. Rather,

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it is a sign of just how unwarranted this conclusion is that even the most charitable reconstructions of the arguments that SEAC scientists may have expected to advance in support of it fail to arrive at premises that provide this conclusion with warrant. For example, SEAC scientists may have been attempting to base their view that the emergence of FSE had no implications for human health on the following line of reasoning which is reconstructed as an argument sequence below: It is already known that domestic cats are susceptible to CJD, so there is no surprise in the fact that they have now been shown to be susceptible to another spongiform encephalopathy, FSE, and certainly nothing relating to human health can be deduced from this fact.

Reconstructed argument sequence: Argument 1: PREMISE 1:

PREMISE 2: CONCLUSION:

If domestic cats are susceptible to CJD, then they will also be susceptible to the bovine-derived spongiform encephalopathy FSE. Domestic cats are susceptible to CJD. Domestic cats are also susceptible to FSE.

Argument 2: PREMISE 1: PREMISE 2: CONCLUSION:

If domestic cats are susceptible to FSE, there are no implications from this fact for human health. Domestic cats are susceptible to FSE. FSE in domestic cats poses no implications for human health.

But if this were SEAC’s attempted justification of their view that FSE had no implications for human health, it would be problematic in at least three ways. Firstly, the spongiform encephalopathies that a particular species is susceptible to can only be established through experimental and natural transmission studies. It is not possible to conclude from the fact that a species is susceptible (not susceptible) to one TSE that it will also be susceptible (not susceptible) to another TSE (premise 1, argument 1), as the mistaken conclusions of scientists regarding the susceptibility of humans to BSE based on scrapie demonstrates. Secondly, domestic cats were only experimentally susceptible to CJD (premise 2, argument 1). The bovine-derived spongiform encephalopathy FSE had developed in cats not as a result of experimental transmission but as a result of natural transmission via the oral route (a food source was the presumed origin of the disease). It is not only conceivable, but is also consistent with the scientific literature on TSEs, that a species may succumb to disease via experimental inoculation when it would not develop disease under natural conditions. So it cannot be concluded that because domestic cats are experimentally susceptible to a TSE that they will be susceptible under natural conditions to the same or a different TSE. Thirdly, something very significant in relation to human health could be deduced from the fact that domestic cats had developed a bovinederived spongiform encephalopathy (contra premise 1, argument 2). Domestic cats were known not to be susceptible to scrapie. Here was evidence that scrapie and BSE had different host ranges. If these diseases had different host ranges, then it

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was possible that they could differ in a further important respect and that BSE might transmit to humans where scrapie had failed to do so. Whichever way we turn in this argument sequence, SEAC’s justification of the conclusion that FSE has no implications for human health encounters considerable difficulties. To the extent that we want to continue in this charitable vein, we will consider a further reconstruction of SEAC’s reasoning in relation to FSE. SEAC scientists may have been attempting to reason as follows: Domestic cats are not susceptible to scrapie. The fact that a domestic cat has developed FSE shows that this new feline disease is not related in any way to scrapie. More conclusively still, it cannot be related to BSE which is bovine scrapie. To the extent that FSE is unrelated to BSE, the emergence of FSE presents no new information about how BSE will behave or about the risks that BSE poses to human health.

Reconstructed argument sequence: Argument 1: PREMISE 1: PREMISE 2: CONCLUSION:

If domestic cats are not susceptible to scrapie, then FSE is not related to scrapie. Domestic cats are not susceptible to scrapie. FSE is not related to scrapie.

Argument 2: PREMISE 1: PREMISE 2: CONCLUSION:

If FSE is not related to scrapie, then FSE is not related to BSE. FSE is not related to scrapie. FSE is not related to BSE.

Argument 3: PREMISE 1: PREMISE 2: CONCLUSION:

If FSE is not related to BSE, then FSE has no implications for the risks that BSE poses to human health. FSE is not related to BSE. FSE has no implications for the risks that BSE poses to human health.

Once again, this reconstructed argument sequence is problematic in several respects. Firstly, it cannot be argued that FSE is not related to scrapie because domestic cats are susceptible to FSE when they are not susceptible to scrapie (premise 1, argument 1). It was known in 1994 that FSE was not related to scrapie. But this claim can only be established through strain-typing studies31 and not through the type of grounds (susceptibility to TSEs in domestic cats) that are being advanced in argument 1 above. This is because factors other than features of the TSE agents themselves (e.g. host genotype) determine the TSEs to which a particular species will be susceptible.32 Secondly, it can only be concluded that FSE is not related to BSE on the grounds that FSE is not related to scrapie (premise 1, argument 2), if it can be assumed that BSE is bovine scrapie. This particular assumption is the basis of the scrapie analogy, which was looking increasingly untenable by the time SEAC scientists were assessing the implications of FSE in their report of

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September 1994. Thirdly, the claim that FSE is not related to BSE (premise 2, argument 3) is also problematic. This claim can only be properly substantiated by means of the results of strain-typing studies. By 1994, these studies revealed this claim to be false, i.e. FSE is related to BSE.33 So, premise 2 of argument 3 is not consistent with the experimental evidence that was available to scientists in 1994. In short, this alternative reconstruction of SEAC’s reasoning in relation to FSE leads us into as many logical pitfalls as the first reconstruction that we examined. If SEAC had a logically compelling case to make in support of its conclusion that FSE posed no implications for human health, it is difficult to imagine what that case would be. It emerges that even the most charitable reconstructions of SEAC’s reasoning fail to arrive at argument sequences that provide rational justification for the claim that the emergence of FSE has few, if any, implications for human health. To the extent that it has not been possible to envisage a rationally acceptable sequence of reasoning that would support this claim, there are grounds for asking what role this claim is playing in SEAC’s deliberations. That role, I contend, is one of distracting the audience, consisting of other scientists and the public, from an altogether more relevant conclusion, a conclusion to the effect that BSE has a different host range from scrapie. Although this conclusion is the only rationally warranted position available to SEAC scientists given what was known at the time, it is nevertheless a conclusion that has adverse consequences for the dominant scrapie analogy in inquiry. To avert any challenge to this analogy, SEAC scientists substituted the only relevant conclusion that could be derived from the available facts (BSE has a different host range from scrapie) with an irrelevant or wrong conclusion to the effect that the emergence of FSE has no implications for human health. Although this latter conclusion was not warranted by the facts of the case, its presence foreclosed a further sequence of reasoning that would terminate in a direct challenge to the scrapie analogy. In arguing to the wrong or irrelevant conclusion, SEAC scientists had certainly committed a logical error of advancing a conclusion that was not warranted by the best available evidence represented as premises. But this logical error, I contend, is revealing of another use of this argument. This was the use of the argument as a deceptive tactic in argumentation that was designed to prevent any challenge to the dominant scrapie analogy in inquiry.

6.3 Summary The temporal context in which the events of the BSE crisis unfolded is of paramount importance to the examination of scientific reasoning that is conducted within this book. This chapter has been no exception in this regard. The late phase of the BSE inquiry presented scientists with unique challenges and conditions. For a model of scientific reasoning to have explanatory value, it must be as capable of addressing these conditions as it is of addressing the conditions that obtain at the outset of inquiry. This model must not only capture how scientists reason when evidence is lacking and knowledge of a topic is limited in the early stage of an inquiry, but also how theses can change their epistemic standing as inquiry proceeds over

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time. These changes lead in some cases to the rejection of claims when contrary evidence emerges and in other cases to the upgrading of claims when validation of their content occurs. This responsiveness to changing conditions across time in inquiry requires that we attribute to scientists only those reasoning strategies that are dynamic rather than static, that are context sensitive rather than context insensitive and that generate theses which are defeasible rather than immutable. It is only such strategies that can be equally well adapted to the pervasive uncertainty of early inquiry, the rapidly changing evidential background of middle inquiry and the epistemic strengthening of theses that occurs in late inquiry. In this chapter, we have seen three different ways in which these reasoning strategies can exist in late inquiry. The first of these ways captures the capacity of these strategies to achieve the epistemic strengthening of theses in late inquiry. The second and third ways reflect uses of these strategies that are contrary to the aims of inquiry and are a subversion of its dialectical processes. We summarise these different uses of these reasoning strategies below. We described in Chapter 5 how certain scientific claims did not survive the emergence of evidence that occurred in the middle phase of inquiry. These claims, which were the presumptive conclusions of analogical and ignorance arguments, were overturned by the results of experimental studies and other investigations. While certain claims fell by the wayside in the middle phase of inquiry, other claims withstood successive challenges to their presumptive status and improved their epistemic standing in inquiry as a result. These upgraded theses were for the first time the basis of knowledge claims in inquiry. One of these theses concerned the risk of CJD transmission from blood and blood products. The whole area of blood safety had such important public health implications that SEAC scientists kept this issue under constant review. By regularly reviewing the medical and scientific literature on CJD transmission through blood, SEAC scientists were in effect exposing the question of blood safety to repeated challenge. To the extent that this challenge failed to overturn the thesis that blood does not pose a risk of CJD transmission, this thesis may be said to have improved its epistemic standing in inquiry. The elevated stature of this thesis attests to a type of dialectical rationality in inquiry whereby the operation of presumption and burden of proof raises the rational standing of claims. Specifically, where the burden of proof that attends a thesis cannot be discharged, the thesis in question may be seen to gain ground in inquiry. It is in the late stages of an inquiry that these dialectical conditions are most likely to be fulfilled and, indeed, were fulfilled in the case of SEAC’s consideration of blood safety. This was one example during the BSE inquiry where the epistemic promise of an early presumption regarding blood safety was delivered in the form of a much strengthened thesis. In this chapter, we have also described two types of dialectical distortion that occurred in the late stage of inquiry. The first of these distortions involved the persistence of analogical reasoning based on scrapie well beyond the point at which this analogy could be supported by the evidence available to investigators. This form of reasoning was only sustained in inquiry through the subversion of the dialectical rights and obligations that exist in inquiry. In specific terms, scientists who attempted to challenge the scrapie origin of BSE, and with it the dominant scrapie

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analogy, were denied their dialectical right to advance claims and to have those claims properly assessed by scientists who formed the consensus view on BSE. These obstructions to the dialectical process had the effect of shielding the scrapie analogy from challenge and allocating to it a burden of proof that simply could not be discharged. The result was that this analogy persisted in inquiry when there was little evidential basis for its continued existence. Stripped of any rational grounds, this analogy became a fossilised presumption in inquiry. As such, it was a relic of an earlier period in inquiry when the scrapie analogy had experienced presumptive warrant, even though that warrant had long since lapsed by the final phase of inquiry. This scenario would be little more than an interesting point about the dialectical processes that can occur in scientific inquiry were it not for the fact that the scrapie analogy was still the basis of BSE risk assessments by SEAC and other scientists in the final phase of inquiry. In short, this particular dialectical distortion had very real (and adverse) consequences for the assessments made and decisions taken by scientists in the final weeks and months of the BSE inquiry. The second dialectical distortion to occur in the final phase of inquiry found SEAC scientists foreclosing a potentially difficult line of reasoning through the institution of an irrelevant or wrong conclusion in argument. The wrong conclusion at issue was a claim to the effect that FSE has no implications for human health. The line of reasoning that was averted by this conclusion would have brought the dominant scrapie analogy under critical scrutiny with possible rejection of this analogy from inquiry. For SEAC scientists, challenge to this analogy was to be avoided at all costs, as the scrapie analogy was still being used to justify risk assessments in relation to BSE in the late stage of inquiry. The use of a wrong or irrelevant conclusion allowed SEAC scientists to at least appear to be assessing the implications of the emergence of FSE whilst at the same time ensuring that the rejection of the scrapie analogy was not one of those implications. By maintaining the appearance of rational argument while simultaneously preventing any challenge to the scrapie analogy, SEAC scientists were using an argument to the wrong conclusion as a fallacy of reasoning or as a deceptive tactic in argumentation (it will be recalled that it is part of the definition of a fallacy that it must at least have the appearance of being a rationally warranted argument; see note 29 in Chapter 5). By the late stage of the BSE inquiry, it was becoming increasingly difficult for investigators to uphold the scrapie analogy in the face of contrary evidence. As scientists continued to defend this analogy and to draw upon it in their risk assessments, a growing number of fallacious arguments began to characterise their reasoning. The argument to the wrong or irrelevant conclusion was one of the fallacious arguments that were used by scientists to maintain this failing analogy.

Notes 1. The ELISA test (enzyme linked immunosorbent assays) is routinely used in laboratories to measure the quantity of a substance by using antibodies to that substance. In the case of BSE, the ELISA used antibodies that recognized heat-stable proteins, that is, proteins present

Notes

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3.

4.

5.

6.

7.

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in rendered material, which had been derived from a variety of ruminant organs and tissues (BSE Inquiry Report, Volume 2: 136). Dr Watson confirmed this in oral evidence to Lord Phillips and his inquiry team on 6 July 1998: ‘speaking for Mr Bradley and I, we were both surprised at the small amount of CNS which did transmit orally to cattle’ (BSE Inquiry 1998: 64). (Dr Watson was the Director of the CVL between 1986 and 1990 and was a member of the Tyrrell Committee and SEAC.) In November 1990, the Neuropathogenesis Unit confirmed that 0.5 g of infective material had been sufficient to orally transmit BSE to sheep. Although this was an even more alarming finding – this was oral transmission across a species barrier – it largely went unrecognized, as Lord Phillips and his inquiry team remarked: ‘Knowledge that 0.5 gram had sufficed for oral infection of a negative line sheep was available as early as November 1990. It is extremely unfortunate that this did not lead to an appreciation of the risks of cross-contamination at this stage’ (BSE Inquiry Report, Volume 6: 522). Lord Phillips and his team remarked of these cases ‘[t]hey did not have glycosylation patterns associated with vCJD. To date, no one has demonstrated a link between these cases and BSE’ (BSE Inquiry Report, Volume 1: 12). The purpose of the review, which was conducted between 13 and 16 February 1995, was to consider the balance, scope and direction of the research programme on TSEs and to ensure that policy customers were receiving value for money from their research. The review examined all MAFF supported R&D on TSEs. During the review, contractors gave presentations on their projects to four independent referees and representatives from the Animal Health Policy Division and Chief Scientist’s Group. The four referees were Professor J. Almond (Reading University, UK), Dr W. Heuston (United States Department of Agriculture, Washington), Dr R. Kimberlin (Scrapie and Related Diseases Advisory Service, Edinburgh) and Dr R. Ridley (Cambridge University). ‘The NPU have informally reported some disturbing results in experiments intended to demonstrate that properly washed embryos from scrapie infected sheep do not transmit infection. Some resulting offspring, which were not expected to succumb, have in fact done so. These results are open to a number of possible interpretations, one being that the disease could be spread through semen. . .The suggestion that semen may be infectious is at variance with our findings on BSE and with previously held views about the epidemiology of scrapie’ (Meldrum 1995: 3). Mr Meldrum remarked of the NPU’s results: ‘Our problem here is that these interim results may have to be released even though they are incomplete and are likely to be misleading. This is an unsatisfactory situation and something we are hoping to resolve through further work with the Central Veterinary Laboratory and the Biotechnology and Biological Sciences Research Council to design better experiments to study possible links between scrapie and BSE in the future. To that end we are arranging a closed scientific meeting in early March to attempt to define what experimental work is necessary to investigate these relationships. . .’ (Meldrum 1995: 3). The final report of the R&D review recommended that the BSE semen transmission investigation should form a ‘minor addition’ to the research study SE0201 on BSE epidemiology. This study was judged in the review to be of ‘high priority and high quality’. The analogy between scrapie and CJD was no more strongly warranted than the analogy between scrapie and BSE. After all, Brown et al. (1987) had concluded based on a review of the world literature that there was no epidemiological link between scrapie and CJD (see note 33 in Chapter 2). In the absence of such a link, there were no grounds for establishing an analogy between these diseases. The minutes of SEAC’s 22nd meeting record that ‘[t]he Committee concluded that there is no new evidence of risk from blood suggesting the necessity for new measures’ (SEAC 1995a: 12). At its 23rd meeting, the minutes record that ‘the Committee felt that it would be inappropriate to notify [recipients of blood from CJD cases] in view of the very small risk involved in relation to the stress caused’ (SEAC 1996: 6).

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10. At the request of the Committee of Proprietary Medicinal Products (CPMP), a meeting was held on 13 February 1995 in Brussels to discuss the risk of CJD transmission via blood derivatives. In a report prepared for the CPMP, scrapie analogy is used to make assessments of the risk of CJD transmission from blood and plasma: ‘The different types of animal TSE, particularly ovine scrapie, have been studied using various experimental models. The different tissues have been classified according to the concentration of the infectious material. . .There is general agreement on the similarity between experimental animal models and human TSEs. The EC classification could thus also apply to human tissues. White blood cells can be placed in category III (low infectivity), whereas plasma is in category IV (no detectable infectivity). The lack of accumulation of the infectious agent in body fluids could account for the lack of reported infectivity’ (European Agency for the Evaluation of Medicinal Products 1995: 4). 11. This is evident, for example, in Mr Meldrum’s letter to the MAFF Permanent Secretary on 28 February 1995. In this letter, Mr Meldrum discussed the findings of an experimental study conducted at the Neuropathogenesis Unit in Edinburgh. This study had revealed infectivity in the spleen of sheep which had been infected with BSE. This finding presented a challenge to the scrapie analogy in that BSE infectivity in cattle had previously been demonstrated only in the brain and cervical spinal cord. Mr Meldrum remarked that ‘this finding will be presentationally awkward because the BSE agent appears to be distributed in a different manner or at a different titre in cattle as against sheep’ (Meldrum 1995: 2). 12. Dr Dealler had previously worked in the University of Leeds Microbiology Department under Professor Lacey. 13. Mr Waldegrave responded to Dr Dealler ‘I take the view that it would be appropriate to continue the practice of relying primarily on [SEAC] to keep the scientific issues under review and to draw to my attention those findings which may require changes to be considered to the safeguards to protect animal or public health’ (Waldegrave 1994: 1). 14. It is clear from Mr Lister’s comments on the matter that his decision to invite Dr Dealler to a SEAC meeting was motivated more by a desire to manage a scientist who was judged to be troublesome than by any desire to have a full and frank exchange of opposing scientific views: ‘It is clear from these conversations that the only thing that will really satisfy Dr Dealler is an invitation to discuss his paper at a full meeting of SEAC. I accept that nothing that SEAC members say is ever likely to persuade him to change his view, but unless he is given this opportunity it will always be easy for him to claim that he has been fobbed off. Dr Dealler is not going to go away and may well get increasingly vocal’ (Lister 1994: 1). 15. Dr Dealler’s comments to Lord Phillips and his inquiry team indicate that he believed that no proper assessment of his views was even possible owing to the widespread acceptance of MAFF’s position on BSE: ‘It seemed initially that Professor Lacey and I were being treated as people who simply did not understand the subject and we had to be taught the truth so that we did understand. It was as if anything that we put forward was treated as invalid if it did not agree with their point of view whereas much of what they were saying the other way was accepted’ (BSE Inquiry Report, Volume 11: 256). Dr Dealler also added: ‘The impression that I got from the meeting was that Dr Tyrrell was accepting MAFF’s position on BSE as fact and as such it would be very difficult to get information to be assessed independently in the UK’ (BSE Inquiry Report, Volume 11: 256). 16. In his letter to Mr Eddy of MAFF, Mr Lister remarks that ‘[w]e could time-limit him by scheduling him for the last item of the day (eg, at 3 pm)’ (Lister 1994: 1). 17. In a letter dated 22 November 1994, Mr Wilesmith conceded to Dr Patterson – a consultant in public health medicine in York – that Dr Dealler’s estimates of the scale of the epidemic were correct: ‘I am afraid that I cannot admit this to people such as Stephen Dealler as he may use it against MAFF who naturally fund our research. Unfortunately the decision has been made by the powers that be that no quantitative estimate is made public. This is one that I continually strive to reverse, but have not yet had any success. However, all I can say is that Stephen Dealler’s ‘all time’ cumulative total is not far out’ (BSE Inquiry Report, Volume 11: 270).

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18. The minutes of this meeting continue: ‘The Committee briefly discussed Dr Dealler’s article from the British Food Journal and concluded that it would be useful to seek an epidemiological critique since the article is very densely drafted and difficult even for a professional epidemiologist to understand fully. . .Professor Pattison would like to strengthen the epidemiological expertise available to SEAC to review work. . .’ (SEAC 1995a: 2). 19. The decision to conduct such a review was taken at SEAC’s 23rd meeting which was held on 5 January 1996. The minutes of the meeting suggest that SEAC scientists may in fact have prejudged the outcome of this review (see statement in italics), notwithstanding the qualification given in brackets below: ‘Dr Kimberlin asked whether Dr Dealler’s paper had been analysed. Professor Pattison advised that Mr Wilesmith had written a critique but that it was difficult to understand and that the paper would also need to be analysed by Dr Hueston. The Committee were of the opinion that it would be useful to have several critiques – in effect a peer review. Dr Hueston agreed that this suggestion would add more weight to SEAC’s rebuttal of the paper (if that was in fact the outcome) and offered to co-ordinate and analyse other critiques. The Committee suggested a number of candidates who could be asked to analyse the paper’ (SEAC 1996: 5). 20. Although the conclusions of the Southwood Working Party were based on the scrapie analogy, it is clear from comments by the Working Party’s chairman, Sir Richard Southwood, that this analogy was somewhat tentative and that BSE could not simply be assumed to behave as scrapie had done. In a letter to a medical correspondent in August 1988, Sir Richard stated: ‘My colleagues and I have made various recommendations based, I have to admit, largely on guesswork and drawing parallels from the existing knowledge of scrapie and CJD’ (BSE Inquiry Report, Volume 4: 45). Paragraph 6.3 of the Southwood Report states that ‘[i]t cannot automatically be assumed that animals and man will react to BSE agent exposure as they have done to scrapie, which in the human case has not led to any clear association with disease. BSE agent may for example be an adapted or particularly virulent form of scrapie agent although the results of the epidemiological study indicate otherwise’ (Southwood Report, 1989: 16). 21. In June 1994, Dr Kenneth Calman (Chief Medical Officer) and Mr Keith Meldrum (Chief Veterinary Officer) released a joint statement on the findings of ongoing research on BSE. This statement included claims to the effect that ‘[t]here is no evidence that BSE can cause CJD in humans’ and ‘there is. . .not the slightest evidence that eating beef or hamburgers causes CJD’. 22. The report states that ‘[t]he occupational history of [CJD] cases, controls and their spouses and their parents were also investigated to identify employment in the following areas: medical/nursing/dentistry, etc; laboratory work involving animals; work in pharmaceutical laboratories; work in other research laboratories; livestock farming/veterinary medicine; work in abattoirs/butchers’ shops or other direct contact with animal carcasses; other occupations involving contact with animal products (eg leather workers). There was no evidence that cases were more likely than controls to have worked in any of the above categories. . .Nor was there any convincing evidence that spouses or parents of cases were more likely to have worked in any of these occupations than those of controls’ (CJD Surveillance Unit 1995: 22; italics added). 23. When lexical items are discussed within the context of argument analysis, it is usually in relation to words like ‘so’ and ‘therefore’ which may be taken to indicate the presence of a conclusion of an argument. But as the examples of ‘no new evidence’ and ‘still no evidence’ demonstrate, a much wider range of lexical items need to be considered by analysts during the reconstruction and evaluation of arguments. These words do more than just contribute to the semantics of the propositions in which they occur. As is discussed in the main text, they may be taken to indicate particular dimensions of the process of scientific inquiry, including the iterative nature of some deliberations (questions such as blood safety were returned to time and again by investigators) and the temporal context in which those deliberations are conducted.

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24. SEAC’s reasoning can be reconstructed as follows, where the conclusion of an ignorance argument forms a minor premise in an argument based on modus ponens inference: Argument from ignorance: PREMISE: CONCLUSION:

There is a lack of evidence that CJD is transmitted via blood and blood products. CJD is not transmitted via blood and blood products.

Modus ponens: MAJOR PREMISE: MINOR PREMISE: CONCLUSION:

If CJD is not transmitted via blood and blood products, then there is no justification for recalling blood products. CJD is not transmitted via blood and blood products. There is no justification for recalling blood products.

25. This is evident in one of two questions that the Department of Health posed to SEAC: ‘Does any further work need to be done to support the UK’s current position that there is no conclusive scientific or epidemiological evidence of transmission via blood or blood products?’ (SEAC 1995a: 10). 26. There is little new in the idea that a scientific thesis can improve its epistemic standing in inquiry by surviving attempts to refute it. This idea is the basis of Karl Popper’s programme in the philosophy of science. As Bechtel (1988: 33) characterises that programme, ‘[a] scientist should begin by making conjectures about how the world is and then seek to disprove them. If the hypothesis is disproved, then it should be discarded. If, on the other hand, a scientist tries diligently to disprove a hypothesis, and fails, the hypothesis gains in stature’. It is interesting to note that this process of refutation in science trades upon the same logical structure (modus tollens argument) as the argument from ignorance: ‘[Popper] recommended abandoning the whole endeavor of seeking well-confirmed theories, and proposed instead that scientists focus on demonstrating that some hypotheses are false. His reason for making this shift was that although there is no valid deductive or even good inductive form of reasoning from which we could derive a general proposition from specific instances, there is a valid argument form according to which we can show that evidence disproves an hypothesis. This form is modus tollens or denying the consequent: If H, then P Not P ____ Therefore, not H. If H is the hypothesis in question and P is a prediction that follows from it, then when P turns out to be false we can infer that H is false’ (Bechtel 1988: 33). 27. Walton (2004: 71) classifies arguing to the wrong conclusion as one of the fallacies of relevance, a significant category of informal fallacies which includes ‘two that could be called pure fallacies of relevance – the wrong conclusion (ignoratio elenchi, wrong conclusion, missing the point) fallacy and the red herring (digression, diversion) fallacy.’ Walton (2004) also provides a comprehensive overview of different definitions of this fallacy. 28. This is the essence of the following definition by Copi and Cohen (2009: 134): ‘The ignoratio elenchi is, we may say, a catchall class of fallacies: fallacies in which the premises simply fail to connect to the intended conclusion with the coherence that rational argument requires’. 29. This is the thrust of the following definition: ‘The simplest type of fallacy of relevance occurs in cases where the chain of argumentation starting from the premises proves the wrong conclusion, i.e., a proposition that may look like the conclusion to be proved, but is a different conclusion. This is the fallacy of ignoratio elenchi, or ignorance of refutation, described by Aristotle’ (Walton 2004: 72; italics added).

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30. While this conclusion was more implied that explicitly stated in the extract quoted in the main text from SEAC’s report, it was nonetheless the belief of the committee that FSE would not have implications for human health. The minutes of SEAC’s 5th meeting held on 19 September 1990 record that ‘the Committee did not believe that the disease in cats was of direct relevance to human health’ (SEAC 1990f: 3). 31. See discussion of Fraser et al. (1994) in note 14 in Chapter 5. 32. That features of TSE agents and host genotype both play a role in determining susceptibility to TSEs in any species is evident in the following comments by Bradley (1997: 92): ‘From the collective studies of experimental and natural disease it seems there are natural restraints which resist the transmission of spongiform encephalopathy from one species to another under natural conditions. One is the strain of agent. The other is the variation in the PrP genotype between the donor and recipient species’. 33. See discussion of Fraser et al. (1994) in note 14 in Chapter 5.

Chapter 7

Political and Commercial Interests in the BSE Inquiry

7.1 Introduction The account of the reasoning of BSE scientists in Chapters 4, 5, and 6 has emphasised logical and epistemic features of argument to the exclusion of a vast range of other factors that have an influence on the reasoning process. These factors, which include psychological states1 and emotions2 as well as a range of vested interests, are as significant determinants of the reasoning process as are the logical factors that have traditionally been the focus of study by theorists of reasoning. In the context of the UK’s BSE epidemic, two main types of interest were never far from the risk assessments and other decisions arrived at by scientists. These interests included political considerations of various shades and the concerns of commercial organisations connected to the British beef industry. The role of these interests during the BSE crisis varied from that of directly influencing scientific decision-making and other judgements to creating contexts in which only certain views and opinions could be readily expressed. In an effort to present a complete picture of how scientists reasoned during the BSE affair, this chapter will examine the different ways in which political and commercial interests influenced scientific reasoning in the 10-year period between 1986 and 1996. In keeping with the philosophical orientation of this book, and specifically its concern with the informal fallacies, it will be argued that many of these interests manifested themselves in various types of incorrect or fallacious reasoning. But before we examine individual episodes in the BSE inquiry during which this fallacious reasoning occurred, we return to an earlier distinction between the argumentative strategy of inquiry and the various arguments that are subsumed by this strategy. This distinction provides an important starting point for the discussion of political and commercial interests and reasoning that follows.

7.2 Reasoning and Non-scientific Interests in the BSE Inquiry In earlier chapters, it has been helpful to think of the scientific argumentation that occurred during the BSE inquiry as being conducted on two levels. These levels consisted of an overarching argumentative strategy and a series of arguments that L. Cummings, Rethinking the BSE Crisis, DOI 10.1007/978-90-481-9504-6_7,  C Springer Science+Business Media B.V. 2010

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were subsumed by this strategy. The argumentative strategy, it was claimed, spanned the entire duration of the BSE inquiry. This strategy received rational warrant, at least in the early stage of inquiry, from a range of arguments that scientists used to justify their risk assessments and other decisions relating to BSE. In the middle phase of inquiry, this strategy began to separate from the various arguments that had previously provided it with rational support. While scientists and others continued to argue that beef was safe to eat and that BSE would not transmit to humans as part of the argumentative strategy of inquiry, these claims only appeared to be rationally warranted and were only supported by fallacious arguments. The factors that brought about this separation of the argumentative strategy of inquiry from its rational base were numerous. But they included most significantly the growing dominance of a range of non-scientific interests. These interests became particularly prominent during the middle phase of inquiry as media interest in BSE increased and politicians and commercial representatives began to undertake forceful defences of the British beef industry. This period in the inquiry will provide many of the examples of fallacious reasoning that we will examine in subsequent sections. However, the late phase of inquiry also found scientists and others arguing fallaciously as strenuous efforts were made to continue defending claims that had long since ceased to enjoy the support of rationally warranted arguments. Examples of fallacious reasoning from this period will also be considered. A number of other preliminary comments are in order before we embark fully upon this chapter. The relationship of science to politics, economics and commerce is an overriding theme of the present chapter. Scientific committees and working parties such as SEAC and the Southwood Working Party were established with the purpose of providing independent advice to the government on various aspects of BSE. This advice was then made available to the public through the government’s most senior scientists, the Chief Medical Officer and the Chief Veterinary Officer. This linear model of the communication of scientific advice from its origin (expert scientific bodies) to its eventual audience (the general public) is simplistic, to say the least. In reality, scientific advice was often extensively reworked prior to publication with various political considerations in mind.3 Even when this advice was made available to the public, it was often selectively quoted and extensively qualified in an effort to minimise any adverse reaction.4 Also, scientists were acutely aware of the need to negotiate political and commercial interests in their risk assessments of BSE and of the extent to which this need often compromised the objectivity of their deliberations.5 So the picture to emerge is a complex one in which scientific inquiry during the BSE epidemic was awash with extraneous influences, some of which were detrimental to the aims of inquiry, and all of which had to be addressed to some degree. The success or otherwise with which this was achieved will become apparent in the sections that follow. In the meantime, the reader should be aware that while BSE scientists may have aspired to attain objectivity and impartiality in their inquiries, the reality of their scientific practice was such that these ideals were often subordinated to other concerns. To the extent that science was compelled to engage with a number of other arenas, it is necessary to establish the type of political, governmental, economic and commercial contexts in which scientific inquiry into BSE was conducted. Between 1986

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and 1996, successive Conservative governments led by Prime Ministers Margaret Thatcher and then John Major were in charge of handling of the BSE crisis. It was the policy of these governments to establish expert scientific committees to consider the implications of BSE and then to act on the advice of these committees.6 This policy was enacted through two governmental departments, the Department of Health and the Ministry of Agriculture, Fisheries and Food. Reflecting the significance of the health and agricultural portfolios within government, these departments were headed by senior ministers who were also members of the Cabinet. Much of the everyday work of running departments was delegated to two or more junior ministers7 who were either Parliamentary Secretaries or Ministers of State. Like senior ministers, these positions were also political appointments. Below junior ministers were Permanent Secretaries, the most senior officials (Grade 1) in the civil service. While it was the role of senior and junior ministers to see that government policy on an issue was enacted within departments, individuals who held appointments within the civil service were obliged to remain impartial and to conduct their duties without political affiliation or interference.8 We will see in the sections to follow that the issue of BSE demanded very close interaction and cooperation between individuals who held political appointments within government departments and those who held positions as professional civil servants. The nature of this relationship will be considered at various points in the discussion to follow. The economic context within which BSE emerged was never distant from the deliberations of scientists and others. It is not difficult to see why this was the case. Beef and dairy farming was the largest sector of UK agriculture when BSE first appeared in British cattle. Nearly 38% of the entire agricultural output of the UK, some £5 billion, was earned from the production of milk, fattened cattle and calves. The UK’s cattle population of some 12.7 million animals produced 97% of the beef and veal that was needed to supply the domestic market. Sufficient liquid milk was produced in the UK to meet 100% of the domestic demand for milk and 70% of the domestic demand for butter and cheese (BSE Inquiry Report, Volume 1: 23). In 1988, approximately 10,000 head of cattle and 7,000 head of purebred breeding cattle were exported, a trade that was valued at £5 million and £5.5 million, respectively (BSE Inquiry Report, Volume 10: 59). Before March 1996, an estimated 130,000 people were employed in the UK’s beef and cattle sector (BSE Inquiry Report, Volume 10: 1). Even apart from the impact of BSE on agricultural output and employment, there were economic implications of all the major decisions that were taken to control BSE. For example, the government introduced a compensation scheme in August 1988 which compensated farmers for 50% of the market value of any animal with BSE or suspected of having BSE (this was raised in February 1990 to 100% of the market value of the animal). Between 1988 and 1996, total expenditure on compensation and ex gratia payments to farmers came to £135 million (BSE Inquiry Report, Volume 10: 16). We will engage with economic considerations time and again in the following discussion. A number of bodies represented different aspects of the beef and dairy industry during the BSE epidemic. These bodies included the Meat and Livestock Commission (MLC), the Federation of United Kingdom Milk Marketing Boards

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(the Federation) and the UK Agricultural Supply Trade Association (UKASTA). The MLC was a non-departmental public body whose role was to promote greater efficiency in the livestock industry. It was established under the Agriculture Act 1967 and its members were appointed by the Minister of Agriculture (BSE Inquiry Report, Volume 12: 10).9 Of all industry bodies, the MLC was particularly active during the BSE affair, even to the point of offering incorrect assurances about the safety of beef.10 It was advised by Dr Richard Kimberlin, whom we have encountered in previous chapters through his work as a witness to the Southwood Working Party and a member of the Tyrrell Committee and SEAC. In 1986, the Federation consisted of the five Milk Marketing Boards in the UK. It was established in 1962 to assist in the development of UK dairy policy and to present a united position for dairy farmers in discussions with government (BSE Inquiry Report, Volume 12: 9). Along with other bodies, the Milk Marketing Board pointed out a discrepancy regarding the use of milk from BSE suspects.11 This was to lead to the introduction on 30 December 1988 of the Bovine Spongiform Encephalopathy (No. 2) Order 1988 which placed a ban on the use of such milk other than for the purpose of feeding the cow’s own calf. The feed producers’ trade association UKASTA was very actively involved in discussions with MAFF about measures designed to control BSE. Amongst its actions, UKASTA drew up a code of practice to try to minimise cross-contamination of feedstuffs during the production process (BSE Inquiry Report, Volume 1: 27). This Association was another aspect of the complex commercial context in which the BSE crisis unfolded. Finally, a couple of introductory comments are in order about the type of reasoning that we may expect to find being used by scientists and others when a range of non-scientific interests predominated during inquiry. To the extent that interests are always the interests of particular individuals or groups of individuals, it is to be expected that many of the arguments which we will examine in this chapter focus on attributes of the arguers who produce these arguments. These attributes may describe some aspect of an arguer’s professional identity such as their expertise in a particular discipline or topic. Or they may capture aspects of an arguer’s personal identity such as their moral character. It may be legitimate in argument to make reference to one of these attributes to support a claim that the arguer is advancing. For example, genuine expertise on the part of an arguer in a scientific or technical discipline is a strong ground in support of a claim that an arguer is advancing within that discipline. More often than not, however, these attributes are used in argument to render the claims of an arguer invalid or at least weaker than they might otherwise be. Attacks against an arguer’s mental competence or moral character, for example, are rarely legitimate and are intended to invalidate the claims advanced by this arguer. Two informal fallacies embody this attribute-based form of reasoning, the argumentum ad verecundiam (argument from authority) and argumentum ad hominem (argument against the man). Variants of both types of argument were used extensively by scientists and others during the BSE crisis, often with a view to securing some argumentative gain, e.g. the acceptance of claims about beef safety or the dismissal of challenges to the consensus view of BSE. We will examine both types of argument in detail below.

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So we may expect to find a preponderance of attribute-based reasoning in use in inquiry when investigators are mindful of satisfying a range of non-scientific interests. But non-scientific interests also manifested themselves in the reasoning of scientists during the BSE inquiry in one further respect. In Chapters 4, 5, and 6, we described how analogical and ignorance arguments formed the mainstay of scientific reasoning during the BSE crisis. In particular, analogical reasoning based on scrapie shaped BSE risk assessments continuously throughout the period between 1986 and 1996. This period extended from the very earliest stage of inquiry, when this form of reasoning was particularly strongly warranted, to the late phase of inquiry, when analogical reasoning continued to be used despite a lack of evidential warrant in its support. Notwithstanding the dominance of this form of reasoning, there were occasions during the BSE inquiry when investigators sought to distance themselves from the scrapie analogy and any reasoning based on it. When these occasions are examined, they may be seen to be influenced to a very large degree by non-scientific interests such as the protection of the UK’s export trade. As we argued in Chapters 5 and 6, there are conditions under which it was appropriate for investigators to suspend their commitment to analogical reasoning based on scrapie (even if, as we also argued, this suspension did not actually occur during the course of inquiry). A question that we will also consider below is whether the protection of certain economic and other interests constitutes such a condition.

7.2.1 Argument from Authority The notion of expertise was integral to all the scientific deliberations that took place during the inquiry into BSE. An expert knowledge of TSEs was not within the purview of most scientists, even less the various government ministers and officials who had to develop policy to control the spread of BSE. During the BSE crisis, scientific advisory groups such as SEAC were established with a view to satisfying this demand for expert knowledge. The constitution of these groups reflected the diverse medical and veterinary disciplines that converged on the study of TSEs. Such was the need to maintain the expert status of these groups that extensive efforts were made to review and, if necessary, change their membership to reflect the type of risk assessments that these groups were being asked to undertake.12 These efforts would have been to no avail were it not for the fact that expertise carries real probative weight in scientific and other deliberations. Indeed, in the same way that it is rational to accept the results of experimental studies as revealing certain truths about nature, it is also rational to accept the testimony of someone who is an established expert in a particular field or discipline as revealing facts about the world around us. Expertise is thus revered with considerable justification. But it may also be abused and misused by scientists and others.13 Abuses and misuses occur when someone lacks expertise in the area or discipline in which he claims expertise (charlatans exist in science as in other areas of life) or has genuine expertise in one area but then makes statements from a position of apparent expertise in an unrelated area.14 There is a fine line between genuine, true expertise and fraudulent, false expertise

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and any negotiation of this line must be based upon a careful assessment of the case in hand. Such an assessment will be integral to the examination of expertise appeals in argument which will be conducted in this section. Before embarking on our analysis of authority appeals during the BSE crisis, it is instructive to consider the type of grounds that had led earlier generations of philosophers and logicians to dismiss appeals to expertise or authority in argument as fallacious.15 The basis of this argument’s fallaciousness, it was argued, is its dependence on the opinions and judgements of individuals, both of which are ‘subjective elements’ that offend against the objectivity that is aspired to in a scientific context. While not subscribing to this view of the argument, Woods and Walton (1974: 136) capture the considerations that motivate it as follows: . . .to allow an appeal to authority as a genuine form of acceptable argument is to throw scientific objectivity to the winds. . .an appeal to authority, having intrinsically inexact and subjective elements about it, must be ruled out of the domain of science entirely.

This rejection of authority appeals is motivated by a suspicion of the cognitive agent and of the subjectivity that such an agent brings to scientific deliberations.16 This subjectivity is not an adequate basis, it is argued, to form a scientific epistemology that is able to deliver objective knowledge claims. But an epistemology that demands the exclusion of cognitive agents is not a workable epistemology for scientific inquiry or, indeed, for most other human affairs. To the extent that appeals to authority are fallacious in scientific inquiry, their fallaciousness should not reside in the mere fact that expert testimony is being used but, rather, in the fact that the quality of that testimony can be called into question. In order to interrogate the quality of expert testimony, we must engage with cognitive, dialectical and presumptive considerations that have no place in traditional epistemologies. Like the other arguments that we have examined in this book, we will pursue a presumptive analysis of the argument from authority in the discussion below. The essence of this analysis is that authority appeals can give rise to presumptively warranted claims which, under the right conditions, may become the basis of objective knowledge claims in inquiry. Indeed, authority appeals are often most rationally compelling when objective knowledge from other sources is lacking or unavailable in inquiry and when decisions and other courses of action cannot be postponed until such knowledge becomes available. We will return to these points subsequently. So our starting point in this discussion is that contra certain philosophers, no authority appeal should be ruled out of court simply by virtue of being an authority appeal. Some of these appeals are warranted and are capable of delivering theses that can become objective knowledge claims in inquiry and it is the task of argument analysts to establish which of these arguments fulfil these criteria. To embark on this task, we must first examine the types of authority appeals that were made during the BSE inquiry. To this end, we examine a number of assurances that were given about the safety of beef by medical, political and commercial figures in May 1990. The first of these assurances occurred on 15 May 1990. In a letter to Lady Wilcox (Chairperson of the National Consumer Council), the Minister of Agriculture, Fisheries and Food, Mr John Gummer, described how ‘independent

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experts have concluded that BSE is most unlikely to have any implications for human health’ (BSE Inquiry Report, Volume 6: 368; italics added). On 16 May 1990, the Department of Health issued a press release in which the Chief Medical Officer, Sir Donald Acheson, was reported as saying: I have taken advice from the leading scientific and medical experts in the field. I have checked with them again today. They have consistently advised me in the past that there is no scientific justification for not eating British beef and this continues to be their advice. I therefore have no hesitation in saying that beef can be eaten safely by everyone, both adults and children, including patients in hospital (Department of Health 1990: 1; italics added).

The following day on 17 May 1990, the MLC issued a press release entitled ‘British Beef is Safe’. This release stated that: . . .the most eminent and distinguished scientists in Britain and in the rest of Europe have concluded there is no evidence of any threat to human health as a result of this animal health problem (BSE Inquiry Report, Volume 6: 377; italics added).

So numerous were the appeals to authority during this period that these examples could be readily multiplied.17 However, the three extracts that we have cited can be used to demonstrate the main features of the authority appeals that were made during the BSE inquiry. The expertise of the different authorities that are appealed to in these extracts is represented in various ways. The professional standing of scientists and experts is indicated through the use of adjectives like ‘eminent’, ‘distinguished’ and ‘leading’. To reflect the impartiality of experts, they are described as being ‘independent’. Finally, in an attempt to establish the extent of their expertise, scientists are represented as having eminence in ‘Britain and in the rest of Europe’, all countries that are deemed to have advanced scientific communities. The aim of these combined linguistic devices is to emphasise that the expertise at issue in these cases is genuine and real as opposed to false and illusory (although a critical examination of the sources of expertise in these cases may reveal these claims to be little more than instances of linguistic exaggeration). Using an argumentation scheme for appeals to expert opinion advanced by Walton (1997: 258), we may say that these various statements are used to ground the first premise in the argument below, in which A is a proposition, E is an expert and D is a domain of knowledge: E is an expert in domain D. E asserts that A is known to be true. A is within D. Therefore, A may (plausibly) be taken to be true. Applied to the above authority appeals relating to the safety of beef, this scheme assumes the following form: PREMISE 1: PREMISE 2:

Members of BSE scientific committees are experts in the study of TSEs. Members of BSE scientific committees assert that the proposition ‘beef is safe’ is known to be true.

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‘Beef is safe’ is a proposition within the disciplines that study TSEs. Therefore, ‘beef is safe’ may plausibly be taken to be true.

The conclusion of this argument is warranted to the extent that (1) the scientific committees that provided advice to the government on BSE did indeed contain experts in the fields or disciplines that study TSEs, (2) these scientific experts subscribed to the view that beef is safe and (3) an assessment of the safety of beef falls within the fields or disciplines that study TSEs. The consistent advice of both the Southwood Working Party and SEAC was that BSE posed little, if any, risk to human health and that beef was safe to eat as a result.18 So premise (2) of the above argument is strongly warranted. The same can be said of premise (3). In order to determine that beef is safe to eat, something must be known about the BSE infectivity of bovine tissues (particularly skeletal muscle), the efficiency of the oral route in transmitting the BSE agent, the susceptibility of humans to prion diseases, etc. This knowledge is only to be found in the various disciplines that converge on the study of TSEs. So there is also considerable warrant for premise (3) in the above argument. However, the same cannot be so readily said of premise (1) in this argument. It is true that certain scientists on the committees that advised the government about BSE were experts on TSEs – Dr Richard Kimberlin, who was a member of SEAC, is a case in point. However, the Southwood Working Party contained no experts on TSEs, a point that attracted criticism from certain sections of the print media and which was directly interrogated by Lord Phillips and his inquiry team.19 So the rational standing of the above authority appeals hinges on whether the scientific committees that provided advice to the government on BSE embodied true expertise in the area of TSEs. For Lord Phillips and his co-investigators these committees contained such expertise; for certain others, this expertise was noticeably lacking.20 These examples of authority appeals are also interesting for what they can tell us about the wider epistemic conditions in which arguments from authority may be used. The question of the safety of beef could not be directly investigated. Experimental studies could certainly establish if the BSE agent was to be found in bovine skeletal muscle and the concentration of any agent in this tissue. But the question of safety would always come back to the concentration of BSE agent in beef that would be capable of orally transmitting disease to humans. Yet, ethical restrictions on the use of human subjects in research meant that this issue could not be experimentally tested. The best and, in fact, the only way to proceed in these circumstances was for government ministers to solicit the opinion of scientific experts and to use this opinion to formulate policies for dealing with BSE. To the extent that the cognitive authority of these experts was called upon to address a question that could not be experimentally investigated, the argument from authority can be seen to facilitate the progression of inquiry in the absence of other sources of evidence and knowledge.21 Like the other presumptive arguments that we have examined in this book, the argument from authority was used to licence decisions and other courses of action that would not have been possible where a requirement for knowledge in place in inquiry.22 Its function is thus akin to the argument forms that were used in

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the early stage of the BSE inquiry, forms which, it was argued, were specific adaptations of cognitive rationality to the uncertainty that exists in the emergent phase of a scientific inquiry. Yet again, it can be seen that one of the so-called informal fallacies had a significant epistemic contribution to make to inquiry into BSE, a contribution that is overlooked within traditional characterisations of the argument from authority. Thus far, we have considered a beneficial use of the argument from authority during the BSE inquiry (even though, as we have seen, some doubt exists as to whether individual authority appeals used in this inquiry were sufficiently warranted to qualify as examples of this use). However, the argument from authority was also skilfully manipulated on occasion during the BSE inquiry to achieve certain argumentative gains that had nothing to do with advancing scientific inquiry. On one such occasion at least, this manipulation was serving the commercial interests of one of the industry organisations described above, the Meat and Livestock Commission. We examine this particular case in the rest of this section. In an attempt to address growing public concern about BSE, the MLC distributed a video entitled ‘Beef – The Facts’ to local authorities in 1990. In this video, Mr Colin Maclean, Technical Director of the MLC, claimed: In 1988 the Government commissioned a report from a group of eminent scientists led by Professor Richard Southwood of Oxford University. They reported eighteen months ago that if the current meat industry practices continued, the chance of transmission of BSE from cattle to man by any method was remote – if they do nothing. Finally, to quote the Government’s Chief Medical Officer, Sir Donald Acheson ‘Beef can be eaten safely by everyone, both adults and children, including patients in the National Health Service.’ (BSE Inquiry Report, Volume 6: 378; italics added).

Two authority appeals advanced by Mr Maclean in this extract address the question of BSE transmission from cattle to man and the question of the safety of beef for human consumption. The expert sources that are cited in relation to each of these questions are, respectively: • Eminent scientists led by Professor Richard Southwood of Oxford University • Government’s Chief Medical Officer, Sir Donald Acheson Each member of the Southwood Working Party was a respected authority in his specialist field.23 Moreover, the scope of their combined specialisms in zoology, virology, clinical neurology and veterinary science certainly equipped the working party to make authoritative statements on a whole range of scientific issues. Notwithstanding the considerable collective expertise of these scientists, it is still open to question whether this expertise qualified them to make an assessment of a matter relating to TSEs. The more important issue for our present purposes is not whether this was a warranted appeal to authority, but the fact that an appeal to authority was made at all. In his appeal, Mr Maclean marked the authority of the Southwood scientists through his use of the adjective ‘eminent’ and the academic title (Professor) and institutional affiliation (Oxford University) of the chairman of

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the party. Sir Donald Acheson, the second of our expert sources, was not personally qualified to make pronouncements on the safety of beef for human consumption – the question of the safety of any animal product for human consumption depends for an answer as much on veterinary expertise as on medical expertise and, as such, lies outside of the exclusively medical competence of the Chief Medical Officer. However, through consultations with veterinary and medical experts, Sir Donald acquired a form of indirect expertise on the question of the safety of beef and an appeal to his authority in argument was an appeal to this indirect expertise. So, two arguments from authority were advanced by Mr Maclean in support of the MLC’s position that BSE was unlikely to transmit from cattle to man and that, consequently, beef was safe to eat. However, the fallaciousness of Mr Maclean’s reasoning does not lie in either of these arguments. Rather, the fallaciousness of his reasoning only truly emerges when these two appeals to authority are examined in the context of the following extract from the same MLC video: One person has suggested that in order to infect cattle the agent may have changed, mutated, and so it can change again to infect humans. There is now sound scientific evidence that this is simply not the case (BSE Inquiry Report, Volume 6: 378; italics added).

I want to contend that an appeal to expertise is necessary in this extract and that Mr Maclean quite deliberately avoids using such an appeal. To see that such an appeal is necessary, we need only consider the wider argumentative context in which the above extract occurs. Mr Maclean produces two appeals to expertise in an attempt to support the MLC’s claims that beef is safe to eat and that BSE cannot transmit from cattle to humans. On the question of transmission, he then goes on to address a viewpoint which the MLC opposes (that BSE may yet transmit to humans because the causative agent may mutate). In the interests of achieving balance in argument, it is necessary for an arguer to accord the same rights of cognitive authority to each of the experts who are making contributions to a debate. At a minimum, this requires that the arguer state the name, professional title and affiliation of the expert in question. It is evident from the above extract that Mr Maclean neglects to fulfil even this minimum requirement – the source of a viewpoint that is opposed by the MLC is merely referred to as one person. What motivates this neglect, I contend, is Mr Maclean’s desire to remove authority from his opponent in argument and, in so doing, invalidate this opponent’s claims – the source of this claim, he is implying, lacks cognitive authority with the result that the claim itself has no rational standing. Moreover, this claim is further weakened on account of its juxtaposition with two authority arguments that support the MLC’s position. It emerges that the fallaciousness of Mr Maclean’s reasoning lies not in any unwarranted appeal to authority but in the failure to use an authority appeal when the argumentative context effectively demands such an appeal. This last claim warrants further examination. It is commonplace for fallacy theorists to use the term ‘fallacy’ only when certain argumentative errors have been committed. On some occasions, these errors take the form of the violation of a rule of dialogue or of inference. On other occasions, arguers use premises that do not support the conclusion of an argument or that

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support a different conclusion. Typically, these errors are antithetical to the fulfilment of one or more of the purposes for which we engage in argument, whether this is the resolution of a dispute or the demonstration of a scientific thesis. However, it is clear that an arguer can also act in ways that are antithetical to the fulfilment of these purposes by failing to do certain things. For example, an arguer may fail to use available evidence to support a claim and this would be as much of an argumentative flaw as the arguer who uses weak evidence to support a claim. In the same way, the arguer who uses an unwarranted appeal to authority and the arguer who fails to appeal to authority when such an appeal should be used to support a claim are both acting in ways that preclude the fulfilment of one or more of the purposes of argument (it would be as difficult to make a legal or scientific case in support of a thesis if an arguer failed to appeal to authority – assuming such an appeal could be legitimately made – as it would if an arguer made fallacious authority appeals). This extended conception of fallacy – a fallacy is as much about what is not done in argument as it is about what is done that is incorrect – can now be applied to the reasoning employed by Mr Maclean. It is clear that the MLC was under considerable pressure to address growing public concerns about the safety of beef. Media speculation about the potential risks posed by BSE to human health threatened to destabilise the UK’s beef industry. In a letter to Mr John MacGregor (Secretary of State, MAFF), Mr Geoffrey John (Chairman of the MLC) remarked: At its meeting today [25 May 1989], the Commission expressed very considerable and urgent concern about the effect of the current BSE issue on the public perception of the meat industry, and potentially on beef sales. You, of course, will be fully aware of recent media interest in the subject (BSE Inquiry Report, Volume 6: 134).

It was against this increasingly difficult background that Mr Maclean of the MLC set about attempting to alleviate the public’s fears about BSE. To this end, he embarked upon an argumentative monologue, in which he is seen both to advance claims and to respond to counter-claims. However, given the looming threat to the beef industry, it is clear that Mr Maclean’s overwhelming concern was not simply to provide the public with facts upon which it could base its own assessment of risk. Rather, his primary concern was to defend the British beef industry and, particularly, to argue forcefully in support of the claim that beef was safe to eat. Mr Maclean promoted this interest in two ways. Firstly, he advanced two appeals to expertise in support of claims that it was within his organisation’s interest to defend. Secondly, he failed to accord proper rights of cognitive authority to the source24 of an opposing claim. Mr Maclean’s dual strategy served to erode the authority of the source that produced this opposing claim which, in turn, enabled him to imply that there was no rational basis to this claim. In this case, Mr Maclean was not making an unwarranted appeal to authority – in fact, he made no appeal to authority whatsoever. To this extent, his error was quite unlike the flaws that are typically associated with fallacious appeals to authority. Notwithstanding this fact, Mr Maclean was still reasoning fallaciously when he failed to use authority in a context that demanded its use (Cummings 2005).

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7.2.2 Argument Against the Person Logicians have long recognised the widespread tendency of arguers to attempt to reject an opponent’s claim by attacking some attribute of the person who is advancing that claim. This type of argument is variously known as argumentum ad hominem, argument against the person or, more literally, ‘argument directed to the man’. The attribute in question may be some aspect of an individual’s moral character, mental competence or a range of other personality and character traits. There are occasions on which it is relevant to challenge a claim by appeal to an attribute of the arguer who has advanced that claim. For example, a candidate for the position of mayor who argues that he alone has the moral scrupulousness to hold public office deserves to have this claim challenged by reference to his conviction for financial irregularities 5 years earlier. Similarly, the scientist who is known to have engaged in plagiarism of his colleagues’ work should not be surprised to find his scientific peers less than willing to accept the veracity of his various claims and conclusions. When this type of argument is used fallaciously, however, its fallaciousness resides in the fact that some attribute, which is judged to be irrelevant25 to the claim under discussion, is being advanced as a logical ground against the claim. In fact, it is not unusual to find ad hominem argument used most extensively when an arguer lacks logical grounds against a claim. In the absence of such grounds, he attempts to reject his opponent’s claim by bringing forward some negative attribute of his opponent. Although characterisations of the fallacy vary, it is generally recognised that two variants of ad hominem argument exist: abusive ad hominem (a direct attack on an opponent’s character, trustworthiness, etc.) and circumstantial ad hominem (criticism of the personal circumstances of an opponent in argument).26 We will examine both forms of this fallacy in this section. During scientific inquiry into BSE, ad hominem arguments were used with considerable frequency. It is revealing of the nature of this inquiry and of ad hominem argument to ask why this was the case. We described above how non-scientific interests came to dominate scientific inquiry into BSE at various points. The promotion of these interests by those who held them was less a logical pursuit than it was an exercise in upholding certain claims, often at all costs. In fact, the protection of these interests frequently required individuals and organisations to assume logically indefensible positions and to advance claims and counter-claims which enjoyed little, if any, rational warrant. It is not difficult to envisage how ad hominem arguments flourished under these conditions. These arguments function by replacing logical grounds against a claim by grounds that appeal to some negative attribute of the proponent of a claim. If logical grounds could not be brought against a claim because such grounds did not exist, and yet the imperative in argument was nevertheless to overturn a claim that was contrary to certain interests, the arguer who is committed to these interests has little alternative but to fall back on features of his opponent’s character to defeat the claim in question. To the extent that statements about an opponent’s character are used to overturn a claim when logical grounds do not exist for this purpose, we may reasonably predict increased use of ad hominem arguments during times in the BSE inquiry when scientific investigators were attempting to

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defend increasingly untenable views. We will see below that this prediction is borne out – ad hominem arguments were used extensively against certain dissenting scientists in the late phase of inquiry when it was becoming increasingly apparent that the consensus view of BSE could no longer be rationally defended. We described in Chapter 6 how a small number of scientists in the late phase of the scientific inquiry into BSE began to question the established view of this bovine disease. In specific terms, these scientists, who included Professor Richard Lacey and Dr Stephen Dealler, challenged the idea that BSE was derived from scrapie in sheep. The problem that this challenge created for the consensus view of BSE was that if an ovine origin of BSE could not be assumed, then the scrapie analogy itself along with all the risk assessments that had been based on this analogy began to look decidedly weak. In Chapter 6, various argumentative tactics were described whereby the established view of BSE was protected from this potentially devastating challenge. These tactics were intended to deny dissenting scientists certain dialectical rights in inquiry such as the opportunity to present their views and to have those views rationally assessed by their scientific peers. However, there was a further way in which mainstream scientists sought to undermine the views of those who attempted to challenge the scrapie origin of BSE. That way was to discredit the scientists who were involved in launching this challenge through the use of a series of ad hominem arguments. These arguments had a number of different targets including attacks on the professional competence and even the mental competence of the scientists in question, as well as attempts to throw doubt on the motivations of these scientists for challenging the consensus view of BSE. We will examine a number of these ad hominem arguments below before considering how these arguments were used to serve certain non-scientific interests during the scientific inquiry into BSE. Attempts to undermine the professional competence of dissenting scientists were integral to a large number of the abusive ad hominem arguments that were made during the BSE inquiry. They included claims to the effect that these scientists lacked subject knowledge, that they had inadequately acquainted themselves with the existing literature in the area, and that their work was not publishable in the most prestigious scientific journals. On occasion, these claims even went as far as suggesting that these individuals did not deserve to be called ‘scientists’. The mental competence of dissenting scientists was also variously attacked with claims made to the effect that certain assessments relating to BSE were beyond the mental abilities of these scientists. Dissenting scientists were also presented as being divorced from reality and not sufficiently rational to contribute to the scientific debate about BSE.27 An example of each of these abusive claims is given below. The target of each of these claims is Professor Lacey’s published work. Specifically, example (1a) is taken from a correspondence between Mr Bradley (Head of the Pathology Department, CVL) and Mr Eddy (MAFF Head of Animal Health Division) on 20 November 1994. The subject of the correspondence is Professor Lacey’s paper entitled ‘Bovine Spongiform Encephalopathy: A “Progress” Report’ which was published in the British Food Journal in 1994. Examples (1b), (2a), (2b), (4), (5a), (5b) and (7) are taken from a review of Professor Lacey’s paper ‘BSE: The

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Gathering Crisis’ by Mr Wilesmith (Head of Epidemiology, CVL). This paper was published in the British Food Journal in 1993. Finally, examples (3) and (6) are from a correspondence on 2 December 1994 between Mr Eddy and Mr Cahn (Principal Private Secretary, MAFF). The subject of the correspondence is Professor Lacey’s forthcoming book Mad Cow Disease: The History of BSE in Britain. Abusive claims about Professor Lacey’s professional competence: Example (1): Inadequate subject knowledge (a) This article is badly written, makes wrong deductions and exposes his [Lacey’s] own and Dr Dealler’s superficial and inaccurate knowledge of the subject area. (b) The last part of this sentence, relating to the detection of infectivity in cattle feed, uncovers an epidemiological and microbiological ineptitude. Example (2): Inadequate acquaintance with literature (a) . . .if Lacey had read the whole literature, digested it and understood it he would have no doubt written something more appropriate. (b) if he had really read the Southwood Report and the derivative paper Wilesmith and others (1988) there was no change of view. Example (3): Low standing of published journal articles . . .you might find it helpful to have a short Q&A brief on the main arguments which Professor Lacey has recently been pedalling in a series of scientific papers which are basically different versions of the same theme, published in different fringe journals. Example (4): Failure to warrant title of ‘scientist’ This is truly amazing from a so-called scientist. It is a selective presentation with a total disregard of the complete results presented in the paper. Abusive claims about Professor Lacey’s mental competence: Example (5): Poor mental abilities (a) What he [Professor Lacey] does not (consciously) realise is that the 4 year old animals represent the greatest number of cases and therefore weight the apparently ‘age unknown’ category. The animals of course are in a transit category whilst we obtain the questionnaires. A process which is very complicated and on present experience is beyond the mental abilities of Lacey. (b) I do not need to comment on Lacey’s stupid misinterpretation of the whole system and more particularly the House of Commons Agriculture Committee.

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Example (6): Detachment from reality In 1990 the Agriculture Select Committee considered evidence from him [Professor Lacey] and others and reached the conclusion that he seemed to lose touch completely with the real world and showed a tendency to extrapolate sensational conclusions from incomplete evidence. Example (7): Unfit to contribute to scientific debate The third sentence is a clear exhibition of Lacey’s innumeracy and inability to contribute to the scientific discussion of the problem in a constructive manner. Collectively, these claims became the basis of an abusive ad hominem argument in which the views of Professor Lacey and other dissenting scientists were discredited by attempts to portray these individuals as lacking on one or more indicators of professional and mental competence. The claim that scrapie was not the origin of BSE, it was being argued, was not credible when it came from scientists who were not particularly well acquainted with the relevant scientific issues and who were not even capable of understanding and assessing those issues. Yet, this was not the only type of ad hominem argument advanced against scientists who attempted to challenge the consensus view of BSE. Circumstantial ad hominem arguments were also frequently used against dissenting scientists. One version of this type of argument is ‘used to suggest that the opponents’ conclusion should be rejected because their judgment is warped, dictated by their special situation rather than by reasoning or evidence’ (Copi and Cohen 2009: 130). It is clear that on several occasions during the BSE crisis, MAFF scientists and parliamentary committees attempted to undermine the views of Professor Lacey and Dr Dealler by highlighting particular features of the circumstances of these scientists. These features, it was suggested, had led these scientists to adopt views that were a direct challenge both to the government’s handling of BSE and to the scientific consensus on BSE. The first circumstantial ad hominem argument we will examine occurred in the fifth report on BSE of the House of Commons Agriculture Committee which was published on 10 July 1990. Amongst their conclusions, the Committee stated: Professor Lacey. . .showed a tendency to extrapolate sensational conclusions from incomplete evidence in order to publicise his long-standing concerns about food safety. . .We do not doubt the sincerity of Professor Lacey’s concerns, but we must question the judgement of television producers and newspaper editors who beat a path to his door as an authority on all aspects of food safety (Agriculture Committee 1990: xxi, paragraph 74).

By the time BSE emerged, Professor Lacey had already been a vocal critic of the handling of previous food scares.28 This critical stance had seen him assume a high profile in both the print and broadcast media.29 The implication of the Committee’s remarks was that Professor Lacey’s position on these earlier food scares, and particularly his previous media work, disqualified him from offering an objective scientific opinion on the issue of BSE. To the extent that he had a proven track record of producing exaggerated claims in the media, the Agriculture Committee30 was arguing, Professor Lacey was incapable of making a sound assessment of the human

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health risks of BSE. By portraying Professor Lacey as an alarmist who enjoyed making extreme statements to the media, the Agriculture Committee was attempting to argue that this scientist’s views on BSE were influenced more by his agenda for publicity on food scares than by any reasoned consideration of the scientific facts and evidence relating to this new bovine disease. The Agriculture Committee’s ad hominem argument was intended to undermine and, to a large extent, succeeded in undermining Professor Lacey’s status as a legitimate scientific actor in the BSE affair. The second example of circumstantial ad hominem argument which we will consider is directly related to the case just examined. It concerns a written correspondence on 25 July 1990 between Mr Bradley of the CVL and Dr Joe Gibbs of the National Institutes of Health in Maryland, USA. Dr Gibbs had previously written to Mr Bradley to enquire about the identity of Dr Dealler (who was seeking a meeting with Dr Gibbs on a trip to the US) and to explore the possibility of undertaking collaborative research with Mr Bradley. Mr Bradley stated in his response: He [Dr Dealler] works with Professor Lacey who has been a vigorous antagonist of the Ministry on many aspects of BSE control. We have recently had a House of Commons Select Committee on Agriculture looking at the BSE problem and the way the Government has tackled it. As a result of the interviews of Professor Lacey by the Committee, he has been very much discredited as an alarmist. I do not know Dr Dealler’s relationship to Professor Lacey but they both work for the same employer and apparently in the same Department. I do not know him myself. I have gathered via the grapevine, colleagues in the University were not particularly enamoured with Professor Lacey’s high profile and sensationalist approach. However, I just do not know where Dr Dealler stands on this issue. Nevertheless, I would advise caution in forming a close liaison with the Department, particularly on the subject of meat and bone meal analysis, if that is the intention (Bradley 1990: 1).

Mr Bradley, I contend, is using this response to launch a circumstantial ad hominem argument against Dr Dealler’s views on meat and bone meal. He achieves this in a stepwise fashion. As a first step, Mr Bradley attempts to discredit Professor Lacey by portraying him as an alarmist (first paragraph) who does not have the support of his academic colleagues (second paragraph). The second step finds Mr Bradley attempting to link Dr Dealler, and by implication his views, to Professor Lacey through the shared employer and academic department of these scientists. In effect, Mr Bradley is implying that Dr Dealler is not to be trusted to deliver an objective scientific opinion on meat and bone meal and BSE in general on account of his association with the discredited scientist Professor Lacey. Mr Bradley has perpetrated against Dr Dealler a form of circumstantial ad hominem argument called ‘poisoning the well’, in which an aspect of Dr Dealler’s circumstances or background (specifically, his professional association with another scientist) is used to discredit him in argument. If there were any doubt that this has been Mr Bradley’s argumentative intention in this context, that doubt is effectively dispelled through Mr Bradley’s final comment which explicitly advises Dr Gibbs not to establish a research collaboration with the department that employs Dr Dealler. That a deceptive argumentative tactic is at work in this extract is further demonstrated by Mr Bradley’s use of three statements declaring a lack of knowledge of, respectively,

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Dr Dealler’s relationship to Professor Lacey, Dr Dealler himself and Dr Dealler’s stance on meat and bone meal. These statements have the effect of distancing Mr Bradley from any accusation that he is perpetrating a circumstantial ad hominem attack on Dr Dealler, while at the same time providing essential cover for that attack to go ahead. Thus far, we have established that abusive and circumstantial ad hominem arguments were advanced against Professor Lacey and Dr Dealler during the late stage of the BSE inquiry. We have also characterised these arguments as most likely to be used against an opponent in argument when an arguer lacks logical grounds against an opponent’s thesis and attempts to substitute some negative attribute of the opponent in place of these grounds. Furthermore, we said that it became increasingly difficult for government scientists to advance logical grounds against those scientists who were challenging the consensus view of BSE in the final stage of inquiry into this disease – by that stage, substantial evidence had amassed against an ovine origin of BSE. But we have yet to establish the factors that so forcefully motivated government scientists to pursue ad hominem attacks against dissenting scientists. These factors, I contend, can be loosely characterised as a set of political, commercial and economic interests that would have been directly compromised had the views of dissenting scientists been allowed to gain prominence in inquiry. The political response to BSE ranged from public reassurances that beef was safe to eat to the introduction of legislation and bans to control the spread of BSE. This response was directly premised on the belief that BSE had been caused by the transmission of sheep scrapie to cattle. To the extent that an ovine origin of BSE could no longer be assumed, the response of politicians to this new bovine disease began to appear misguided. To prevent an unravelling of the government’s position on BSE, parliamentary bodies and government (mainly MAFF) scientists undertook a strident campaign of rebuttal against dissenting scientists.31 This campaign consisted for the most part in ad hominem arguments which were not warranted and which did not contribute to a rational discussion of the scientific issues relating to BSE.32 Of course, political interests during the BSE inquiry were inextricably linked with economic and commercial interests. Dissenting scientists such as Professor Lacey were calling for measures to be taken in relation to BSE that would have had considerable economic implications for the country as a whole and for the beef industry in particular had they been implemented. In an article in The Sunday Times on 13 May 1990, Professor Lacey called for the slaughter of all herds that had at least one BSE case, a cull that would see some 6 million animals destroyed.33 Dr Dealler told Mr Bradley during a visit to the CVL on 15 April 1994 that he would ban the consumption of liver and kidney from cattle over 6 months and all tissues from cattle over 21/2 years. Liver and kidney were excluded from the human SBO ban and there was no existing ban on the use of tissues from cattle over 30 months.34 So this measure, if it were to be adopted, would have considerable economic implications for industry, as Dr Dealler himself acknowledged.35 In a memorandum submitted to the Agriculture Committee on 13 June 1990, Professor Lacey and Dr Dealler made five recommendations. The first of these recommendations related to rendering (processing) plants. It stated that ‘[t]here is a clear case for the total prohibition

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of the use of the bone meal fraction from rendered animal and poultry remains in those species’ (Agriculture Committee 1990: 22). Although a ban had been in place on feeding ruminant protein to ruminants since July 1988 (the ruminant feed ban), MAFF had always resisted banning the use of cattle offal in pig and poultry feed.36 A total prohibition on rendered animal material in the feed of all species posed considerable commercial and economic challenges not only to the rendering industry, which would no longer have customers for its products, but also to abattoirs, which would have to pay for disposal of material that previously would have been recycled by means of rendering.37 The economic and commercial implications of such an all-encompassing ban were evident to all, particularly to the government and its scientists.38 In short, every measure implemented to control BSE had very immediate economic and commercial implications which it was not irrational for politicians, scientists and others to consider as part of their decision-making. These implications were all the greater in the case of the recommendations of dissenting scientists, who were more inclined than government scientists to recommend the most extensive courses of action possible in order to protect public health.39 Of course, it was somewhat easier for dissenting scientists to propose wide-ranging measures to control BSE. These scientists did not have to balance the competing demands of serving the public health interest and avoiding legal action40 – protecting public health was the primary, or even only, concern of these scientists.41 Moreover, the work of dissenting scientists was funded through university departments and was not in the service of a research agenda determined by government departments such as MAFF.42 The lack of competing interests on the part of dissenting scientists certainly facilitated these scientists in pursuing a public health response to BSE with singular focus. But at the same time the pronouncements of these scientists created considerable unease for government officials and scientists who faced growing public clamour for effective action to be taken against BSE. To the extent that MAFF scientists were not prepared to endorse the sweeping measures proposed by Professor Lacey and other dissenting scientists, some means needed to be found of isolating the views of these scientists from further scientific consideration. This isolation was achieved through a series of abusive and circumstantial ad hominem arguments against these scientists. In effect, MAFF’s strategy for dealing with dissenting scientists was to exclude them as rational actors within the wider scientific and public debates on BSE.

7.2.3 Argument from Analogy In Chapters 4, 5, and 6, we described how analogical reasoning based on scrapie was used extensively by scientists during the BSE inquiry. This reasoning strategy, which received some initial degree of presumptive warrant from the early epidemiological investigations of John Wilesmith and his colleagues at the CVL, became the basis of BSE risk assessments since the disease first emerged in cattle in 1986 until the announcement in March 1996 to British Parliament that BSE was the probable

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cause of cases of CJD in young people. The presence and influence of this form of reasoning during the BSE inquiry cannot be overestimated – analogical reasoning based on scrapie really was the main plank of both the government’s and scientists’ response to BSE. For the most part, this reasoning strategy produced the type of reassuring conclusions about BSE that government scientists were eager to promote. To the extent that scrapie had not transmitted to humans and did not pose a risk to human health, so it was argued that BSE was unlikely to have any implications for human health. This conclusion was the basis of further reassurances about the safety of beef, reassurances that served to shore up the large and lucrative domestic beef markets. However, there was at least one area in which analogical reasoning based on scrapie presented MAFF scientists and officials with considerable difficulty. That area related to beef exports around the world. On 30 October 1987, Mr Suich (Animal Health Division, MAFF) sent a letter to Mr Faulkner (British Embassy, The Hague), a copy of which was circulated to other British Embassies in Australia, New Zealand, USA and Europe. In this letter, Mr Suich stated in relation to BSE: [T]he fact that it so far appears to be a uniquely British disorder could prejudice our cattle exports if it is publicised in inaccurate or exaggerated terms. It would be particularly misleading if it were to be described as ‘scrapie in cattle’. Scrapie is a disease of sheep, the existence of which in British flocks is an impediment to our export trade, but although it is also an encephalopathy there is no evidence that BSE is attributable to the same cause as scrapie and it is important to distinguish between the two conditions (Suich 1987: 1; underlining in original).

In this extract, Mr Suich is seen to dissociate the new disease of BSE from scrapie in sheep in a move that was specifically designed to protect British exports of beef and cattle to other countries around the world. Certainly, this export trade was of huge significance to the UK’s economy. In the period in which Mr Suich was writing, the total value of UK beef and cattle exports to the European Union alone was over £300 million (BSE Inquiry Report, Volume 10: 51). The loss of such a trade would have had considerable adverse implications for all those directly and indirectly involved in the British beef industry. This industry, Mr Suich was arguing, could not be exposed to the same damaging restrictions that had been imposed on sheep exports on account of scrapie. Some means needed to be found of protecting beef and cattle against the inevitable comparisons43 with scrapie in sheep that would be made in export countries. To avoid adverse consequences for the beef industry, MAFF officials worked hard to distinguish BSE from scrapie through a series of denials that there was any connection between these diseases.44 But to the extent that MAFF’s denials occurred alongside a domestic public health response to BSE that was increasingly drawing upon an analogy with scrapie to validate risk assessments of BSE, these denials can be seen to have had more than a ring of logical inconsistency about them. It emerges that even that most dominant of reasoning strategies during the BSE inquiry – analogical reasoning based on scrapie – was not immune to the pressures of economic and commercial interests. This strategy, it can be seen, was simultaneously advocated and denounced in accordance with the particular interests that happened to prevail at the time.

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7.3 Summary No process of reasoning can be conducted in the absence of extra-logical factors and considerations. To the extent that reasoning is always the reasoning of one or more cognitive agents, logical processes must operate alongside a range of other attributes of the reasoner, such as beliefs and emotional states, goals and preferences, to name just a few. Specifically, logical processes must also interact with the interests that a reasoner is seeking to promote or challenge. In this chapter, we have attempted to characterise those interests as they applied to scientists who grappled with the problem of BSE. Scientific inquiry into BSE was conducted in a context that was heavily infused with political, commercial and economic interests. These interests shaped the reasoning processes of scientists in various ways. On some occasions, they led scientists to substitute logical grounds against a claim or thesis with grounds that were little more than an attack on an opposing scientist’s professional and mental competence. The ad hominem arguments through which this was achieved served to distract the audience (here represented by the public) from the real logical error which was being committed, that there were no logical grounds which could be brought against an opponent’s thesis in argument. On other occasions, these interests manifested themselves in the attempt to deny one’s opponent in argument proper rights of cognitive authority. On still other occasions, upholding certain interests led scientists into logical inconsistency as they attempted to reject the scrapie analogy with a view to protecting exports while simultaneously adopting this analogy as a basis for the public health response to BSE. Interests and the reasoning processes they influenced co-existed in many ways during the BSE inquiry. It is unfortunate that so many of those ways involved logical anomalies that were not conducive to attaining the aims of inquiry. Of course, it is not always irrational for scientists to consider certain interests during their deliberations on an issue. That a certain course of action has potentially severe economic consequences should be taken into consideration in deciding which of two equally effective public health measures should be pursued. But the interests that dominated the BSE inquiry were more often than not in direct conflict with each other and, particularly, with the aim of protecting public health. This conflict came to manifest itself in various forms of fallacious reasoning as scientists sought to uphold certain interests often at the expense of logical considerations. So MAFF scientists, for example, were able to protect political and economic interests through their use of fallacious ad hominem arguments against dissenting scientists, arguments which masked the fact that MAFF scientists lacked logical grounds against the claims of these scientists. In effect, the promotion of certain interests during the BSE inquiry served to distort logical, rational processes within this inquiry. In earlier chapters, we found it useful to conceive of those points in inquiry when logical, rational processes were subordinated to other concerns in terms of a distinction between the argumentative strategy of inquiry and the arguments that are subsumed by this strategy. Applied to the discussion of the current chapter, we may say that non-scientific interests held considerable sway in shaping the argumentative strategy of the BSE inquiry. Meanwhile, the arguments that were

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being used to support that strategy only did so fallaciously. While the argumentative strategy of the BSE inquiry was pulling in the direction of the promotion of certain interests, rationally warranted arguments were leading some scientists in a quite different direction, that of challenging the consensus view of BSE. The result was the separation of these two (normally interconnected) argumentative levels of inquiry.

Notes 1. Philip Johnson-Laird and co-workers have devised a mental models theory of deductive reasoning that can explain, amongst other things, the effects of beliefs on the reasoning process. Johnson-Laird and Byrne (1991: 125) state that ‘[a]ccording to rule theories, any effect of belief or prejudice on deduction can operate only by biasing the initial interpretation of the premises or else by acting as a post-deductive “censor” that throws out conclusions offensive to the reasoner’s views about the world. There cannot be any effect on the process of deduction itself because formal rules are by definition blind to content. The model theory also predicts these effects, but in addition it suggests that the deductive process itself can be affected by beliefs. In particular, reasoners will search for refuting models more assiduously if their initial conclusion is unbelievable than if it is believable’. Amos Tversky and Daniel Kahneman have also examined the role of beliefs in reasoning. In their landmark article ‘Judgment under Uncertainty: Heuristics and Biases’, these investigators describe a number of heuristics that reasoners use in probabilistic reasoning: ‘Many decisions are based on beliefs concerning the likelihood of uncertain events. . .people rely on a limited number of heuristic principles which reduce the complex tasks of assessing probabilities and predicting values to simpler judgmental operations. In general, these heuristics are quite useful, but sometimes they lead to severe and systematic errors’ (1974: 1124). One such error is known as the gambler’s fallacy, the belief that random processes self-correct: ‘if [a random] sequence has strayed from the population proportion, a corrective bias in the other direction is expected. This has been called the gambler’s fallacy’ (Tversky and Kahneman 2004: 193). 2. An account of argumentation that gives due consideration to the role of emotion in reasoning is advanced by Gilbert (1997: 26): ‘[C]ertain very human factors such as emotion and intuition have been viewed as extraneous to proper argumentation and solely the domain of other disciplines (Psychology and Communication Theory) or, worse, the concern of sophists and manipulators. . .Emotion, intuition, and physicality are not plagues that stalk the land of Reason, but perfectly natural and ordinary components of all human endeavor’. 3. Such reworking took place in the report of the Southwood Working Party. Sir Richard Southwood had originally sought to include a final general conclusion in the report that criticised and urged reform of the agricultural practices, principally rendering, that were credited with causing the BSE problem. Reporting to the Chief Medical Officer, Dr Pickles (Department of Health lead on BSE, 1988–1991) stated ‘alarm bells will be ringing already in MAFF and they may attempt to steer Sir Richard away from a general statement of this sort’ (BSE Inquiry Report, Volume 4: 37). MAFF certainly did attempt to steer Sir Richard away from this conclusion. Mr Donald Thompson (MAFF Parliamentary Secretary, 1986–1989) went as far as remarking ‘I cannot say how strongly I regard this matter. Of course we must take all due care but the environmental, economic and the competition consequences would be dire if Prof. S was to go forward’ (BSE Inquiry Report, Volume 4: 38). Following MAFF’s intervention, paragraph 9.4 of the Southwood Report, which had described the risks of rendering as ‘inevitable’, was amended to read: ‘we believe that the risks from inadequately sterilised animal products are such that this method of disposing of animal waste should be changed so as to eliminate these novel pathways for pathogens’ (BSE Inquiry Report, Volume 4: 39).

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4. In evidence to Lord Phillips and his team, Mr Brian Dickinson of MAFF’s Food Safety Group remarked that ‘[t]here was a stronger danger of being misinterpreted one way rather than the other, and we tended to make more reassuring sounding statements than might ideally have been said’ (BSE Inquiry Report, Volume 1: 265). 5. Several comments during evidence to Lord Phillips and his inquiry team attest to the difficulty of the situation in which scientists were operating. In responding to questions about advice on the safety of beef that SEAC provided to the Chief Medical Officer on 24 July 1990, Dr Tyrrell stated: ‘I think we had already sold the pass; we had already said, ‘We are going to be involved in doing things to help a CMO’. We had given up the idea of trying to stand back and do nothing else but evaluate science at a distance and impartially. I think that was something which seemed to be part of what we had got ourselves involved in willy nilly’ (BSE Inquiry Report, Volume 11: 71). Mr Brian Dickinson, a member of MAFF’s Food Safety Group, told Lord Phillips and his inquiry team: ‘Given the strength of public debate on the matter [of BSE] at the time one was aware of slightly leaning into the wind. You could not just stand upright and give a totally impartial, objective view of what was the situation’ (BSE Inquiry Report, Volume 1: 265). 6. This policy was articulated by Margaret Thatcher during Prime Minister’s Questions on 28 February 1989. In response to a question demanding the banning of offal for human consumption from Mr John Evans of the Opposition benches, Margaret Thatcher replied: ‘We set up a committee of experts under Professor Southwood. We published the report in full. We referred it to the Chief Medical Officer of Health and we accepted the recommendations of both, precisely. There is no point whatsoever in setting up a committee of experts, in having a Chief Medical Officer of Health, in receiving their advice and then not accepting it’ (BSE Inquiry Report, Volume 1: 109). 7. ‘Junior Ministers processed a heavy load of day-to-day business, including much parliamentary business (for example adjournment debates and the committee stages of Bills) and answering letters from MPs’ (BSE Inquiry Report, Volume 15: 4). 8. The responsibilities of civil servants were laid out in guidance drawn up in 1985 by Sir Robert Armstrong. This guidance – The Duties and Responsibilities of Civil Servants in Relation to Ministers (often known as the ‘Armstrong Memorandum’) – stated that ‘it is the duty of the civil servant to make available to the Minister all the information and experience at his or her disposal which may have a bearing on the policy decisions to which the Minister is committed or which he is preparing to make, and to give to the Minister honest and impartial advice, without fear or favour, and whether the advice accords with the Minister’s view or not’ (Hansard, 26 February 1985, col. 129, para. 5). 9. It has been frequently argued in the literature on the BSE crisis that there was a conflict between the two main functions of MAFF. Seguin (2000: 294) characterises this tension as follows: ‘the crisis was due to the tension between the two functions of the Ministry of Agriculture, Fisheries and Food (MAFF), namely promoting the interests of the farming industry and protecting public health’. This tension is clearly evident in the case of the MLC. It was the task of the MLC to promote industry interests, yet membership of the Commission was at the gift of the Minister of Agriculture who had to uphold the public health interest. 10. Lord Phillips and his inquiry team remarked of the MLC that it ‘was particularly assiduous in seeking to counter the suggestion that it might be dangerous to eat beef. Regrettably this enthusiasm led on occasion to statements which were not scientifically correct’ (BSE Inquiry Report, Volume 1: 127). 11. In a letter to the Southwood Working Party on 9 November 1988, the Chief Veterinary Officer, Mr Meldrum, wrote ‘MAFF are now coming under some pressure to destroy the milk derived from animals suspected of being affected with BSE. The veterinary profession, in particular the Veterinary Public Health Committee of the British Veterinary Association, the Milk Marketing Board, the general public and media have all pointed to the discrepancy between our policy on carcase disposal and continued consumption of milk from suspect animals’. 12. The minutes of SEAC’s first meeting held on 1 May 1990 record that ‘[a]lthough the core membership was small, additional experts could be involved for particular topics as

Notes

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14.

15.

16.

17.

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necessary’ (SEAC 1990e: 1). Some of these ‘additional experts’ included Professor Ingrid Allen, a neuropathologist, who joined SEAC shortly after its formation to strengthen its human health expertise; Professor Richard Barlow, a pathologist and veterinarian, who was confirmed as a SEAC member in September 1990; and Mr David Pepper, a veterinary surgeon in private practice, who attended his first SEAC meeting on 1 November 1990 (BSE Inquiry Report, Volume 11: 41–42). The whole area of scientific expertise has been particularly contentious since a US Supreme Court ruling in June 1993. This ruling, which was made as part of the Daubert versus Merrell Dow Pharmaceuticals, Inc decision, requires that trial judges now evaluate the relevance and reliability of expert testimony. Michaels (2005: S5) states that ‘[w]hat began as a well-intentioned attempt to improve the quality of evidentiary science has had troubling consequences. . .on the basis of a lay judge’s ruling, respected scientists have been barred from offering expert testimony in civil cases’. The Daubert ruling raises interesting questions about who is qualified to decide if someone has requisite expertise in a particular area. Clearly, Michaels does not believe that trial judges are so qualified. ‘The most blatant of the fallacious appeals to authority occur where a legitimate expert in a given area makes a judgement that does not fall within it, but where added credibility is given to his judgement simply by virtue of his being an expert in some area’ (Woods and Walton 1974: 143; italics in original). Mr Cahn (Principal Private Secretary, MAFF) would appear to be charging Professor Lacey, a vocal critic of MAFF’s handling of the BSE crisis, with just exactly this lack of expertise when he stated in a memo that ‘Professor Lacey has now ventured outside his specialist field of microbiology into neurology’. This memo was sent to Mr Eddy (MAFF Head of Animal Health Division) on 29 September 1994. For an excellent overview of the historical background of appeals to authority, the reader is referred to Chapter 2 in Walton (1997). Earlier philosophers and logicians were not unanimously of the view that this type of argument was a fallacy. Walton (1997) describes, for example, how the argument from authority was recognised as a reasonable form of argument in medieval logic. The emergence of scientific thinking, however, brought about a significant shift in how this argument was perceived. As Walton (1997: 48) states: ‘Once scientific thinking became established as the accepted framework of knowledge, . . .the say-so of any authority could come into conflict with scientific findings, based on observation and experiment. According to this new way of thinking, which we have now come to accept, the opinion of the authority must give way in such a conflict. The “subjective” opinion of the authority must give way to the hard evidence of scientifically verified, “objective”, knowledge. This new conventional wisdom, where scientific knowledge has priority over an authority’s opinion, suggested that appeal to authority may not be very reliable as a type of argument. This, in turn, made it possible that such an argument could be misleading, sophistical, or fallacious’. This distrust of the cognitive agent has also led argumentation and fallacy theorists to eschew arguer-relative notions when they are framing normative criteria for the evaluation of arguments. These notions are inherently subjective and, hence, not adequate to the task of evaluating arguments, it is argued. On this point, see note 17 in Chapter 2. Mr Colin Maclean, in an MLC press release on 14 May 1990, remarked: ‘All the scientific evidence – as opposed to rumour, conjecture and guess – provided by leading veterinary surgeons and scientists in the U.K. and the rest of the EEC has indicated that U.K. beef is perfectly safe to eat’ (BSE Inquiry Report, Volume 6: 363; italics added). Dr Pickles, principal medical officer in the Department of Health, issued in May 1990 a minute to health and local authorities. It read: ‘The Government have taken advice from the leading scientific experts in this field. They have consistently advised us that there is no scientific justification to avoid eating British beef. Beef can be eaten safely by everyone both adults and children including patients within the NHS’ (BSE Inquiry Report, Volume 6: 365; italics added). A draft of this statement, agreed by the Chief Medical Officer, Department of Health Press Office and MAFF, read: ‘According to the advice of outside experts to the Government there is no scientific justification to avoid eating British beef. Beef can be eaten safely by

188

18.

19.

20.

21.

22.

7 Political and Commercial Interests in the BSE Inquiry everyone both adults and children [including patients within the NHS]’ (BSE Inquiry Report, Volume 6: 365; italics added). In the letter to Lady Wilcox, mentioned in the main text, Mr Gummer stated: ‘British beef is therefore not a public health risk and can be eaten with complete confidence – a view endorsed by the European Community’s top scientists’ (BSE Inquiry Report, Volume 6: 368; italics added). Finally, in a press release in May 1990 by the MAFF Food Safety Directorate, the question ‘Isn’t it true that not enough is known about BSE to ensure the public is protected?’ was addressed as follows: ‘Although BSE is a recent development, a similar disease in sheep, scrapie, has been studied extensively. That research provides a solid foundation for dealing with BSE. Our policy has been endorsed by the EC’s independent scientific advisors’ (BSE Inquiry Report, Volume 6: 370; italics added). To recap, the Southwood Working Party concluded that the risk of BSE transmission to humans was ‘remote’. SEAC’s position on the safety of beef was set out in a paper to the Chief Medical Officer on 24 July 1990. It stated that ‘we believe there is no scientific justification for not eating British beef and that it can be eaten by everyone’ (SEAC 1990d: 2). In an article entitled ‘A Culture of Secrecy that Risked Our Lives’ in the Sunday Times on 29 October 2000, Jonathan Carr Brown argued that ‘The Southwood working party did not contain a single expert in prions. Phillips [Chairman of the BSE Inquiry] declines to comment on this glaring omission’ (12). Lord Phillips and his inquiry team did actually comment on this lack of a TSE expert in the Southwood Working Party. However, as can be seen from the inquiry team’s comments below, this particular lack of expertise was not viewed as being problematic: ‘The Southwood Working Party consisted of Sir Richard Southwood, Professor of Zoology at Oxford University; Professor Anthony Epstein FRS, a virologist; Professor Sir John Walton, a neurologist; and Dr William Martin, a veterinarian who had just retired from the Directorship of the Moredun Research Institute in Edinburgh. Sir Richard emphasised to us that they were not experts in the narrow sense of having particular expertise in TSEs. Each was, however, a scientist of the highest standing in his field and together they were well placed to consider the available data and to give a considered view as to what implications these suggested that BSE might have for human health’ (BSE Inquiry Report, Volume 1: 48). An interesting analysis of the lack of TSE expertise in the Southwood Working Party is given by Seguin (2000). Sir Richard Southwood, who selected the members who would work alongside him, was concerned to ensure the independence and impartiality of the working party. He also wanted to avoid choosing a member who was involved in the controversy surrounding the nature of the agents that cause TSEs. But, as Seguin (2000: 298) remarks ‘Southwood’s avowed concern about the Committee’s independence gives rise to an alternative interpretation. The logic underlying his choice of members was that science should be independent of commercial and organisational interests, such as the farming industry or university departments. The exclusion of TSE researchers shows that he also expected scientists to be devoid of cognitive interests’. ‘Appeals to expert opinion can be a legitimate form of obtaining advice or guidance for drawing tentative conclusions on an issue or problem where objective knowledge is unavailable or inconclusive’ (Walton 2008: 209). The idea that authority appeals can advance scientific inquiry by facilitating decisions in the practical sphere when evidence is lacking or otherwise limited is consistent with the view of the informal fallacies that we have been presenting in this book. Walton (2008: 212) captures this use of authority appeals as follows: ‘Good scientific method is based on the idea of reproducible evidence. In other words, it is better to do an experiment yourself than rely on the say-so of someone else who has done it and claimed certain results. But does that mean we should always mistrust and reject the say-so of an authority as fallacious? It need not, if our reliance on cognitive authority is only regarded as a means of supplementing experimental investigation in those cases where an immediate decision is required and independent experimental investigation is not possible or practical’.

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23. Jasanoff (1997: 227–8) compares British and American processes for obtaining expert advice. She claims that British advisory committees, such as were used during the BSE crisis, privilege the trustworthiness of individuals over the rationality of views or technical competence: ‘In British advisory committees, trust is created through embodiment in trustworthy people: peers, professors, tested public servants, representatives of established interest groups or responsible citizen organizations. Over and above any demonstrations of technical competence, such individuals have proved their right to represent the public interest through years of devoted service. Many have earned knighthoods or other honours in recognition of their contributions to public life. The most eminent are elevated to the (unelected) House of Lords, where they are in a position to influence some of the nation’s most significant legal and policy decisions. People who have attained this status can be said, with little exaggeration, to constitute an elite tier of civic virtue that stands, and is seen to stand, above self-interest and even party politics’. Two members of the Southwood Working Party, Sir Richard Southwood and Sir John Walton, had knighthoods. By the time Lord Phillips conducted his inquiry into the BSE affair, a further member of the working party, Sir Anthony Epstein, had received a knighthood and Sir John Walton had received a peerage (Lord Walton). 24. Although we cannot say with certainty who this source was, as Mr Maclean expresses this claim, it is consistent with views advanced by Dr Richard Kimberlin, an independent consultant in TSEs. In an article entitled ‘Transmissible Encephalopathies in Animals’, submitted for publication in the Canadian Journal of Veterinary Research in June 1989, Dr Kimberlin refers to the possibility of a change in the agent on crossing the species barrier, a change which could put humans at risk of transmission of BSE from cattle (see Kimberlin 1990). 25. The irrelevance of the attribute to the question-at-issue is why ad hominem argument is classified as a fallacy of (ir)relevance by logicians. Copi and Cohen (2009: 127) subscribe to this classification of the fallacy: ‘Of all the fallacies of irrelevance, the argument against the person, or ad hominem, is among the most pernicious’. 26. Although Copi and Cohen (2009) recognise two forms (abusive and circumstantial) of ad hominem argument, Walton (2008) describes a third form, called ‘poisoning the well’, in addition to the abusive and circumstantial variants. This third type of ad hominem occurs where ‘the critic questions the sincerity or objectivity of an arguer by suggesting that the arguer has something to gain by supporting the argument he has advocated’ (Walton 2008: 170). Copi and Cohen classify ‘poisoning the well’ as a type of circumstantial ad hominem argument. For an interesting discussion of the circumstantial ad hominem fallacy in the context of an important epidemiological issue – the health effects of environmental tobacco smoke (passive smoking) – the reader is referred to Battersby (2006). 27. These attacks on the mental competence of dissenting scientists are akin to a type of abusive ad hominem argument that Walton (2008: 171) describes as follows: ‘the personal attack will question the arguer’s credibility, or ability to enter into reasoned argument. For example, it may even be suggested that the arguer is insane or mentally imbalanced, and that therefore no serious attention can be paid to his argument’. 28. These food scares included salmonella, listeriosis and E.-coli 0157. In a statement to Lord Phillips and his inquiry team on 4 March 1998, Professor Lacey described the reaction to his attempts to raise concerns about these diseases: ‘The concerns, which I expressed from 1988 about salmonella in eggs inevitably led to criticism from the egg farmers and their Parliamentary supporters. Similarly when I made known my concerns in 1989 about processed foods, including cooked chicken, soft cheeses and cooked chill foods, this led to similar people disparaging me. I also pointed out at this time that E.-coli 0157 was a potential problem with cooked meat. Therefore I was aware that with this background, raising the profile of BSE would generate anger from those with a vested interest. Despite that, my training and professional responsibility required me to give priority to the welfare of the public’ (Lacey 1998: 2). 29. This high media profile continued with the BSE problem. In Professor Lacey’s statement to the BSE Inquiry on 4 March 1998, he indicates something of the speed with which he assumed

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32.

33.

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7 Political and Commercial Interests in the BSE Inquiry media prominence in relation to BSE: ‘I became dramatically involved with the BSE issue when I took a chance telephone call from a London radio station on 10 May 1990. I was asked if I would give a telephone interview with a Mr Andrew Neil. . .little realizing that the Andrew Neil in question was. . .the then editor of The Sunday Times. We talked about food matters in general, including BSE. I explained that the numbers of cattle confirmed as having BSE were still rising, implying that BSE must be spreading between cattle and that all the infected herds should be destroyed. On the next day, a journalist from The Sunday Times telephoned and I repeated these comments. On Sunday 13 May the paper carried the front-page headline “Leading food scientist calls for slaughter of 6m cows”. The next day, 14 May, the telephone at work never stopped ringing’ (Lacey 1998: 3). It is clear from comments in the report of the Agriculture Committee that the mix of publicity and science was not appreciated by committee members. Professor Lacey is almost certainly one of the ‘irresponsible scientists’ described in this extract from the report: ‘We accept that BEEF IS UNSAFE merits a bigger headline than BEEF IS SAFE, but deprecate the extensive publicity given to some pretty threadbare scientific theories, on an issue where the overwhelming scientific consensus was that public alarm was unjustified. Unless journalists exercise greater responsibility and research their facts properly, the public will be subjected to quite unnecessary anxiety and one sector of the UK food industry after another torpedoed by the pronouncements of one or two irresponsible scientists’ (Agriculture Committee 1990: xxi, paragraph 73). That this campaign was a considered strategy on the part of MAFF is evident from the following comments taken from a written correspondence between Mr Wilesmith and Mr Bradley on 18 May 1993. In relation to Professor Lacey, Mr Wilesmith states: ‘As you are aware, I feel that we have two basic options for dealing with this tendentious individual who has failed to apply any scientific scholarship to his so-called critique of BSE. The first is to ignore him and hope that he will keep digging his own grave. The second is to launch an all out attack at every opportunity particularly with respect to his published musings. On some reflection I do not favour the first option as I am sure that he will find an escape route. I therefore tend towards the second option. . .’ (Wilesmith 1993: 1). It was also the view of Lord Phillips and his inquiry team that at least some of the criticism of Professor Lacey and Dr Dealler’s work by MAFF scientists was unwarranted. In relation to an article by these authors entitled ‘Transmissible Spongiform Encephalopathies: The Threat of BSE to Man’ which published in Food Microbiology on 30 August 1990, Lord Phillips and his co-investigators concluded: ‘That article did not deserve the opprobrium it received from MAFF officials. It was a careful review of the subject and the authors stated in clear terms that ‘in discussing the possible effect on man, the most pessimistic view has been taken so far’. Most of the criticisms of the article do not have regard to that important qualification’ (BSE Inquiry Report, Volume 11: 275). The article, which was written by Richard Palmer and Ian Birrell, was entitled ‘Leading Food Scientist Calls for Slaughter of 6m Cows’. It stated: ‘The risks of humans catching “mad cow” disease are now so great that 6m cattle need to be slaughtered, one of Britain’s leading food scientists said yesterday. Professor Richard Lacey, a former government health adviser, said people should not eat beef until half the herds in Britain, each of which had at least one infected cow, had been destroyed and beef had been proved safe to eat again’. A ban on the consumption of tissues from cattle over 30 months was only introduced following the announcement to British Parliament in March 1996 that BSE was most probably the cause of a new variant of CJD identified in young people. On 3 April 1996, Mr Hogg (Minister of Agriculture, Fisheries and Food, 1995–1997) announced in Parliament that ‘[a]rrangements will be introduced to ensure that all bovine animals over the age of 30 months at the time of slaughter will not enter the food or animal feed chains’. During Dr Dealler’s visit to the CVL, Mr Bradley described how he ‘asked Dr Dealler what actions he would immediately take if he were Minister of Agriculture, Fisheries and Food

Notes

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tomorrow. He said he would immediately ban the consumption of all liver and kidney from cattle over 6 months old for human consumption and no tissues whatever from cattle over 21/2 years old would be permitted for such sale. He calculated that slaughter of cattle and disposal might cost the industry £40 billion but it was essential to protect public health’ (Bradley 1994b: 4). MAFF conducted its own calculations of the costs that would be incurred if a ban on cattle over 30 months was implemented. In a written correspondence to the Minister on 18 March 1996, Mr Packer (Permanent Secretary, MAFF) stated that ‘[t]he cost of such a course of action would be enormous. Compensation to producers for cull cows alone compulsorily slaughtered would be of the order of £350 million per year at current market prices. A further £200 million per year might be incurred in slaughter and disposal costs’ (Packer 1996: 4). The Agriculture Committee summarised MAFF’s grounds for resisting such a ban: ‘MAFF has so far resisted it [a ban on cattle offal in poultry and pig feed] on the grounds that there is not yet the scientific evidence to warrant it: in the view of their own experts, pigs are not at risk because they are natural scavengers (and have evolved defences against pathogens) and poultry are not at risk because there is an enormous zoological divide between cattle and poultry’ (Agriculture Committee 1990: xix; paragraph 64). This cycle of adverse commercial consequences of statutory and voluntary bans on meat and bone meal was clearly captured by the Agriculture Committee: ‘An industry which has been dramatically affected has been the rendering industry, whose representatives painted a gloomy picture of their present commercial prospects. A number of bankruptcies have already been reported and more are feared. Previously they were buying offals etc from the primary producers, rendering them and then selling the by-product as meat and bone meal to the compounders for inclusion in animal feed. Because, however, it was the inclusion of meat and bone meal from sheep in cattle feed which is thought to have created BSE, and because UKASTA (the compounders’ trade association) has responded to public anxiety about meat and bone meal from cattle by excluding specified offals from other feed rations, the renderers have no market for the offals they have rendered. They in turn have to charge the abattoirs for the offals, instead of buying them, with the result that they have become, in their own words, a “waste disposal service”. Meanwhile thousands of tonnes of treated but unsellable meat and bone meal are piling up in their store rooms’ (Agriculture Committee 1990: xxi–xxii; paragraph 78). When it appeared that Sir Richard Southwood and his colleagues were going to recommend the complete cessation of the practice of feeding animal materials to herbivores as one of the general conclusions in the Southwood Report (see note 3, this chapter), this prompted considerable consternation amongst MAFF officials. In a correspondence in January 1989 between Mr John Suich (Animal Health Division, MAFF) and Mr Andrews (Permanent Secretary, MAFF), which was copied to Mr Meldrum (Chief Veterinary Officer), this issue was addressed as follows: ‘BSE is. . .being used as a peg on which to hang a controversial recommendation which goes far wider than Professor Southwood’s remit. If implemented it would have serious consequences not least for the rendering industry, which processes over 100,000 tonnes of raw material every month, thus providing a source of animal feed and industrial raw material, and also a ‘waste disposal’ service for the slaughtering industry. . .I would suggest that, at the very least, the members of the Working Party should be made aware of what the rendering industry does and its scale of activity so that they can reflect on the implications of the draft recommendation’ (BSE Inquiry Report, Volume 4: 38). Of course, all parties in the BSE crisis claimed that they were applying the precautionary principle in their assessments of the risks that were posed by BSE (see note 14, Chapter 3). For example, in written evidence to the Lord Phillips inquiry, Sir Kenneth Calman (Chief Medical Officer, 1991–1998) stated that ‘[t]he Department of Health has always adopted a precautionary approach in relation to public health issues arising from BSE in their deliberations with MAFF’ (BSE Inquiry Report, Volume 11: 181). Even within this precautionary approach, however, there were some actors who characterised the most minimal measures as being ‘purely precautionary’ (i.e. not really necessary at all) or

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42. 43.

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7 Political and Commercial Interests in the BSE Inquiry ‘ultra-precautionary’, and other actors who proposed drastic measures as a precautionary response. These two groups of actors were represented by MAFF scientists and officials and dissenting scientists, respectively. The precautionary principle is discussed further in Section 8.3.1. MAFF officials and scientists were particularly concerned not to be seen to take any action that would not be supported by scientific evidence. Such unsupported action, it was argued, would almost certainly face legal challenge from the industry or commercial organisations that would be affected by this action. This concern about legal challenges can be seen in the following correspondence on 21 September 1993 between Mr Bell and Mr Taylor on the subject of MAFF’s policy on artificial insemination: ‘It was decided that this policy would apply until there was scientific evidence to show conclusively whether or not bovine semen is a vehicle for BSE transmission. Legal advice was that any legal challenge to have a suspension lifted would be based on whether MAFF had acted unreasonably in suspending approval. If MAFF acted with caution because of uncertainty of scientific knowledge, such a challenge would be unlikely to succeed’ (BSE Inquiry Report, Volume 5: 569–70). The last sentence in this quotation is an expression of the precautionary principle (see note 39 in this chapter, note 14 in Chapter 3 and Section 8.3.1). That the public health interest was not being served, according to dissenting scientists, by the government’s response to BSE is evident from the following comments by Professor Lacey and Dr Dealler to the Agriculture Committee. In relation to comments in the report of the Southwood Working Party, Lacey and Dealler stated ‘what this sentence is really saying is that we propose to permit a gigantic long term experiment to see how many of us acquire a fatal infection that should have been entirely avoidable’ (Agriculture Committee 1990: 21). Lacey and Dealler commented as follows about statements in the Tyrrell report: ‘So this means doing nothing for 20 years, except to watch the change in prevalence in CJD is the way to reassure the public! In two sentences, the government’s intent is revealed in absolute clarity. Its action is intended somehow to reassure, rather than to take any curative action. What do members of the public think of this treatment of them?’ (Agriculture Committee 1990:22). At least one MAFF scientist, Mr Wilesmith, felt constrained in his actions by his research funding provider. For his full comments, see note 17 in Chapter 6. MAFF, too, knew that these comparisons were inevitable, hence their desire to restrict information about this new bovine disease. This restriction of information is evident in the following correspondence on 13 May 1987 between Dr Williams (Assistant CVO) and Mr Hancock (State Veterinary Service, South West England) about a letter submitted for publication to the Veterinary Record: ‘Further to our telephone conversation this morning, I am now confirming that the letter to the Veterinary Record which I cleared earlier in the week should not be published. I explained to you that this condition has been discussed by the CVO and the Director of CVL, and because of possible effects on exports and the political implications it had been decided that, at this stage, no account should be published’ (Williams 1987: 1). In fact, MAFF’s strategy went somewhat further than explicit denials of the type advanced by Mr Suich. It was the opinion of Lord Phillips and his co-investigators that this strategy involved an embargo on any comparison between BSE and scrapie. This opinion of MAFF’s approach to the emergence of BSE is supported by comments like the following. In a written statement to the Lord Phillips inquiry, Dr Williams (Assistant CVO) stated ‘My understanding was that the CVO had prohibited BSE being referred to as ‘bovine scrapie’’ (BSE Inquiry Report, Volume 3: 54). In July 1987, Mr Bradley circulated a memorandum relating to a paper that Dr Jeffrey of the CVL had written about spongiform encephalopathy in a nyala. The memorandum stated ‘It is unlikely that approval will be given to publish if comparisons are made with scrapie or this is mentioned’ (BSE Inquiry Report, Volume 3: 54).

Chapter 8

Learning the Lessons of the BSE Crisis

8.1 Introduction By any standard, the BSE crisis was a most difficult period in the public health of the UK. This period saw a previously unknown TSE emerge in cattle and then transmit to humans, a scenario which by August 2009 had cost 164 people their lives in the UK1 and which has resulted in an unknown number of other people incubating variant CJD (vCJD).2 The economic damage caused by this disease has been considerable. In April 2000, the government estimated that by the end of the 2001/2002 financial year, the total net cost of the BSE crisis to the Exchequer would be £3.7 billion (BSE Inquiry Report, Volume 10: 1). Less quantifiable consequences have also stemmed from this crisis.3 Chief amongst them has been significant damage to the public’s ability to trust the pronouncements of government on matters of food safety and risk.4 The scientific community has suffered inestimable damage to its expertise and to its capacity to provide objective, consistent scientific advice to the public.5 With such serious consequences emanating from the BSE affair, it is incumbent on all those who were involved in this tragic episode to reflect on the events that took place and to consider how things could have been done better. Such a reflective exercise has, of course, been conducted by Lord Phillips and his inquiry team who examined all the events that took place during the BSE epidemic and drew a wide-ranging set of lessons from these events.6 A reflective purpose is also a central motivation of the current chapter. However, the focus of this reflection – scientific reasoning in contexts of uncertainty – is altogether narrower than that undertaken during the public inquiry into BSE. Moreover, the question of reasoning in contexts of uncertainty was omitted from Lord Phillips’ inquiry into BSE7 and has also been overlooked within the vast literature that has been written on the topic of BSE both before and after this inquiry was conducted. The purpose of this chapter will be to bring together the various features that we have identified in the reasoning of scientists during the BSE epidemic. The aim is to arrive at a model that will provide a new conceptual framework for scientists who are charged with managing emerging infectious diseases like BSE in contexts of uncertainty. This model will be informed by the informal logical analysis of arguments used by BSE scientists that was undertaken in Chapters 4, 5, 6, and 7 inclusive. This

L. Cummings, Rethinking the BSE Crisis, DOI 10.1007/978-90-481-9504-6_8,  C Springer Science+Business Media B.V. 2010

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analysis has its roots in philosophical disciplines. However, it is undertaken with a distinctly scientific purpose in mind. That purpose is one of responding to the call from public health scientists and epidemiologists for new modes of reasoning that can cope with uncertainty (see Section 2.2). It is to be expected that philosophy and science should cooperate on the response to this call. Both these intellectual enterprises, after all, must address the concept of uncertainty (science in an altogether more urgent way) and are concerned with the various logical operations that are integral to reasoning (philosophy in an altogether more abstract way). Yet, their cooperation has been stifled through disciplinary boundaries and other obstructions to greater integration. Chief amongst these obstructions is philosophy’s failure to give proper consideration to the cognitive agent in matters of reasoning with all the chaos that this entails (e.g. taking cognitive shortcuts, assessing arguments with suboptimal logical acuity). The scientific reasoner must seem a strange beast indeed to the philosopher or logician who cannot conceive of reasoning in terms other than the preservation of truth relations among propositions. For its part, science must look beyond its technical resources to the conceptual wealth of philosophy if it is to make genuine progress in generating the new ways of thinking that are needed to address increasingly complex public health problems. The model of reasoning that will be proposed in this chapter is an important step on the road to achieving greater integration of these disciplines. To the extent that philosophy and public health science need to join forces in devising new modes of reasoning that are equipped to cope with uncertainty, I believe that the so-called informal fallacies are the place to begin this venture. These fallacies represent an important logical resource of reasoners that has for too long been treated with suspicion and more than a little contempt. Yet, it is the very feature of these arguments which has traditionally seen them despised by philosophers that puts them in good standing for the theorist who is investigating reasoning under uncertainty. That feature is their ability to exist in conditions where high status epistemic concepts such as knowledge are not to be found. The fallacies occupy a logical place where reasoning occurs against the odds, so few are the epistemic resources that are available to reasoners. But quite apart from being a weak or misguided response to this lack of resources, the fallacies act as guides through the paucity of evidence and knowledge that attends certain contexts. They are thus rational adaptations to the uncertainty of these contexts. This view of the fallacies as strategies or heuristics for tentatively inching forward in a process of reasoning in the absence of even minimal evidence or knowledge is largely an anathema to logicians and philosophers of a traditional bent. Fallacy analysis, these philosophers argue, should resist the type of cognitive characterisation that is integral to this view. Nor should features of context play a role in any determination of the rational standing of these arguments. And, finally, the very fact that fallacies are to be found where knowledge is lacking is proof, if proof were needed, that there are no redeeming features to these arguments. But this response sacrifices too much for some rather high-minded and outdated preconceptions about the logical value of the fallacies. Most present-day fallacy theorists are not inclined to adhere to the view that the fallacies are of dubious logical worth. But acknowledging, as Douglas Walton and

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others do, that there are non-fallacious variants of the fallacies or that the fallacies can best be analysed within a pragma-dialectical framework8 doesn’t quite go far enough for our present purposes. For contributions of this type often lack the theoretical power to explain how these arguments function within the rational procedures of different domains such as inquiry in science (as witnessed by the fact that we have not found it useful to employ the Gricean and Searlean communicative insights that are integral to pragma-dialectics in the argument analyses undertaken in Chapters 4–7). If the analyses of earlier chapters have demonstrated anything, it is that the rational merits and weaknesses of arguments are not particularly well characterised in terms of rules, either rules on the performance of speech acts à la pragma-dialectics or any other type of rules (none of the analyses in Chapters 4, 5, 6, and 7 appealed to rules in order to characterise the strength or weakness of arguments). Nor is it even helpful to conceive of a standard list of fallacies which contains arguments that are inherently weak. Some of the weak arguments that we examined in earlier chapters are not to be found in any list of fallacies, and other arguments that have historically been labelled as fallacies were shown to be anything but fallacious. The assumption of a standard list of fallacies has had a particularly constraining effect on the development of theoretical frameworks, as these frameworks are constructed to prohibit certain argument forms while permitting other forms. It emerges that even recent theoretical approaches that take a more positive view of the logical worth of fallacies still have some way to go if they are to shed certain rather unhelpful assumptions about the fallacies. If philosophical accounts of the fallacies need to make some adjustments in order to accommodate a greater alliance with public health science, then public health science must also facilitate greater disciplinary integration by undertaking some changes to its practice. Chief amongst these changes is a diminution of the preoccupation, in epidemiology in particular, with statistical techniques that are designed to establish correlations. This should be accompanied by an increase in thinking about the informal arguments that epidemiologists must advance in order to give rational weight to the various associations they establish.9 Battersby (2006: 50) effectively makes this point in the case of correlations, only some of which can qualify as causal claims and only after they are supported by rationally warranted arguments: [S]tatistical inference is often not adequate for establishing correlations in most studies. It is never adequate for establishing causal claims. Correlations are necessary but not sufficient for a causal claim. Epidemiologists therefore must use informal arguments to make their case for a causal claim.

Epidemiologists must re-engage with the critical base of their discipline, a critical base in which arguments are advanced about the correlations that satisfy criteria for causal claims, for example.10 In this way, the epidemiologist’s challenge is to become more like an informal logician who reflects on the arguments that must be advanced in order to determine which of the many statistical associations that can be established through the application of techniques warrant rational acceptance. This re-engagement with the critical base of epidemiology will not be easy, even for a discipline that is more aware than most scientific disciplines of the need to reflect

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on its processes of knowledge generation.11 After all, if epidemiologists are to start thinking like informal logicians about the arguments in their field, it may be feared that they could come to apply these critical skills of a whole range of argumentative practices. One such practice could be the relationship in epidemiology between argumentation and corporate influences.12 Notwithstanding the difficulty in overcoming hurdles to greater engagement with the critical base of epidemiology, this engagement must occur if philosophy and public health science are to make progress on areas of joint concern. As well as becoming an informal logician, the epidemiologist can secure a greater convergence of philosophy and public health science by becoming an epistemologist. An epistemological concept, the concept of presumption, has been integral to the account of the informal fallacies that we have been developing in this book. In this way, informal fallacies have been shown to facilitate scientific inquiry in a context of uncertainty, a capacity which, it has been argued, is directly attributable to the presumptive nature of the arguments in question. Specifically, these arguments have been shown to licence decisions in the practical sphere in the absence of complete deliberation and to respond to shifting evidential considerations during inquiry because the presumptions on which they are based display an orientation to action and context sensitivity, amongst other features (see Section 3.2). A concept that can confer such epistemic gains on inquiry, particularly in a context of uncertainty, has obvious relevance to the discipline of epidemiology and should be firmly embraced by epidemiologists and other public health scientists. Historically, epidemiology has made considerable strides when it has opened itself to the conceptual influences of other disciplines. Krieger (2000) describes epidemiology’s long-standing relationship to the social sciences, a relationship that has seen certain social scientific concepts have a substantial impact on the work of epidemiologists.13 Amongst the many benefits of this relationship for epidemiology have been new ways of conceiving of social inequalities14 and racial/ethnic disparities15 in health. In the same way, I believe that it is only when epidemiologists open themselves to epistemological concepts that we will begin to see significant progress on questions of joint interest to philosophy and public health science.16 Of course, the question of joint interest to philosophy and public health science that we have been examining in this book is how best to develop a model of scientific reasoning that is adapted to conditions of uncertainty. We argued in Chapter 3 that a model based on presumption was best equipped to address the three aspects of this question: the scientific inquiry within which reasoning about BSE proceeded; the type of uncertainty that beset this inquiry; and the strategies (informal fallacies) that scientists used to facilitate their reasoning in this context. To the extent that we have committed ourselves to a presumptive framework, our model must assume certain features. It must exhibit defeasibility: the various structures and processes posited within the model must be capable of being overturned, if conditions dictate that this should occur. The model must display an orientation to action: the reasoning that is captured by the model must be the basis of courses of action and decisions in the practical sphere that cannot await the completion of extensive inquiries and other investigations. It must exhibit rational justification: the structures and processes

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within the model are not arbitrary and must possess the minimal degree of rational warrant that is befitting of presumption. The model must display context sensitivity: it must be capable of varying its structures and processes in accordance with the conditions that exist at any particular point in time. So what constitutes evidence in support of a thesis or proof of a claim, for example, will be different in knowledge abundant contexts and contexts in which knowledge is lacking. Finally, the model must reflect the epistemic status of presumption. Initially at least, presumption has a lowly epistemic status. However, this status can be improved over time. Our model of reasoning will need to accommodate the changes, both positive and negative, that can occur in the epistemic standing of presumptions. It should be emphasised that these general features of the model may not actually be fulfilled by scientific reasoners in practice. Scientists may operate in inquiry with a standard of evidence that is in excess of that which can be achieved in a particular context. The actual reasoning of scientists may, therefore, not exhibit context sensitivity. Scientists may also fail to give effect to the defeasibility of the model by continuing to adhere to a claim in the face of contrary evidence. But neither of these scientific performances detracts from the fact that it should be possible in principle for the structures and processes within the model to vary in accordance with conditions in particular contexts and to be overturned by the emergence of contrary evidence. In not permitting these scientific performances to undermine the features of the model, we are not thereby diminishing the importance of the reasoning practices of scientists to this model. In fact, the need to achieve a model of scientific reasoning that can more closely reflect some of the characteristics of actual scientific reasoning has been one of the main motivations of the current study. But it is a reminder that if our model is to have any normative weight, it must be informed by, rather than reduced to, the reasoning practices of scientists. In placing high value on the role that the fallacies can play in this project, we are not taking the extreme view that there is no such thing as fallacious reasoning. We have seen numerous examples in earlier chapters of very weak scientific reasoning that, if anything, frustrated the aims of inquiry into BSE. If we want to emerge from this undertaking with a model of reasoning that is at once logically respectable and scientifically viable, we need to give this weak reasoning as much of a wide berth as the ideas of a theorist who refuses to engage with the actual reasoning practices of scientists.

8.2 A Model of Reasoning in Scientific Inquiry In keeping with the significance that we have accorded to the temporal context in which scientific reasoning takes place, we will outline the various aspects of our model in the three time phases that we have identified in the BSE inquiry. Our purpose in identifying these phases was to emphasise the fact that a scientific inquiry can assume different states as it evolves over time. Each of these states is characterised by unique epistemic conditions and other features that have a profound effect on the type of reasoning strategies that are employed by scientists. For each stage

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of inquiry, these conditions will be laid bare alongside a number of other considerations that impact more or less directly on the reasoning of scientists. We begin by describing the goals of each phase of inquiry. Goals in inquiry might include the gathering of evidence to support a particular hypothesis about the origin of an emerging infectious disease, the justification of disease control measures or the simple initiation of inquiry. The scientific conditions that characterise each phase of inquiry will also be addressed. These conditions might include technical issues such as the types of experiments that can be conducted or organisational issues such as the establishment of expert advisory committees. The epistemic conditions in each phase of inquiry will be discussed. Here we might address not just obvious considerations such as the lack of knowledge in a certain phase of inquiry, but also issues such as the changing epistemic status of theses. Finally, we will consider the reasoning strategies that scientists use in each phase of inquiry. Some of these strategies facilitate scientists in achieving the goals of a phase of inquiry. As well as these facilitative strategies, scientists can use non-facilitative strategies that frustrate the attainment of one or more goals in a phase of inquiry. Both types of strategy will be discussed.

8.2.1 A Model of Reasoning in Early Inquiry Newly emerging infectious diseases such as BSE have a habit of catching the scientific community in a state of less than complete preparedness. An important element in improving the scientific response to these diseases must surely be the development of an explicit model of reasoning that can help guide scientists in their early decision-making. At a minimum, this model should stipulate (i) the goals towards the fulfilment of which the model is contributing, (ii) the conditions under which the model is to be applied and (iii) the reasoning strategies that can address the goals of early inquiry within the conditions that obtain at this point in inquiry. We examine each of these components in turn below. Goals: Upon identifying a new disease entity, scientific investigators have an overriding goal: to launch a formal process of scientific inquiry within the shortest timescale possible. Where a new disease entity is infectious or a potential zoonosis, there is even greater urgency to embark on inquiry – any delay or inaction could pose considerable risks to animal and human health while the transmission routes of the disease remain unknown to scientists. The pressing demand to launch inquiry assumes precedence over other competing demands on scientific investigators. For example, the concern to avoid incurring error in inquiry is temporarily suspended as scientists forge ahead in an attitude of optimistic exploration. This attitude does not involve throwing all caution to the wind, but it does involve the calculation that the risk of error cannot be allowed to outweigh the altogether more pressing need to initiate inquiry. A further goal in the early phase of scientific inquiry is to arrive at decisions that become the basis of disease control measures in the absence of all but the most preliminary investigations. Of necessity, disease containment actions must be initiated in advance of the facts about a new disease. Ultimately,

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these actions may be found to be ineffective or based on an incorrect understanding of the transmission properties and other features of the disease in question. Yet, these possible outcomes should not deter scientists from undertaking the type of pre-inquiry decision-making that is an essential part of the early scientific response to a newly emerging infectious disease. The goals of early scientific inquiry are thus twofold: (1) to initiate inquiry, a goal which is only made possible through the temporary suspension of a number of other desiderata in inquiry and (2) to arrive at decisions relating to disease containment in advance of all but the most preliminary investigations. Scientific Conditions: The results of initial epidemiological investigations become available to scientists during the early weeks and months following the emergence of a new infectious disease. In an effort to identify the new disease entity, scientists also undertake various laboratory analyses that examine the histopathology and molecular properties of the disease in question. However, at this early stage of inquiry, no direct experimentation has yet been undertaken and is still some way off in the future. The scientific community can be in different states of organisational readiness to address the new disease. In the case of pandemic influenza, for example, the global scientific community is particularly well prepared to mount a rapid and effective early response through its organisation via international agencies such as WHO.17 This reflects more generally WHO’s well developed systems for dealing with outbreaks of infectious disease.18 In the case of little known diseases like the TSEs, the situation is quite different. Although expertise existed in TSEs when BSE first emerged in 1986, this was to be found among small, disparate research groups and individuals across both medical and veterinary fields. This expertise had never been formally organised and had never been collectively called upon to assess the implications of the emergence of a new TSE for human health. Inevitably, this lack of organisation in the scientific community produces delays in the community’s response to a new infectious disease and certainly did so in the case of BSE. The result was that it took until June 1988, nearly 2 years after BSE was identified as a new disease entity, before scientific experts in the form of the Southwood Working Party were brought together to consider this bovine disorder (and even then the range of this expertise was questioned; see note 19 in Chapter 7). The early response to a new infectious disease may therefore have to proceed in a less scientifically informed state that would ideally be the case. Epistemic Conditions: Of the three time phases that we identified in the BSE inquiry, the early phase was undoubtedly the most challenging for scientists in epistemic terms. The only direct knowledge scientists had of BSE was gleaned from John Wilesmith’s early epidemiological investigations and from molecular and histopathological studies conducted by Hope et al. (1988) and Wells et al. (1987), respectively. With so few findings about BSE available to investigators, scientists were compelled to bridge gaps in their knowledge by drawing on what was already known about other TSEs. Scrapie was the most extensively investigated TSE by the time BSE emerged and was also believed to be the origin of this new bovine disease. As such, it became a natural template for scientific judgements about how BSE might behave. However, to the extent that this template provided

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only indirect information about BSE, the various claims which the template was used to justify were at best weakly warranted. The type of epistemic strategy which is exemplified by the case of scientists in the early phase of BSE inquiry can be characterized as follows. Scientists respond to the uncertainty of early inquiry by achieving a downward adjustment in the epistemic standards that must be met in order to advance claims. These lowered epistemic standards allow scientists to seek out possible sources of presumption in inquiry. One such source is the use of analogical templates, which are based on a disease that is related to, and better known than, the newly emergent disease under investigation. The presumptive theses to emerge from these sources are certainly not knowledge claims, although this fact does not preclude them becoming knowledge claims as inquiry proceeds. What these presumptive claims do achieve, however, is the facilitation of inquiry until such times as other theses, which are more strongly warranted, can be obtained. Reasoning Strategies: Reasoning based on the analogical template that we have just described became a highly productive strategy for scientists during the BSE inquiry, particularly in the early phase of this inquiry. This strategy formed the basis of early risk assessments about BSE and was also used to justify measures that were taken in order to control the spread of the disease. But it was not the only facilitative reasoning strategy that was at the disposal of scientists during the adverse epistemic conditions of early inquiry. The argument from ignorance was used to effectively order questions for investigation in early inquiry. This reasoning strategy sought to prioritise those questions that had a reasonable prospect of being addressed within the epistemic and scientific conditions of early inquiry. Where a question was not consistent with those conditions – the question of the transmissibility of BSE to humans could not be experimentally investigated and, given the long incubation period of TSEs, natural transmission might take many years to be revealed – the argument from ignorance served to exclude that question from further, active consideration in inquiry. Question-begging argument also proved to be a highly valuable reasoning strategy for scientists in the early stage of inquiry. Typically, this argument is associated with the misguided attempt to use in reasoning the conclusion that the arguer is attempting to establish. However, by allowing scientists to use within their reasoning the proposition they were attempting to prove, this argument form permitted investigators to move forward in inquiry and establish lines of evidence that were independent of the conclusion. Question-begging argument thus transformed points in inquiry that were essentially impassable into much needed opportunities for evidence gathering. The facilitative reasoning strategies that we have just described are not intended to be exhaustive of the strategies that are beneficial to scientists at the outset of inquiry. But they do exemplify an important type of reasoning that has been almost completely overlooked by theorists who are concerned to examine how scientists reason in contexts of uncertainty. Each strategy owes its facilitative capacity to the fact that uncertainty is part of the logical structure (some would say logical flaw) of the argument associated with the strategy. For example, in question-begging argument uncertainty characterises one of the premises of the argument – to the extent that this premise is the conclusion, it exhibits the uncertainty of the conclusion and

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cannot satisfy the epistemic requirement that premises in an argument must be more certain than the conclusion to be proved. But given that this requirement may be held in abeyance as scientists attempt to embark on inquiry, the uncertainty of the premise of a question-begging argument is less a logical anomaly than it is a feature of this argument which makes it particularly well adapted to the adverse epistemic conditions of early inquiry. Non-facilitative forms of reasoning in the early stage of inquiry are those arguments which fail to reflect the wider epistemic conditions under which they are advanced. Deductive arguments which proceed, by definition, from premises that are certain (known to be true) to a conclusion that is uncertain (not known to be true) are poorly suited to the epistemic conditions of early inquiry. So while the circular pattern of reasoning evident in question-begging argument prospers under the conditions of early scientific inquiry, the linear pattern of reasoning that is typical of deductive arguments is altogether less well adapted to the pervasive uncertainty of early inquiry.

8.2.2 A Model of Reasoning in Middle Inquiry Following early investigations of BSE, inquiry into this new bovine disease entered a phase of intensive scientific activity. The middle stage of inquiry saw the relatively tardy and even disorganised response19 of the early weeks and months of the BSE crisis yield to a wide-ranging programme of research into BSE that was already producing results by the end of this period. We describe below the goals that motivated scientific reasoning during this middle stage of inquiry, the conditions that characterised this phase of investigation and the reasoning strategies which facilitated and hindered scientists in their attainment of these goals. Goals: To the extent that measures to control BSE had been implemented in early inquiry on the basis of tentative evidence, an overriding goal of scientists in the middle phase of inquiry was to establish a stronger rational basis for these various courses of action. In this way, the pathogenesis study, which was initiated at the CVL in December 1991, was undertaken with a view to justifying the terms of the human SBO ban (in the event, of course, the results of this study achieved an extension of the ban). The capacity of evidence from studies of this type to validate and revise earlier actions in relation to BSE is related to the fact that this evidence is obtained through experimental investigation. Its probative weight is therefore altogether greater than the evidence of early inquiry, which was established through less direct means such as analogies with other TSEs. Apart from the post-implementation justification of disease containment measures, another important goal of scientists in the middle stage of inquiry was the development of a body of knowledge about BSE. The tentative claims of early inquiry were exposed for the first time in the middle stage of inquiry to results from experimental studies and to findings of natural transmissions of BSE to a range of species. For some of these claims, this exposure marked the end of their journey in inquiry – the force of emerging evidence overturned these claims (or, as we argued in Chapter 5, emerging evidence should have overturned many more claims than actually occurred in the

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BSE inquiry). But for those claims that withstood the emergence of evidence in the middle phase of inquiry, integration within a body of knowledge about BSE was for the first time more than a theoretical possibility. This was the stage in inquiry when the prospect of knowledge that is implicit in presumptions looked as if it might actually be realised. Scientific Conditions: The middle stage of inquiry saw scientists embarking on an organised programme of experimental and other research in relation to BSE. Priorities for research were determined by the Tyrrell Committee,20 while recommended projects were undertaken at centres such as the Central Veterinary Laboratory and the Neuropathogenesis Unit in accordance with the expertise and facilities of these centres. Epidemiological studies, which had been so prominent in the emergent phase of inquiry, continued to occupy a position of significance during the middle stage of inquiry21 with epidemiological work an integral part of the Tyrrell recommendations and the basis of early studies of natural transmission of BSE to species that are not susceptible to scrapie (e.g. Kirkwood et al. 1990; Kirkwood and Cunningham 1994). During the same period, scientific advice to government about the risks that BSE posed to human health became the responsibility of a single expert committee, the Spongiform Encephalopathy Advisory Committee. From these various developments we can draw conclusions about the scientific conditions under which investigators were operating in the middle phase of inquiry. Firstly, how the scientific response to BSE should proceed became as much a focus of rational deliberation as BSE itself. In this way, the research that should be undertaken and the use of the results of that research to inform BSE risk assessments and justify disease containment measures became the primary scientific activity of expert committees during this period. Secondly, the ongoing prominence of epidemiological work during this phase of inquiry is indicative of just how long scientists were expecting to wait for BSE experiments to begin producing results. TSEs were known to have lengthy incubation periods, in some cases of many years. Epidemiological work provided a much needed means of characterising BSE while scientists awaited the results of experimental studies. Epistemic Conditions: As evidence from studies began to emerge in the middle phase of inquiry, the epistemic challenge for scientists was less about bridging gaps in knowledge and more about integrating this evidence within a body of knowledge. Some evidence that emerged during the middle stage of inquiry served to expand this body of knowledge by contributing new propositions to it (the finding of the dose required to achieve oral transmission of BSE to cattle is a case in point). Other evidence called into question the rational bases of disease containment measures and BSE risk assessments. By right, this evidence should have achieved a significant revision of the rational approach to scientific decision-making (specifically, scientists should have relinquished their reliance on analogical reasoning based on scrapie). On a few occasions, contrary evidence did overturn earlier decisions (e.g. the finding of BSE infectivity in calves less than 6 months old led scientists to call for an extension to the human SBO ban). However, the fact that this did not occur more widely, we argued, was an indication that the normal dialectical processes of presumption and burden of proof were subverted in inquiry. From these evidential

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developments in middle inquiry, several points emerge. Firstly, the development of a knowledge base supersedes the bridging of knowledge gaps as the primary epistemic activity in the middle phase of inquiry. Secondly, a lack of knowledge or evidence is not the only obstruction to progress in inquiry. The progress of inquiry can be frustrated even in the presence of abundant evidence, if this evidence is not permitted to have its full probative weight. Thirdly, although a body of knowledge begins to take shape in the middle phase of inquiry, it is in a state of constant flux as some theses are added to it, other theses are removed from it and still other theses vary their epistemic standing within it. Reasoning Strategies: In order to be responsive to the emergence of evidence in the middle stage of inquiry, scientists must have access to a set of defeasible, context-sensitive reasoning strategies. These strategies allow scientists to revise their commitments to theses in a proportionate manner to reflect changes in the evidential base of inquiry. In some contexts, a proportionate revision may involve the rejection of a single claim which can no longer be supported by the available evidence. In other contexts, a proportionate revision may involve the rejection of several claims, all of which are indefensible given their shared reliance on an insupportable claim. It has been argued that the so-called informal fallacies are uniquely equipped to respond to changes in the evidential base of inquiry. The defeasibility and context-sensitivity of these argument forms stem from the presumptive theses that constitute these forms. When the presumptive character of these arguments is allowed to stand in inquiry, the reasoning strategies based on these arguments can be seen to facilitate inquiry by enabling scientists to respond to the emergence of evidence. However, when this presumptive character is distorted, as occurred during the middle phase of the BSE inquiry, these same reasoning strategies frustrate the very argumentative purposes for which they are brought forward. In this case, rather than responding to emerging evidence, these strategies serve only to protect a developing body of claims from any evidential challenge. To the extent that emerging evidence is not able to bring about revisions in the epistemic commitments of scientists, these commitments progressively become detached from the evidential base of inquiry. In the BSE inquiry, this detachment found scientists continuing to argue that BSE would not transmit to humans and that beef was safe to eat even when the evidence available to scientists failed to support either of these claims. If correctly employed, presumptive strategies can guide the reasoning of scientists as they deal with new evidence about an infectious disease in the middle phase of inquiry. However, these same strategies have another important function for scientists during this phase of inquiry. While the defeasibility and context-sensitivity of these strategies equips them to respond to the emergence of new evidence, another feature – the capacity for the theses that are warranted by these strategies to improve their epistemic standing in inquiry – is integral to the knowledge generation function of these strategies. For presumptive theses that withstand the emergence of evidence in middle inquiry, the prospect of these theses improving their epistemic standing in inquiry and, eventually, attaining the status of knowledge claims becomes increasingly real.22 To the extent that reasoning strategies such as the argument from ignorance and analogical argument are based on presumptive claims, we can expect

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these strategies to be vehicles of knowledge generation in inquiry. In the early phase of inquiry, the raison d’être of presumptive reasoning strategies is to bridge gaps in scientific knowledge with no guarantee that this will result in any long-term epistemic gains for inquiry. By the middle phase of inquiry, investigators are beginning to see some epistemic return for their initial commitment to these strategies, as a number of the theses that are warranted by means of them are able to contribute for the first time to the knowledge base of inquiry. The capacity of presumptive reasoning strategies to generate knowledge in inquiry is not always evident to investigators at the outset of inquiry. But for those investigators who make an early investment in these strategies, the middle phase of inquiry is where they can begin to see some return for their efforts in terms of the development of a body of knowledge.

8.2.3 A Model of Reasoning in Late Inquiry As with other infectious disease epidemics, BSE cases have now decreased to an almost negligible level. From a peak of 36,680 cases in 1992, cases of BSE fell to 8,013 in 1996 (the end of the period we are studying) and only 7 cases were recorded in 2009 by the UK’s Department for Environment, Food and Rural Affairs. However, unlike other infectious disease epidemics, even as BSE cases were in decline, a related epidemic in humans in the form of variant CJD was emerging. It is not an exaggeration to say that scientists in the late phase of the BSE inquiry appeared to be taken aback by this serious human health development. We explained this response in terms of an unassailable scientific consensus about BSE which had served to reassure scientists and the public alike that BSE would not transmit to humans. This lack of scientific preparedness for the emergence of variant CJD was entirely avoidable and, indeed, could have been avoided if scientists had engaged in a more robust form of reasoning. We examine the main components of that reasoning below within a wider consideration of reasoning in the final stage of scientific inquiry. Goals: With the attainment of knowledge now well and truly within the grasp of scientists, theory construction becomes the focus of scientific effort in the late stage of inquiry. To this end, a number of priorities or concerns that were temporarily suspended in early inquiry once again assume significance. We described in Section 8.2.1 above how the need to initiate scientific inquiry into an infectious disease is so great that scientists at the outset of inquiry are prepared to suspend their concern for the avoidance of error. However, this suspension is relatively short-lived and by the middle and final stages of inquiry, investigators are positively inclined to ensure that their developing theories of a disease are consistent with the best scientific evidence that is available to them. Error at these later stages of inquiry is much more costly in cognitive and epistemic terms than in the early phase of inquiry. At the outset of inquiry, there are few epistemic commitments resting on presumptions. So if a particular presumption is found to be lacking, it can be rejected without necessitating a more widespread revision of scientific theses. However, a presumption that has been elevated to a knowledge claim in inquiry and integrated within a theory threatens to destabilise that theory should it be shown subsequently to be unwarranted. We

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also described in Section 8.2.1 how an epistemic priority requirement on argument was held in abeyance at the outset of inquiry. This required that scientists argue from theses that are more certain than, or better known than, the thesis to be proved through argument. In the uncertainty of early inquiry, the satisfaction of this requirement would have seen scientists having to abandon the possibility of even initiating inquiry. This epistemic priority requirement can be more readily satisfied in the late phase of inquiry, when there are many more theses, which can fulfil what it stipulates, at the disposal of investigators. Scientific Conditions: To the extent that theory construction is the goal of late inquiry, certain scientific conditions must be in place for this goal to be realised. The emergence of evidence during the middle phase of inquiry is certainly essential for theory construction to proceed. But this evidence is inadequate in itself to determine a single, correct theory of an emerging infectious disease and, indeed, may even be consistent with more than one theoretical account of such a disease.23 This was amply demonstrated in the BSE inquiry when two groups of scientists – government scientists and dissenting scientists – developed two opposing theoretical views of BSE which were based on the same set of evidence from experimental and epidemiological studies. These views contained quite different claims about the origin of BSE, the transmissibility of BSE to humans and much else besides. The key factors in deciding which of these views should be accepted as most likely to be a true account of this new bovine disease were all dialectical in nature.24 In this way, the failure of government scientists to afford dissenting scientists opportunities in which to present their claims and to bring forth evidence in support of those claims25 was the type of consideration that we described in Chapter 6 as serving to undermine the consensus view of BSE. Presumption and burden of proof form the dialectical engine of the process of inquiry that has been presented in this book. Through the interplay of these concepts, the rational grounds of a thesis are laid bare. The same dialectical considerations, which are the basis of presumption and burden of proof, can now be seen to guide theory construction in the late phase of scientific inquiry. While the consensus view of BSE enjoyed the support of most scientists who investigated the disease, it was a view that failed by the dialectical standards of inquiry. The scientific context in which a consensus view of BSE developed was one in which dialectical considerations relating to theory construction were increasingly subordinated to a range of non-scientific interests. These interests motivated government scientists to protect the consensus view from criticism, as this view contained reassuring claims to the effect that BSE had negligible implications for human health. The attempt to suppress the normal dialectical processes of inquiry had concrete consequences for scientists who undertook to challenge the consensus view of BSE. These dissenting scientists found their professional standing undermined, access to data and research materials restricted26 and the publication and funding of their work challenged.27 In short, the working conditions of these scientists ensured that they would be unable to mount an effective challenge to the consensus view of government scientists. In the absence of such a challenge, theory construction during the BSE inquiry consisted in the promotion at all costs of a

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particular position (the consensus view) rather than in a dialectical exercise between competing theoretical views. The lesson to emerge from theoretical developments during the BSE crisis is that any condition which frustrates this dialectical exercise is an obstruction to robust theory construction in inquiry. These conditions may include behaviours such as denying scientists opportunities in which to present their views. Dissenting scientists, for example, wished to discuss their research work with SEAC scientists but were prevented from attending SEAC meetings. However, they may also include a number of more fundamental conditions, the existence of any one of which can make dialectical interventions by scientists all but impossible. For example, dissenting scientists were denied the use of the data and materials that were needed in order to undertake their research. Epistemic Conditions: Of all stages of inquiry, the late stage has traditionally been the focus of discussion of philosophers of science and logicians.28 This is because this stage embodies epistemic concepts like certainty and reasoning processes such as deduction that have historically been of interest to these theorists. By late inquiry, scientists are not contending with a lack of knowledge as was the case in early inquiry. However, a knowledge problem of sorts nevertheless confronts investigators in the final phase of inquiry. Warranted theses have to be integrated into a body of knowledge, from within which they can enter into a number of deductive relations with other theses. However, not every deductive consequence of these theses is interesting, relevant or significant enough to form propositions that should undergo further testing in inquiry. Scientists must therefore manage the potentially large number of deductive implications that can be generated by this body of knowledge with a view to pursuing only those implications that are most likely to make a positive contribution to theory construction. But deduction does much more in late inquiry than generate propositions for further scientific testing. Deduction from certain and known theses confers certainty on all derived theses. This is in stark contrast to early inquiry, when scientists attempted to bridge a lack of certainty through the use of presumptive reasoning strategies. Certainty preservation assumes significance in late inquiry, as this is a time in inquiry when substantial epistemic commitments on the part of scientists rest on a small number of foundational theses. Disruption to one of these theses can have adverse consequences for investigators, who must face the prospect of substantial revisions to their other commitments should one of these foundational claims be invalidated. Of course, these deliberations bore little resemblance to how scientific theorising actually proceeded in the late stage of the BSE inquiry. The theses that government scientists used in theory construction did not emerge from a dialectical process in which claims grew in epistemic stature as they survived successive cycles of challenge during inquiry. Certainly, the theses advanced by these scientists persisted over the course of inquiry. But this persistence was only achieved by shielding these claims from criticism by dissenting scientists. To the extent that these claims entered theory construction in late inquiry in a less than warranted state, no process of deduction based on them would ever produce sound conclusions regardless of the validity of its rules of inference. This scenario demonstrates that the really important epistemic work of inquiry lies in establishing strongly warranted theses

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that can then participate in deductive reasoning – no deductive process can confer on its premises the type of certainty and warrant that comes from a thoroughgoing dialectical examination of the rational merits of a thesis. This scenario also demonstrates that theorists have been somewhat remiss in attending for the most part to later, deductive stages of scientific inquiry. Clearly, these stages can find scientists engaged in some very weak theory construction if earlier phases in inquiry have failed to deliver strongly warranted theses upon which construction can proceed. The traditional (mainly positivist) characterisation of early inquiry as a non-logical process has seen this important stage of scientific inquiry dismissed as mere creative guesswork. Yet, logical processes are very much in evidence in the formative stage of a scientific inquiry, as we demonstrated in Chapter 4. Moreover, it is these processes that must work well if scientists are to have anything even approximating a strongly warranted thesis for use in theory construction in late inquiry. Reasoning Strategies: It should be clear from the preceding section that deduction from certain, known premises is the dominant mode of reasoning in the final stage of scientific inquiry. It is not difficult to see why this is the case. It is only in the final stage of inquiry that scientists have access to strongly warranted theses for use as premises in deductive arguments. But even in this deductive phase of inquiry, the strategies that we have identified as facilitating early inquiry can once again be seen to play an important role in scientific reasoning. One such strategy, the argument from ignorance, has the status of a deductively valid argument when certain conditions are satisfied (see note 23 in Chapter 4). These conditions are that an exhaustive search has been conducted of a knowledge base that is closed, i.e. the base must contain all the relevant information pertaining to a particular question. In Chapter 6, we described two uses of the argument from ignorance by SEAC scientists that fulfilled these conditions. These uses were evident during SEAC’s deliberations concerning the safety of blood and its further assessment of the risk of BSE transmission through bovine eyeballs. With these conditions fulfilled, it was left for a modus tollens inference to generate deductively valid conclusions to the effect that blood did not pose a risk of CJD transmission and that there was no risk of BSE transmission through bovine eyeballs. As well as prioritising questions for investigation in early inquiry, the argument from ignorance, as these examples demonstrate, is able to contribute to theory construction in late inquiry by extending the knowledge base of inquiry. This argument is able to perform these diverse epistemic functions because it is as much at home in the exacting epistemic conditions of late inquiry as it is in the tentative epistemic circumstances of early inquiry. The argument from ignorance is particularly well adapted to the late, deductive phase of inquiry on account of its logical structure. Unlike other informal fallacies that we have studied in this book, this argument has a deductive logical structure which it owes to its dependence on modus tollens, a valid rule of deductive inference. Although the deductive operations of late inquiry preclude the use of presumptive reasoning strategies by scientists, these strategies are nevertheless pivotal to reasoning in this phase of inquiry. For it is through these strategies that the premises of deductive arguments are generated. The certain, known theses that constitute the premises of deductions in late inquiry are the epistemic product of

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reasoning undertaken in earlier stages of inquiry. These theses acquire their rational standing in inquiry through dialectical exchanges between scientists. Accounts of deductive reasoning never interrogate the origin of the theses that form premises in deductive arguments.29 According to these accounts, deduction proceeds by definition from premises that are true theses with no explanation of the epistemic and other processes that give rise to these theses in the first place. Of course, the deductive logician can easily avoid such an explanatory task by assigning it to the inductive logician. It is not the deductive logician’s task, after all, to describe the processes through which premises are established, but to capture deductive relations between established propositions. But this is not a stance that is open to the applied logician who is seeking to characterise the reasoning of public health scientists. In this case, the epistemic course that theses take en route to becoming premises in deductive arguments is relevant in any consideration of the reasoning of these scientists.30 And to understand this course, we must engage with the presumptive reasoning strategies that were discussed in earlier chapters. This final stage of scientific inquiry completes our model of reasoning, which is shown in its entirety in Diagram 8.1. EARLY INQUIRY Goals: To initiate inquiry. Two sub-goals must first be achieved: the suspension of epistemic priority requirements and error avoidance considerations To arrive at decisions relating to disease control measures Scientific Conditions: Initial epidemiological findings and laboratory results become available Varying levels of preparedness found in scientific community in accordance with involvement of international organisations (e.g. WHO) and presence of well organised research groupings Epistemic Conditions: Pervasive uncertainty exists in limited scientific evidence and knowledge Knowledge gaps bridged by establishing analogical template for new disease based on parallels with related diseases, etc. Reasoning Strategies: Facilitative strategies include analogical argument, argument from ignorance and question-begging argument. All function by conferring epistemic gains on inquiry Non-facilitative strategies include any form of reasoning that insists on a strict epistemic priority requirement (e.g. deductive reasoning)

MIDDLE INQUIRY Goals: To justify disease control measures postimplementation To develop a body of knowledge about new infectious disease Scientific Conditions: Scientists reflect on the scientific response (e.g. research to be conducted) to a new infectious disease Scientists embark on an organised programme of experimental and other research Scientific advice-giving is rationalised within a single, expert committee Epistemic Conditions: Development of knowledge base supersedes bridging of knowledge gaps as primary epistemic activity Scientific findings are integrated into a body of knowledge which must accommodate changing status of theses Emerging evidence assessed against preexisting scientific commitments, disease control measures, etc. Reasoning Strategies: Only defeasible, context-sensitive (i.e. presumptive) reasoning strategies are responsive to the emergence of evidence Presumptive reasoning strategies are integral to knowledge generation through their capacity to raise the epistemic standing of theses

LATE INQUIRY Goals: To engage in theory construction. Previously suspended requirements (e.g. epistemic priority requirement) are reinstated To select theory for acceptance which best satisfies certain scientific desiderata (e.g. explanatory power) and criteria (e.g. dialectical criteria) Scientific Conditions: Scientists begin to coalesce behind a small number of (often competing) theoretical views Scientists must have access to working conditions, that make dialectical interventions possible, for robust theory construction to occur Epistemic Conditions: Scientists must manage deductive implications of accepted theses by drawing only those consequences that can contribute to theory construction Theory acceptance may be guided, legitimately or otherwise, by non-scientific interests Scientists aim for certainty preservation by deriving claims from certain, foundational theses Reasoning Strategies: Deduction from certain, known premises is the dominant mode of reasoning On account of their deductive logical structure, some informal fallacies (e.g. argument from ignorance) can participate in deductive reasoning Premises used in deductions are generated by presumptive reasoning strategies at work in earlier stages of inquiry

Diagram 8.1 A model of scientific reasoning under uncertainty

8.3 The Model, Risk Analysis and Public Health Science A number of risk analysis concepts shaped the public health response to BSE. These concepts, which included the precautionary principle and ALARP principle, have yet to be described in any detail. This lack of earlier description is not an oversight. Rather, it reflects part of the argumentative purpose of this book. That purpose is

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to contend that if the model of reasoning discussed in the last section is to have relevance to the work of public health scientists, then it must be consistent with the concepts that inform the work of these scientists. This includes risk analysis concepts which should be capable of being fully integrated within the proposed model. In this final section, we examine two such concepts both in their own terms and in terms of how they came to be employed by scientists during the BSE crisis. From this examination, we will glean a number of key attributes of these concepts which at a minimum should be accommodated by our reasoning model. To the extent that these attributes are only poorly accommodated by this model, we should be led to consider if our model is truly adequate to address the challenges and issues that confront public health scientists. In such a case, a rational response might be to use the exposure of the model to features of scientific risk analysis to achieve some conceptual fine-tuning of the model. If our model can readily accommodate these attributes, then there is at least a reasonable basis for claiming that it has certain merits for public health science. In any event, an analysis of the conceptual interrelationships between our model of reasoning and the tools of scientific risk analysis can only serve to highlight the features of both of these concerns and bring these two important dimensions of public health science into closer alignment with each other.

8.3.1 The Precautionary Principle Although the precautionary principle was developed in the field of environmental health, it has been used extensively in a range of circumstances relating to public health (Martuzzi and Bertollini 2004). An important public health application of the principle occurred during the BSE crisis. Throughout the years that the BSE epidemic raged, scientists and government officials repeatedly invoked this principle in order to justify measures that were taken to control the spread of the disease and to limit its risk to human health. In evidence to Lord Phillips and his colleagues, Dr Calman (Chief Medical Officer, 1991–1998) stated that ‘[t]he Department of Health has always adopted a precautionary approach in relation to public health issues arising from BSE in their deliberations with MAFF’ (BSE Inquiry Report, Volume 6: 508). On 9 November 1995, Mr Hogg (Minister of Agriculture, Fisheries and Food, 1995–1997) met with representatives of slaughterhouse operators to discuss the handling of specified bovine offals. A note of the meeting recorded that ‘[a]lthough there was at present no evidence that BSE might be a threat to public health, we had to take a precautionary approach, basing our controls on the presumption that BSE might be a threat’ (BSE Inquiry Report, Volume 6: 599). On some occasions at least, it is clear that the precautionary principle was applied in name only during deliberations relating to BSE.31 However, the extent to which this principle was successfully applied during the BSE epidemic is more appropriately topic of discussion for another context. In this section, we are concerned to examine the main features of this principle and to consider if these features can be fully integrated within our proposed model of reasoning.

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Unsurprisingly, definitions of the precautionary principle vary. But in general, a number of central elements can be identified across all or most of these definitions. The first feature is that the principle is presumed to apply when courses of action must be taken in situations of uncertainty: The Precautionary Principle (PP) is a valuable tool for developing adequate courses of action in situations where there is large uncertainty. Such uncertainty can derive from: patchy scientific evidence about the health effects of an agent; sporadic reports of episodical adverse effects, unconfirmed or not reproducible; or limited knowledge of the dynamics of complex systems, resulting in effective ignorance on a series of chain events. Uncertainty can be of different magnitude and degree, but essentially discussion around the PP has focused on elements and criteria that should be addressed when making decisions under this kind of “undetermined” uncertainty, i.e., not easily measured or quantified (Martuzzi and Bertollini 2004: 43).

Moreover, this uncertainty cannot be used as a reason to delay action.32 Rather, the precautionary principle urges action in advance of possession of scientific evidence and knowledge of scientific facts: . . .the PP prescribes that uncertainty cannot be used as a pretext to delay action (Martuzzi and Bertollini 2004: 44). In order to protect the environment, the precautionary approach shall be widely applied by States according to their capabilities. Where there are threats of serious or irreversible damage, lack of full scientific certainty shall not be used as a reason for postponing costeffective measures to prevent environmental degradation.33

The second noteworthy feature of the precautionary principle relates to burden of proof. Typically in inquiry, the burden is on those who doubt the safety of some proposed activity or agent to demonstrate that it is harmful.34 The application of the precautionary principle reverses this burden of proof. The burden of proof is no longer on those who seek to demonstrate that an activity or agent is harmful. Rather, the burden is on those who are proposing a new activity or agent to demonstrate that it is safe: ‘the burden of proof might be reversed, from “recipients” to prove that an agent or technology is harmful to “proponents”, to prove that it is innocuous’ (Martuzzi and Bertollini 2004: 44). This reversal of burden of proof is clearly evident in the note of Mr Hogg’s meeting with representatives of slaughterhouse operators (see above). In this case, there was a presumption that BSE might be a threat to human health and a burden of proof on those who disagree with this view to show that BSE poses no risk. The third feature frequently discussed in relation to the precautionary principle is proportionality. This requires that any actions or measures that are undertaken under the auspices of the precautionary principle must be proportionate to the risks posed by a certain activity or agent. Specifically, measures should not be in excess of those risks:35 The principle of proportionality has an impact on the choice of possible measures, and in the trade context, this could mean that one adopts measures that would be the least traderestrictive. In general terms, the normative line of thinking here is that a proportionate application of the precautionary principle involves the least onerous measure while still attaining the legitimate objective (von Schomberg 2006: 27).

8.3

The Model, Risk Analysis and Public Health Science

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So the precautionary principle applies in contexts of uncertainty (which is not, in itself, grounds to delay action), involves a reversal of the burden of proof in inquiry and is intimately connected to a requirement for proportionality. To the extent that the model of reasoning which we outlined in the last section is to have relevance to public health scientists, this model must be able to accommodate features of the risk analysis concepts that these scientists use, including these features of the precautionary principle. This can be easily demonstrated on account of the presumptive nature of this model. We described in Section 3.3 how presumption was able to integrate the disciplines that converge on scientific inquiry (uncertainty, it was claimed, attends the convergence of different disciplines on a scientific inquiry), accommodate the prioritization of uncertainties in inquiry and capture the temporality of uncertainty. To this extent, presumption was able to address the main dimensions and forms of uncertainty that confront scientists in inquiry. A fortiori, a presumptive model of scientific reasoning is able to accommodate an uncertainty-gravitating notion like the precautionary principle. Also, presumption was characterised in Section 3.2 as a ‘means of extrication’ from deliberation when some action is called for in advance of the completion of deliberation (i.e. before evidence has been fully gathered and considered). A presumptive model of reasoning will, therefore, have little difficulty in handling a precautionary principle that calls for action to be taken in the absence of scientific evidence and certainty. So it can be said that our model of scientific reasoning adequately addresses the first of our three features of the precautionary principle, the capacity of this principle to apply to contexts of uncertainty. Our presumptive model of reasoning is also equipped to accommodate the precautionary principle’s reversal of burden of proof and requirement for proportionality. By definition, presumption is a dialectical notion. Any model of reasoning based on the concept of presumption inevitably assumes the dialectical character of this concept. The reversal of burden of proof demanded by the precautionary principle is a dialectical stipulation about the party in inquiry which should assume responsibility for demonstrating that a particular agent or activity poses no risk to health or to the environment. This dialectical stipulation is readily accommodated within a presumptive model of reasoning that is itself dialectical through and through. Proportionality is a context-sensitive notion. An action or measure that is proportionate to the risks of an agent or activity in one context may be in excess of what is required in another context. For example, it may be proportionate to ban the use of a certain chemical in food products even if there is only minimal evidence of risk to human health if the chemical in question can be readily replaced by a safe alternative. However, if no safe alternative exists, a complete ban may be judged to be a disproportionate response to the risk posed by the chemical.36 Context sensitivity was one of five features of presumption examined in Section 3.2. Presumption, it was argued, is intimately tied to context along a number of parameters including the evidence that can overturn a presumption and that can bring about its rational validation. A presumptive model of reasoning inherits the context sensitivity of the presumptions that constitute this model. This model is thus ideally equipped to accommodate the context sensitivity of the concept of proportionality that attends the precautionary principle.

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8.3.2 As Low As Reasonably Practicable A further risk analysis concept that was used extensively during the BSE affair was ALARP (as low as reasonably practicable).37 This concept contains an imperative to reduce risk until such times when further risk reduction activities incur costs (the latter broadly construed38 ) that exceed any gain from these activities: The principle of ALARP (As low as reasonably practicable) describes the way in which risk is treated legally and by the HSE (Health and Safety Executive) in the UK. The concept is that all reasonable measures will be taken in respect of risks which lie in the ‘tolerable’ zone to reduce them further until the cost of further risk reduction is grossly disproportionate to the benefit (Smith 2001: 129).

ALARP had been a familiar risk analysis concept within government since the 1983 publication by the Royal Society of Risk Assessment: A Study Group Report. Notwithstanding this fact, the use of this principle was largely implicit in the deliberations that followed the emergence of BSE in 1986.39 One of the few explicit statements of this principle by a key actor in the BSE story was the following account by the Southwood Working Party which was given in evidence to Lord Phillips and his colleagues: Our approach to risk was in accord with the then developing application of analysis to public risk which involved the balancing of the perceived magnitude of the risk against the practicability or achievability of successive steps for its reduction. The magnitude of a risk comprises both its likelihood and the scale of the danger (BSE Inquiry Report, Volume 1: 52).

Despite this explicit statement of adherence to the ALARP principle, it was the opinion of Lord Phillips and his co-investigators that this principle was on occasion inadequately implemented not just by Southwood scientists but also by other central players in the BSE affair.40 However, as with the precautionary principle of the previous section, we are less concerned with how well scientists implemented the ALARP principle than we are to discover if our model of scientific reasoning can accommodate features of this principle. It is to an examination of this issue that we now turn. The ALARP principle sets out from a position which acknowledges that complete risk reduction is not attainable and that risk must therefore be managed by bringing it within levels that are as low as reasonably achievable or practicable.41 The principle achieves this risk reduction through three components: (1) an imperative to undertake action to reduce the risks of an agent or activity, (2) an expectation that this action will incur costs and (3) a requirement that these costs should be proportionate to any benefit derived from the action. I want to argue that the ALARP principle, and the three components which give it effect, have a functional role in the domain of risk management that is similar to the functional role of presumption in uncertainty management. In the same way that ALARP practitioners acknowledge the impossibility of complete risk reduction, proponents of a presumptive model of scientific reasoning recognise that the total eradication of uncertainty is not attainable in inquiry, particularly inquiry in its emergent phase. Uncertainty is an inherent

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Summary

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feature of scientific inquiry and, like risk, must be brought within levels that are as low as reasonably achievable. A presumptive model of reasoning also has functional equivalents of each of the three ALARP components described above. We described in Section 3.2 how presumption is an action-oriented concept. The actions that are licensed by presumption include cognitive actions (e.g. decisions) that enable investigators to circumvent uncertainty and advance inquiry. Undertaking these actions incurs costs which extend beyond economic considerations to include cognitive costs such as memory and attention. Finally, no presumption or source of presumptions is sustained in inquiry at any cost. A presumption that fails to pay its way in terms of epistemic gains for inquiry will very quickly be relinquished by investigators. Presumption in the epistemic domain, it emerges, is functionally equivalent to ALARP in the domain of risk. Through its functional equivalence to ALARP, a presumptive model of scientific reasoning can accommodate the defining features of this important risk analysis concept.

8.4 Summary This chapter has sought to bring together the various strands of the model of reasoning that we have been developing throughout this book. Central to this model are the informal fallacies, an area of logical inquiry which has historically experienced some neglect but which has proved to be particularly valuable in addressing the difficult epistemic conditions in which scientific reasoners are compelled to operate. Several of these so-called fallacies were found to be anything but fallacious when assessed against the uncertain contexts in which they were advanced. In fact, these fallacies were shown to confer certain epistemic benefits on inquiry, particularly in the early stage of inquiry. An equally neglected area of epistemological inquiry, the concept of presumption, provided the framework for our analysis of the fallacies. A presumptive framework brought the logical and rational features of the fallacies into sharp focus, features which had been obscured by more traditional epistemological analyses. As well as supporting an analysis of the fallacies, a presumptive framework was also used to capture the rational methodology of scientific inquiry à la Rescher. Through this framework, we were able to chart the epistemic course of theses in scientific inquiry, the BSE inquiry specifically included. Only some theses improved their epistemic standing during the inquiry into BSE. Many other theses were overturned by contrary evidence and fell by the wayside in inquiry. Still other theses should have been defeated by this evidence but persisted in inquiry on account of the distortion of the dialectical rules of presumption and burden of proof in inquiry. In any event, the combined presumptive analyses of the informal fallacies on the one hand and scientific inquiry on the other hand opened up new possibilities for a model of scientific reasoning that could address uncertainty. The proposed model of scientific reasoning represents a joint venture between the areas of philosophy and public health science. These areas, it was contended, have not been particularly well integrated to date on account of a number of disciplinary features. Specifically, philosophers have traditionally been concerned to describe

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reasoning in a formal, abstract manner which is concerned more with deductive, truth relations between propositions than with how individuals cope with issues such as uncertainty in their everyday reasoning practice. For their part, public health scientists and epidemiologists have devoted little effort to the type of conceptual work required to generate the new modes of reasoning that are needed to address the complexities of modern public health problems. A combined effort on the part of philosophers and public health scientists to develop new ways of thinking and reasoning about the public health issues (including emerging infectious diseases) that confront us provides us with a rational basis for further progress in this area. The model of reasoning that has been proposed in this book is a first step in this direction. Ultimately, this model may be found to be lacking in ways that reduce its usefulness to the work of public health scientists or that compromise its conceptual credentials for philosophers. However, even if either (or, indeed, both) of these possibilities comes about, this model still has one overriding merit over investigations that have been conducted to date. This is the merit of initiating a form of inquiry that sees much greater potential for progress to be made on important public health questions through the collaboration of the disciplines of philosophy and public health science. If this is the single, enduring feature of this study, then this book will have made a significant contribution to this new area of intellectual inquiry.

Notes 1. There have also been cases of vCJD outside the UK. Collee et al. (2006) report 28 cases outside the UK by February 2006. This figure breaks down as follows: France (16 cases), Ireland (3), USA (2), Canada, Italy, Japan, The Netherlands, Portugal, Saudi Arabia and Spain (1 case each). 2. It is important to establish the prevalence of vCJD if effective measures are to be taken to prevent the iatrogenic transmission of the disease (e.g. through blood transfusions). To this end, studies have been undertaken to establish the prevalence of disease-related prion protein in tonsil and appendix tissue. Clewley et al. (2009) examined 63,007 tonsil samples and found that none of the samples were unequivocally reactive to both enzyme immunoassays used in the study. No disease-related prion protein was detected using immunohistochemistry or immunoblotting either. Frosh et al. (2004) screened 2,000 anonymous surgical tonsillectomy specimens for disease-associated prion protein and found no positive cases. Hilton et al. (2004) examined tissue from 14,964 appendectomies and 1,739 tonsillectomies. Three appendectomy samples showed lymphoreticular accumulation of prion protein, giving an estimated prevalence of 3/12,674 or 237 per million (95% CI 49–692 per million). 3. Although these consequences are unquantifiable, some interesting qualitative work has been conducted into the public’s perceptions of trustworthiness of politicians and scientists on matters of food safety. Green et al. (2005) used focus groups to examine how the public assessed risks associated with food in general, and the BSE problem in particular, in four European countries. These investigators found that ‘participants made routine comments about the lack of trustworthiness of politicians, who were seen as acting in terms of vested interests that were unlikely to be those of the consumer. . .the BSE crisis was seen as a key contributor to this lack of faith. To some extent, ‘experts’ such as scientists were similarly mistrusted. Some

Notes

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5.

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reported frustration with the uncertainties of expert advice on food, but others were sceptical of the neutrality of experts’ (2005: 525–26). Lord Phillips and his colleagues stated that ‘[c]onfidence in government pronouncements about risk was a further casualty of BSE’ (BSE Inquiry Report, Volume 1: xviii). Jasanoff (1997: 223) characterises this breakdown in trust and confidence between the public and government in relation to BSE as ‘civic dislocation’: ‘The phenomenon that I call civic dislocation expressed itself as a mismatch between what governmental institutions were supposed to do for the public and what they did in reality. In the dislocated state, trust in government vanished and people looked to other institutions – the high street butcher, the restaurant, the media, the supermarket – for information and advice to restore their security’. Green et al. (2005: 526) also report that the local butcher was trusted by respondents in their study of focus groups in four European countries to provide reliable information on food safety: ‘[P]articular individuals were seen as reliable sources of both information and safe food. The archetypal embodiment of this kind of trust was the ‘local butcher’, who was suggested across all countries as someone who could be relied upon to provide good quality, safe food and to know the provenance of that food on behalf of the consumer’. Adam (1998: 167) states that: ‘It is my reading of the situation that the public standing of science has been badly damaged by the BSE-CJD episode. Science has suffered a blow to its respectability and its credibility not only through mis/representation by the press but through self-inflicted disastrous ‘performances’ on television. As the crisis broke, for example, viewers were able to watch Professor John Pattison, the chairman of the Government’s BSE advisory committee, change his story from 1 day to the next: on Wednesday 20 March 1996 he stated that the potential number of humans contracting CJD could be anywhere between two-figure numbers and 500,000, thus indicating that the potential was there for a major epidemic. Either scenario, he suggested, was possible; science at this point simply did not have an adequate basis upon which to make predictions or calculate risks. The very next day, however, this same scientist insisted that due to the regulations which the UK Government had put in place in 1989, the risk of contracting CJD was very, very small indeed. On the basis of these measures, he was adamant, the public could be assured that, ‘in the normal sense of the word’, British beef was ‘safe’ to eat’ (italics in original). In fact, Lord Phillips and his co-investigators formulated 73 lessons arranged according to 21 episodes during the BSE affair (e.g. introduction of the ruminant feed ban). A further 52 lessons were arranged according to four topics that were prominent within the inquiry (e.g. use of advisory committees). None of the lessons described by Lord Phillips and his co-investigators relate to the issue of scientific reasoning in contexts of uncertainty. Uncertainty was mentioned in one of the four topics that were considered prominent throughout the inquiry (see note 6 above). The topic in question was ‘Dealing with uncertainty and the communication of risk’. However, the discussion of this topic and the 11 lessons advanced by Lord Phillips and his colleagues dwell entirely on risk communication. This framework is elaborated in note 41 in Chapter 3. That the ascendance of statistical techniques in epidemiology has tended to displace the informal arguments that are needed to make sense of the results of these techniques is evident from the following comments by the prominent American epidemiologist George Willis Comstock. In an interview for the journal Epidemiology in 2003, Comstock was asked how present-day epidemiology differs from the field in which Comstock started his career. He responded: ‘Statistics plays a more prominent role today. Epidemiology back then was based more on logic and whether the results made sense biologically. My early papers don’t have a P value or significance test. The “biostatisticians” were more like today’s project directors. They knew how to carry out studies and how to avoid biases. Technology has improved. We are able to measure more things in different biologic samples. But I don’t think the basic principles of epidemiology have changed at all. It’s just that we now rely more on statistical significance and less on what makes sense’ (Sandler 2003: 624).

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10. Battersby (2006) compares three sets of criteria for causal claims: those advanced in 1964 by the US Surgeon General’s Committee on Smoking and Health; those advanced a year later by the leading biostatistician Bradford Hill; and those advanced by the informal logician Douglas Walton. He remarks that ‘[e]pidemiologists are an important example of disciplinary practitioners who develop and apply epistemological criteria. I have argued that epidemiologists would benefit from seeing the justification of a causal claim as making an “argument for the best explanation”, which involves not only commonly used criteria for justifying a causal claim, but also consideration of arguments against alternative explanations’ (2006: 60). Weed (1995: 915) also sees a need for greater engagement of epidemiology with philosophy on issues relating to causal claims: ‘The philosophy of science is another link between the humanities and epidemiology that is partially in place. Causation and causal inference are central issues, providing epidemiologists the opportunity to answer questions regarding the nature of epidemiological knowledge, the role of logic and reasoning, and constraints on scientific discovery’. 11. Battersby (2006: 41–42) captures the same point as follows: ‘Epidemiology is a highly successful science and to some extent epistemically self-conscious’. 12. Corporate influences have a significant and growing role in epidemiology, largely through the funding of the research work of epidemiologists. For discussion of the pernicious effects of corporate influences on epidemiology, see Pearce (2007, 2008). 13. Baum (2008: 166) states that ‘[c]ollaboration of epidemiologists with social scientists can improve the quality of public health research and interventions’. 14. Krieger (2000: 160) states that ‘[s]tarting in the mid-1990s a new raft of articles – by epidemiologists for epidemiologists – turns critical attention to theoretical frameworks guiding epidemiologic hypotheses and investigations. Challenging the discipline’s dominant focus on individual-level biological and behavioral “risk factors”, as fostered by biomedical and lifestyle approaches to analyzing disease causation, these epidemiologists call for explicit development of epidemiologic theories of disease distribution – informed by relevant social scientific constructs – capable of explaining current and secular trends in social inequalities in health’ (italics in original). 15. Krieger (2000: 160) describes how ‘[r]enewed connections between epidemiology and social sciences in the 1990s also challenge a long-standing epidemiologic practice of conceptualizing and analyzing “race” as an innate biological characteristic. Bringing new insights to unexplained racial/ethnic disparities in health, an emerging body of work examines effects of racial discrimination on somatic health, with measures of exposure extending from individual-level, self-reported experiences of racial discrimination to data on residential segregation and Black political empowerment’. 16. According to Battersby (2006: 41), epidemiology is effectively applied epistemology: ‘I invite those who are interested in applied epistemology . . . to look at epidemiology’. 17. The following extract from the Introduction of WHO’s document Pandemic Influenza Preparedness and Response (2009) reveals the advanced state of readiness of the world’s scientific community for the emergence of pandemic influenza. This level of preparedness was only possible because of the huge international organisational effort mounted by WHO: ‘WHO previously published pandemic preparedness guidance in 1999 and a revision of their guidance in 2005. Since 2005, there have been advances in many areas of preparedness and response planning. For example, stockpiles of antiviral drugs are now a reality and a WHO guideline has been developed to attempt to stop or delay pandemic influenza at its initial emergence. There is increased understanding of past pandemics, strengthened outbreak communications, greater insight on disease spread and approaches to control, and increasingly sophisticated statistical modeling of various aspects of influenza. Extensive practical experience has been gained from responding to outbreaks of highly pathogenic avian influenza A (H5N1) virus infection in poultry and humans, and from conducting pandemic preparedness and response exercises in many countries. There is greater understanding that pandemic preparedness requires the involvement of not only the health sector, but the whole of society.

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In 2007, the International Health Regulations (2005) or IHR (2005) entered into force providing the international community with a framework to address international public heath concerns. In light of these developments, WHO decided to update its guidance to enable countries to be better prepared for the next pandemic. This Guidance serves as the core strategic document in a suite of materials. It is supported by a complement of pandemic preparedness materials and tools. These documents and tools provide detailed information on a broad range of specific recommendations and activities, as well as clear guidance on their implementation’ (World Health Organization 2009: 12). The Global Outbreak and Alert Response Network is one such system. Plant (2008: 46) describes the role of this network when she responded to a call for epidemiological assistance to deal with a ‘respiratory disease of unknown cause’ in Vietnam. The disease in question was subsequently named SARS: ‘I belong to the Global Outbreak and Alert Response Network, a World Health Organization (WHO)-sponsored network which facilitates country, institutional and individual response to outbreaks. This means there is a large army of people available to respond, and the individuals function as surge capacity for the WHO. It is an efficient and rapidly available task force from which people can be quickly mobilized to where they are needed, which means that the WHO has access to the most appropriate responders for different outbreaks’. That scientists failed to make timely use of expert resources in making this response is evident from the following comments of Lord Phillips and his co-investigators: ‘When BSE was identified as a new disease by the CVL in December 1986, it was at once appreciated that two important questions needed to be answered. Was it indeed a TSE? And did it have implications for human health? It was the greatest good fortune that, as a result of the joint initiatives of the Agricultural and Food Research Council (AFRC) and the Medical Research Council (MRC), there existed in the form of the Neuropathogenesis Unit (NPU) a world-renowned centre of expertise in TSEs. We have criticised the delay in seeking the collaboration of the NPU in answering the first important question. We have also criticised the more substantial delay in involving DH [the Department of Health] in the consideration of the second question’ (BSE Inquiry Report, Volume 1: 252). Although the Tyrrell Committee submitted its Interim Report to government in June 1989, it took until January 1990, when the report was finally published, before funding for research projects became available. Lord Phillips and his co-investigators considered if this delay had adverse implications for the projects concerned. Having heard evidence from witnesses that this delay was not detrimental to the scientific work recommended within the report, Lord Phillips and his colleagues concluded: ‘It may be that no time was lost as a result of the delay in publishing the Tyrrell Report, although we are not convinced of this. Publication of the Report would have acted as a spur to the speedy identification of how the recommended research was to be funded. . .It would also have informed the outside world, and in particular the scientific world, of the likelihood of research opportunities, which could have led to a degree of competition for some of the projects. As it was, the CVL and the NPU proceeded to prepare to implement most of the high-priority projects without the peer review that the Tyrrell Committee had advised they should receive’ (BSE Inquiry Report, Volume 11: 37). It is clear from these comments that Lord Phillips and his colleagues did believe there were adverse consequences for scientific research of the delay in publication of the report. In accounts of other infectious disease epidemics, epidemiology has been described as the branch of science that is first to produce a characterisation of a new infectious disease usually in the absence of knowledge. In relation to the AIDS epidemic, Berridge (1996: 23) states that ‘[i]nitially it was epidemiology, in the absence of almost any knowledge of the etiology of the disease, which appeared to offer a means of arriving at some explanatory framework within which it [AIDS] could be placed’. In a US policy context, an epidemiological characterisation of AIDS then yielded to a biomedical explanation of the disease, while epidemiology continued to shape AIDS policy alongside biomedicine in the UK: ‘Gerald Oppenheimer, in his analysis of the relationship between scientific models of AIDS and policy-making in the

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USA, has drawn attention to the initial epidemiological constructions of AIDS which determined policy and which were then replaced by perceptions of AIDS as a set of biomedical problems open to chemical resolution in the period after the discovery of the virus in 1984– 1985. Epidemiology as the engine of policy was replaced by biomedicine, in the US context at least. But in the UK, the relationship between different forms of science and health policy was different. Epidemiology, the rationale for a redefined public-health medicine since the 1960s, continued to define policy along with biomedicine’ (Berridge 1996: 9). In continuing to play a significant role in the characterisation of BSE, even as this disease was increasingly being investigated by other branches of science, epidemiology’s part in the BSE crisis was similar to the role of epidemiology that Berridge describes in the context of AIDS in the UK. The idea that presumptions are a transition stage for scientists en route to a particular epistemic destination is succinctly expressed by Fuller and Collier (2004: 301): ‘[S]cientists are professionally mandated to treat presumptions not as positive accomplishments in their own right, but as way stations to be superseded on the road to inquiry’. However, according to the view of presumption developed in this book, presumptions are not ‘superseded on the road to inquiry’. Rather, they are an integral part of inquiry. This is, of course, an expression of the underdetermination thesis in the philosophy of science. Although different versions of this thesis exist, it may be defined in general as follows: ‘The underdetermination thesis asserts that no body of data or evidence or observation can determine a scientific theory or hypothesis within a theory. . .underdetermination is explicated as the assured possibility of rival theories that are at least as well confirmed as the original theory by all possible data or evidence’ (Norton 2008: 20). To the extent that evidence alone is not sufficient to decide between rival theories, nonempirical factors have been proposed by theorists as a means of singling out a particular theory for acceptance. They include simplicity, breadth of scope, explanatory power, heuristic fecundity and practical success (Magnus 2006). On several occasions during the BSE crisis, dissenting scientists were denied access to information which was needed in order to support their claims. On 21 April 1994, Dr Dealler wrote to John Wilesmith of the CVL to request data that would be used in predicting the number of BSE cases. Mr Wilesmith responded to Dr Dealler on 4 May 1994 by saying that the CVL ‘will not be providing you with any data as I have to cover the costs of all our time and, in this case, the time required to provide these data is not justifiable’. This is confirmed by comments made by Dr Dealler to Lord Phillips and his team. On 5 February 1994, a letter by Dr Dealler and Professor Lacey entitled ‘Suspected Vertical Transmission of BSE’ was published in the Veterinary Record. The letter described a case of BSE in a female Friesian-Holstein calf that had been born nearly a year after the ruminant feed ban: ‘Dr Dealler told us that he was telephoned at home by the local MAFF veterinary officer after the publication of the letter in the Veterinary Record and that MAFF demanded the brain of the animal. Dr Dealler considered that this may have been to make sure that he did not carry out further research’ (BSE Inquiry Report, Volume 11: 264). It is difficult to read the following minutes of the fourth BSE research and development progress meeting held on 21 November 1989 without forming the impression that attempts were being made to block the funding and publication of research work prepared by Dr Harash Narang, another dissenting scientist. Dr Narang was a microbiologist who was employed by the Public Health Laboratory Service at Newcastle General Hospital. The minutes state that ‘Mr Dawson pointed out that he [Dr Narang] had at present no funding and Mr Bradley said this material would only be required if funding was forthcoming. Dr MacOwan said Narang had applied to the Chief Scientist for minimal funding and that if his request for money was granted any information his work produced would be for the Chief Scientist. While to date it was unheard of for the Chief Scientist to stop work being published this was possible. The contract made with the Chief Scientist when funding was granted was to protect the customer. Dr MacOwan asked the meeting to be more specific in their dismissal of Dr Narang’s work as this had a bearing on the result of the request for funding’ (BSE Inquiry Report, Volume 11: 280).

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28. Positivist philosophers of science in particular treated the late stage of scientific inquiry as the only stage worthy of investigation on account of its logical nature. However, even recent work in argumentation theory has tended to privilege this final stage over earlier, discovery stages of inquiry. It is not uncommon, for example, for argumentation theorists to restrict the use of the term ‘inquiry’ only to the activities of this final stage, as can be seen in the following remarks by Douglas Walton (2006: 186): ‘It seems generally that, at the later stages of scientific research, where results are solidified and presented to colleagues and the public, scientific reasoning does take a form of argument very similar to the inquiry. However at the earlier stages, where a lot of creative guesswork is involved in arguments about scientific hypotheses, the inquiry is probably not a very useful model of scientific argument’. In this book, the term ‘inquiry’ has been used to describe both main types of scientific activity. Moreover, I would suggest that if any model of inquiry is unable to capture both types of activity, then it is the model that needs to change rather than theorists restrict the use of the term ‘inquiry’ to the activities of late scientific inquiry. 29. It is as if these theses stand ‘in splendid isolation from [their] probative background’ (Rescher 1977: 117). The actual course of argumentation that led to the premises is not deemed to be relevant to deduction. Rescher captures this point in terms of the relationship between a conclusion and its premises in deductive arguments (to the extent that premises are conclusions of other, prior arguments, Rescher is effectively characterising in this extract the relationship between premises and their background supporting argumentation): ‘To assess the solidity (i.e., validity) of a deductive argument, we must simply determine that the conclusion is such that IF the premises are true, THEN it must be true as well. The way in which the conclusion is linked to the premises – the actual course of argumentation itself – is ultimately irrelevant. In deductive arguments, a thesis can shed its probative antecedents’ (1977: 117; italics in original). 30. The ‘epistemic course’ taken by theses in scientific inquiry – and denied relevance within deduction (see note 29 above) and the deductive sciences (see below) – is at the centre of Rescher’s disputational model of science: ‘These general considerations regarding the probative structure of dialectical contexts have one particularly significant bearing in the specific setting of a disputational model of natural science. They mean that we can never really assess the probative standing of a scientific thesis outside its historical context – outside the background of the actual course of controversy and discussion from which it has emerged. The real-life sequence of argumentation and debate that has brought us to where we are becomes a crucial factor in the rational assessment of this position. The probative or evidential situation in this domain is context-dependent on the details of the historical background in a way that finds no parallel in the deductive sciences that have often (and mistakenly) been taken as the model of scientific rationality in general’ (Rescher 1977: 118). 31. The precautionary principle states that a lack of scientific evidence or certainty should not be used as grounds to delay taking measures which can reduce risks from an activity or agent (see main text). But, as can be seen from the following oral evidence to the BSE Inquiry on 12 June 1998, this central tenet of the principle failed to apply to the government’s handling of BSE: Mr Walker (Counsel for The BSE Inquiry): When you were describing Government policy in this way, are you meaning to say that the scientific advice must be that there is evidence that such and such occurs before the Government can act to stop it? Mr Cruickshank (Animal Health Group, MAFF): Yes, Yes, that was the policy. In waiting for evidence of harm to be obtained before action was taken, the British Government could be described as operating on the basis of a principle of reaction rather than precaution in the manner suggested by Kriebel and Tickner (2001: 1354): ‘Too often, we believe, public health and environmental policies are based on a principle of reaction rather than precaution. Government regulatory agencies are often put in the position of having to wait until evidence of harm is established beyond all reasonable doubt before they can act to prevent harm’ (italics in original).

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32. Scientists and others often exaggerate the uncertainty of evidence upon which regulatory action is based with a view to postponing actions that could protect public health. Michaels and Monforton (2005: S39) state that ‘[e]nvironmental activists can be. . .guilty of using the existence of scientific uncertainty to advance policy aims through an overzealous application of what has been labeled “the precautionary principle”. If the weighing of potential risks and benefits is transformed into a demand for certainty that a policy or action will result in no harm, scientific advances or public health interventions with the potential to genuinely improve the human condition can be disparaged and delayed’ (italics in original). Martuzzi and Bertollini (2004: 44) remark that ‘there might be the danger that the [precautionary principle] is used, or rather misused, against technological development and scientific advancement’. 33. This extract is Principle 15 of the Rio Declaration on Environment and Development. The full Declaration can be found in Annex I of the Report of the United Nations Conference on Environment and Development. The Conference took place in Rio de Janeiro between 3 and 14 June 1992. 34. ‘Characteristically under environmental treaties the burden of proving risk is allocated to those questioning whether a risk-generating activity should proceed. If there is high uncertainty and no likelihood of harm can be established (thus: the threshold is not known to be crossed), activities may proceed’ (Nollkaemper 1996: 85). 35. ‘[T]he proportionate implementation of the precautionary principle is not aimed at categorical bans of products or processes. . .but certainly does not exclude such measures in individual cases’ (von Schomberg 2006: 27). Such ‘categorical bans’ will, in certain cases, be in excess of the risks posed by a product or process. 36. Proportionality was a guiding concept in deliberations concerning the safety of vaccines during the BSE epidemic. The reasoning of scientists on this matter can be characterised as follows. A complete ban on the use of bovine tissues in the production of vaccines was a proportionate response in those cases where non-bovine sources could be readily accessed and there was no risk of disruption to necessary vaccination programmes. However, such a ban was judged to be disproportionate to the perceived risks if non-bovine sources could not be readily established for vaccine production and if disruption to vaccination programmes was threatened. In a letter to Mr Cruickshank (Animal Health Group, MAFF) on 13 January 1989, Mr Scollen (MAFF Animal Health Division) cautioned against action on vaccines that may be judged to be disproportionate: ‘While there is potentially a need for radical – and expensive – action, it is, of course, quite possible that in the course of a few years we will be able to demonstrate the effectiveness of the action already taken to eliminate BSE. Extravagant action now to deal with a contingent risk could then seem to be wholly disproportionate’ (Scollen 1989: 1). Mr Scollen continued ‘[i]n my own view the issues involved centre on an assessment of the risks associated with maintaining or disrupting the supply of vaccines for human health purposes’ (Scollen 1989: 2). 37. The related concept ALARA (as low as reasonably achievable) originated in the atomic energy field. ALARP and ALARA are largely indistinguishable: ‘If there is a substantive difference between the intent of ALARA and ALARP, it’s difficult to establish’ (Manuele 2003: 283). 38. Cost ‘should contain factors relating to time, resource and trouble, not just a financial consideration’ (Maguire 2006: 73). 39. When the ALARP principle was used implicitly, policy decisions could be seen to conform to this principle even though no explicit reference had been made to ALARP during the decisionmaking process. For example, in relation to the two principal policy decisions which were introduced to address the possibility of BSE transmission to humans through food – compulsory slaughter and destruction of cattle with symptoms of BSE and the human SBO ban – Lord Phillips and his colleagues remarked ‘we consider that they constituted a proportionate response that satisfied the ALARP principle, albeit that the policy decisions did not result from the application of that principle’ (BSE Inquiry Report, Volume 1: 230).

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40. The following comments by Lord Phillips and his inquiry team indicate that they believed the ALARP principle was less than successfully implemented on certain occasions: ‘We believe that part of the [Southwood] Working Party’s problem was that they were in no position to reach an informed view of how the ALARP principle should apply’ (BSE Inquiry Report, Volume 1: 53); ‘No reasoned application of the ALARP principle was carried out by MAFF’ (BSE Inquiry Report, Volume 1: 123). 41. ‘If the residual risk for a task or operation is never zero, for what risk level does one strive? At best, we can say that the concept of designing and operating to attain risk levels as low as reasonably achievable or practicable should be applied to the situation being considered’ (Manuele 2003: 282).

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Index

A Aetiology, 12, 44–45 ALARP (as low as reasonably practicable), 208, 212–213, 220–221 Amyloid plaque, 5, 9–11, 15, 19, 50 Appeal to authority, 83, 170, 173–175, 187 See also Argument from authority Arguing to the wrong conclusion, 140, 151–156, 162 Argument analogical, 43, 75–76, 93–96, 98, 99–101, 108, 111, 120–121, 125, 135, 203, 208 See also Argument from analogy analysis, 54, 161 circular, 37, 58, 103–104, 106, 113 See also Question-begging argument deductive, 56, 67, 75, 115, 201, 207–208, 219 evaluation, 39, 53, 59, 84, 109 ignorance, 99–100, 102, 108–109, 118, 126, 128, 148–151, 157, 162, 169 See also Argument from ignorance inductive, 75, 114 reconstruction, 54, 90 Argument from analogy, 75, 92–94, 108, 110, 120–125, 141, 182–183 Argumentation, 32, 48, 64, 67, 76, 79, 81–82, 88, 90, 109, 112, 151–152, 156, 158, 162, 165, 171, 185, 187, 196, 219 Argument from authority, 168–175, 187 See also Appeal to authority Argument from ignorance, 28, 37, 58, 76–77, 84, 92, 97–103, 108, 112–113, 117, 125–128, 134, 140, 147–151, 162, 200, 203, 207–208 Argument against the person, 168, 176–189 See also Argumentum ad hominem

Argumentum ad hominem, 168, 176 abusive, 176, 179, 182, 189 circumstantial, 176, 179–182, 189 See also Argument against the person Artificial intelligence, 74, 76, 83 Astrocytosis, 5 B Belief, 39, 53, 57, 59, 81–82, 184–185 Biochemistry, 72 Blood plasma, 142–143, 160 product, 140, 142, 148–150, 157, 162 transfusion, 142, 214 Born after the ban (BAB), 119–120, 127, 140 Bovine spongiform encephalopathy (BSE), 1, 29, 32, 45, 54, 91, 168, 177 Brain, 1, 4–6, 8, 11, 13–17, 19, 21–26, 29, 31–32, 35, 42–43, 45–46, 50, 54–55, 72, 93–94, 96–97, 117, 125, 131, 135–137, 140, 160, 218 Burden of proof, 64, 66, 80–81, 84, 87, 92, 119, 123, 141, 143–144, 149, 157–158, 202, 205, 210–211, 213 C Cannibalism, 6, 30–31 Central nervous system (CNS), 9, 14, 19, 26, 29, 131, 159 Certainty, 25, 68–69, 82, 92, 206–208, 210–211, 219–220 Chronic wasting disease (CWD), 2, 19–21, 47, 54 Closed world assumption, 84 Cognition, 36, 39–40, 53, 78, 85 Cognitive authority, 172, 174–175, 184, 188 Context sensitivity, 65–66, 73–74, 87, 196–197, 203, 211

239

240

Index

Creutzfeldt-Jakob disease (CJD) familial, 3–4, 95 iatrogenic, 3–4, 214 sporadic, 3–4, 11, 29 variant, 3, 11, 90, 135, 151, 190, 193, 204 Critical thinking, 39, 52

Genetics, 5, 12, 30–31, 44, 54, 70–73, 85, 94, 122 Genotype, 31, 70–71, 73, 155, 163 Gerstmann-Sträussler syndrome (GSS), 2, 10–12, 50 Growth hormone, 3, 94, 137

D Decision making, 26, 33, 85, 95, 100, 102, 165, 182, 198–199, 202 Deduction, 27, 33, 56, 58, 69–70, 75, 80, 88, 113, 178, 185, 206–208, 219 Default, 83, 121 Defeasibility, 57, 61, 63–65, 74–76, 80, 83, 87, 118, 121, 123, 141, 147, 157, 196–197, 203, 208 Dialectic, 53, 60, 64–66, 79–81, 83–84, 88, 103, 113, 119, 123, 134, 141, 143–144, 146–147, 149–150, 157–158, 170, 177, 195, 202, 205–208, 211, 213, 219 Distal ileum, 75, 124, 140–141 Dose, 13, 15, 29, 120–121, 127, 129, 135, 146, 202 Dura mater, 3, 94, 137

H Hadlow, W., 3, 12–15, 17, 30–31 Hamblin, C., 53, 58, 78–79, 103 Hasty generalization, 77, 110 Histopathology, 21, 26, 48, 54, 72, 199 HIV/AIDS, 111, 134, 217–218 Host range, 71–72, 119, 121–122, 141, 146, 152–154, 156 Human specified bovine offal (SBO) ban, 72, 74–75, 90–91, 93–94, 119–120, 123–125, 127, 129, 140–141, 181, 201–202, 220

E Emerging infectious disease, 26, 28, 35, 37, 62, 74, 96, 104, 126, 133, 193, 198–199, 205, 214 Emotion, 165, 184–185 Epidemiology environmental, 41 social, 37, 41–42, 52 Epistemic closure, 77, 84, 99, 126 priority, 58–59, 73, 104, 205, 208 Epistemology, 33, 38–39, 53, 57–60, 80, 103, 113–114, 170, 196, 213, 216 Error, 40, 53, 57, 59, 65–66, 81–82, 85, 92, 118, 198, 204, 208 Expertise, 70, 90, 111, 146, 161, 168–175, 187–188, 193, 199, 202, 217 F Fatal familial insomnia, 29 Feline spongiform encephalopathy (FSE), 122, 126, 136, 151–156, 158, 163 Fore, 1, 5, 7–8, 12, 30–31, 74, 92 G Gajdusek, C., 5–9, 12, 29–31 Gambler’s fallacy, 110, 185 Gelatin(e), 129–132, 136–137

I Immunology, 18, 134 Incubation period, 4–5, 8–9, 12, 14–17, 24–25, 31, 54, 95, 98, 102, 112, 133, 135–136, 200, 202 Induction, 12, 27, 30, 69–70 Inference, 33, 38, 54, 56, 75, 79, 83–84, 98, 100–101, 112, 130, 150, 162, 174, 195, 206–207, 216 Influenza, 41, 54, 199, 216 Informal fallacy, 27–28, 39–40, 74, 76, 78, 88, 117, 134, 162, 165, 168, 173, 188, 196, 203, 207–208, 213 Inoculation intracerebral, 3–5, 9, 11, 13–16, 22, 29, 31, 120 intraperitoneal, 14 subcutaneous, 13 J Jurisprudence, 74 K Knowledge base, 1–2, 22–24, 37, 51, 72, 76, 84, 99–102, 104, 106–107, 109, 112, 126, 128, 151, 203–204, 207–208 gap, 22–28, 92, 203, 208 generation, 70, 92, 196, 203–204, 208 Kuru, 1–2, 5–12, 22, 29–31, 95 L Linguistics, 5, 69, 74, 82–83, 171 Listeria/listeriosis, 110, 189

Index

241

Logic deductive, 58–59, 79, 88, 207–208 formal, 58, 79 informal, 39, 74, 84, 193, 195–196, 216 Lymphoreticular system, 14, 31, 94

Proportionality, 210–211, 220 Prusiner, S., 2, 6, 8, 23, 29, 31, 96 Psychology, 53, 70, 81, 111–112, 165, 185 Public health science, 27, 42, 51, 68–69, 117, 194–196, 208–214

M Meat and bone meal (MBM), 24–25, 32, 41, 43, 47–49, 51, 55, 105–106, 110, 114, 122, 135, 180–181, 191 Mechanically recovered meat (MRM), 127, 136, 140 Media, 91, 101–102, 108, 110, 119, 141, 165–166, 172, 175, 179–180, 186, 189–190, 215 Modus ponens, 130, 162 Modus tollens, 100–101, 150, 162, 207 Molecular biology, 37, 48, 51, 72, 94, 96

Q Question-begging argument, 28, 88, 103–107, 109, 113, 117, 134, 137, 200–201, 208

N Neurology, 11, 173, 187 Neuronal loss, 5, 9 Neuropathology, 11–12, 72, 99, 134–135, 141, 187 Neurosurgery, 3 New Guinea, 1, 5–8, 12 Non-monotonicity, 83 O Optic nerve, 148–151 Oral medicine, 128–132, 136–137 P Pathogenesis, 14–15, 24, 26, 30, 72, 74–75, 90, 95, 105–106, 111, 114, 119, 122, 124–127, 137, 139–142, 146, 150, 159–160, 201–202, 217 Philosophy of science, 38–39, 162, 216, 218 Plausibility, 47–48, 51, 54–58, 72–73, 88, 113 Policy, 51, 69, 82, 89, 110–111, 159, 167–169, 186, 188–189, 192, 217–220 Pragma-dialectics, 83, 195 Precautionary principle, 81, 191–192, 208–212, 219–220 Presumption, 51, 57–85, 87–88, 93, 101–102, 108, 111, 114, 123, 141, 143–144, 147, 149–150, 157–158, 196–197, 200, 202, 204–205, 209–213, 218 Principle of charity, 90 Prion disease, 11, 29, 50, 131, 172 protein, 11, 15–16, 29, 32, 50, 96, 214

R Rationality, 27–28, 59, 77–78, 81, 87, 103, 110, 150–151, 157, 173, 189, 219 Reasoning analogical, 36, 44, 95–97, 108, 111, 120, 122–124, 133–134, 141, 157, 169, 182–183, 202 circular, 107, 109 deductive, 83, 134, 185, 207–208 defeasible, 83 inductive, 33, 67, 75, 117 plausible, 55, 67, 79 presumptive, 65, 74–76, 83, 92, 128, 204, 206–208 probabilistic, 185 Rendering, 24 Rescher, N., 52, 55–56, 60, 62–64, 66, 73, 79–83, 103, 111, 113–114, 213, 219 Risk analysis, 208–213 assessment, 36, 51, 82, 90, 92, 130, 133, 139, 141–143, 146–149, 153, 158, 165–166, 169, 177, 182–183, 200, 202, 212 communication, 215 management, 212 reduction, 212 Ruminant feed ban, 91, 110, 119, 127, 135, 182, 215, 218 S Salmonella, 91, 110, 119, 127, 135, 182, 215, 218 Scepticism, 69, 122 Scientific inquiry, 27, 32, 35, 37, 39, 43, 48, 51–52, 57–61, 63–67, 69–74, 78, 80–81, 87–88, 90, 92, 98, 104, 107, 109, 113, 117–118, 128, 132–133, 147, 158, 161, 166–167, 170, 173, 176–177, 184, 188, 196–208, 211, 219

242 Scrapie, 1–4, 12–17, 22–25, 29–33, 36–37, 43–51, 54–55, 57, 67, 72, 74–75, 90–101, 104–108, 111–112, 114, 119–128, 130, 132, 135–137, 139–144, 146–147, 149, 151–161, 169, 177, 179, 181–184, 188, 192, 199 Scrapie-associated fibril (SAF), 32, 43, 45–46, 50, 54–55, 96–97 Section 4 committee, 89, 94, 110, 128, 130, 132, 137 Severe acute respiratory syndrome (SARS), 41, 62, 111, 217 Sinc gene, 15–16 Social science, 196, 216 Soundness, 58, 88, 138 Southwood Working Party, 33, 99–100, 104, 110, 136–137, 166, 168, 172–173, 185, 188–189, 192, 199, 212, 221 Species barrier, 22, 25, 123, 159, 189 Speech act, 76, 83, 195 Spinal cord, 13, 31, 93, 127, 131, 136, 140, 160 Spleen, 13–16, 19, 31, 135, 138, 160 Spongiform Encephalopathy Advisory Committee (SEAC), 111–112, 119–129, 134–137, 140–163, 166, 168–169, 172, 186–188, 202, 206–207 Syllogism, 79–80 T Thymus, 14, 31, 93–94, 124 Tonsil, 14, 21, 31, 214 Transmissible mink encephalopathy (TME), 2, 13, 15, 17–19, 30, 32, 43, 47, 54, 95 Transmissible spongiform encephalopathy (TSE), 1–2, 5, 10, 12, 17, 19, 22–26, 29, 30, 32, 38, 43–49, 52, 54, 61, 64, 66, 68–70, 72, 75, 79–80, 84, 88, 90–92, 95, 97–100, 102, 104–109, 111, 114, 118, 126, 128, 133, 137, 139, 142–143, 145, 147, 154–156, 159–160, 163, 169, 171–174, 177, 184–185, 188–189,

Index 193, 196, 199–202, 204–205, 211, 215, 217, 219 Transmission experimental, 3, 54, 127, 154 horizontal, 19, 32 iatrogenic, 214 lateral, 13, 94–95 maternal, 13, 17, 70–71, 73, 94–95, 119 natural, 13, 90, 94, 102, 122, 126, 139, 141, 143, 154, 200–202 oral, 32, 47, 102, 104, 122, 130, 159, 202 parenteral, 22, 32 vertical, 17, 218 Tyrrell Committee, 104–106, 111, 114, 119, 125, 159, 168, 202, 217 U Uncertainty, 1–2, 22–23, 25–28, 33, 35–37, 39, 52, 54, 57, 59–60, 68–75, 78, 81–83, 87, 91–92, 95–96, 100, 102, 107–109, 117–118, 123, 125, 133–134, 157, 173, 185, 192–194, 196, 200–201, 205, 208, 210–215, 220 Underdetermination, 218 V Vaccination, 32, 136, 220 Vaccine, 13, 55, 94, 220 Vacuolation, 5, 14–15, 18–19, 26, 31, 43, 45 Validity, 54, 58, 85, 88, 106, 130, 141, 147, 206, 219 Veterinary science, 1, 173 Virology, 32, 72, 134–135, 137, 173 W Walton, D., 58, 62, 76, 109, 162 Woods, J., 40–41, 53, 58, 77, 84–85, 109, 111, 113, 170, 187 World Health Organization (WHO), 68–69, 199, 208, 216–217 Z Zigas, V., 5, 9, 29–30 Zoology, 32, 72, 173, 188 Zoonosis, 92–93, 110, 198