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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