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S248 2006 Congress of Epidemiology Abstracts 990 991 SILENCING OF SCIENCE: THE PHENOMENON AND ITS IMPACT ON PASSIVE SMOKING EPIDEMIOLOGY. *S B Ungar (Division of Social Science, University of Toronto at Scarborough, Ontario, Canada) NEW INFECTIOUS AGENTS. *S Weiss (UMDNJ, School of Public Health, Newark NJ 07107) While science is the main arbiter of societal truth, determining exactly what constitutes sound science is becoming a daunting task, as illustrated by the seemingly strange use of the courts to settle disputes. Openness to new data and ideas, controversy-and yes, error-are critical to sound science; efforts to mute the reporting or circulation of scientific claims undermine the enterprise. Here we outline several cases of silencing of science, with particular focus on the responses of scientific outsiders or ‘‘partisans’’ to the epidemiologic study by Drs. Enstrom and Kabat published in the May 17, 2003 British Medical Journal, which found that secondhand smoke was not as dangerous as conventionally believed. A related examination of media coverage suggests that the public consensus about the negative effects of passive smoke is so strong that it has become part of a regime of truth that cannot be intelligibly questioned. Whereas partisanship and closure subvert science, there is still the problem of established science (or insiders) trying to curb the ‘‘agenda science’’ promoted by tobacco, drug and oil companies. While this ‘‘agenda science’’ seems to impede scientific understanding, insider closure may be as reprehensible and problematic as that attempted by outsiders. Above all, it is important to avoid epistemic conceit here, since science is probably less central to the policy realm than is typically supposed. People demonstrate high levels of scientific ignorance, and passive smoking apparently acquired legs as an issue for reasons other than the intricacies of scientific debates. Modern molecular biology has been evolving rapidly. In this session, an innovative technique used to discover the causative agent of Kaposi’s sarcoma will be described by the discoverer. That epidemiologic puzzles remain more than a decade later highlight the complexities of modern cutting edge infectious disease (and chronic disease) epidemiology and innovative laboratory research. Techniques involving microbial nucleic acid sequences are demonstrating that the known infectious disease universe – which has largely been defined by our ability to culture and isolate in the post-Koch era - are but a small portion of the total microbial universe. What roles do these novel organisms play? It is possible that some may have pivotal roles, even if present in low quantities. While Koch’s postulates are becoming ever less meaningful in the modern era, an appropriate replacement to them remains in need of development and critical scrutiny. 992 993 KS, KSHV AND THE MOLECULAR CASE FOR CAUSATION. *P S Moore (University of Pittsburgh, Pittsburgh, PA) MOLECULAR DETECTION OF NOVEL PATHOGENS: NEW TOOLS FOR UNDERSTANDING EPIDEMIOLOGY AND PATHOGENESIS. *D N Fredricks Kaposi’s sarcoma-associated herpesvirus (KSHV) is the most recently described human tumor virus. Although a wealth of evidence now shows that this virus is the infectious trigger for Kaposi’s sarcoma (KS) and other related tumors, discovery of this virus stirred considerable controversy that lasts until today that has both stimulated and retarded research on this virus. This talk will describe the initial discovery of KSHV and the difficulties in determining its relationship to KS using traditional epidemiologic criteria of causation. This case study demonstrates the importance of using molecular biology together with epidemiology to gain a better understanding of human disease. It illustrates the need to rethink basic epidemiologic principles in light of advances in molecular biology. The use of microbial nucleic acid sequences for the detection and identification of human pathogens has led to critical new insights into the pathogenesis of poorly understood human diseases such as bacterial vaginosis and rhinosporidiosis. These diseases will be discussed to show how new hypotheses to explain epidemiological characteristics can be generated from molecular phylogenetic analyses of the bacterial or protistan parasites implicated. We will review sequence-based methods of pathogen discovery and identification and will demonstrate how these methods have been applied to study cultivation-resistant microbes. We will explore the concept of disease by microbial community and will highlight the challenges to proving disease causation by uncultivated microbes or microbial assemblages. * ¼ Presenter; S ¼ The work was completed while the presenter was a student Am J Epidemiol 2006;163(Suppl):S1–S258