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Causality and the Interpretation of Epidemiologic Evidence
There is an ongoing debate regarding how and when an agent’s or determinant’s impact can be interpreted as causation with respect to some target disease. The so-called criteria of causation, originating from the seminal work of Sir Austin Bradford Hill and Mervyn Susser, are often schematically appl...
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Formato: | Texto |
Lenguaje: | English |
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National Institute of Environmental Health Sciences
2006
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1513293/ https://www.ncbi.nlm.nih.gov/pubmed/16835045 http://dx.doi.org/10.1289/ehp.8297 |
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author | Kundi, Michael |
author_facet | Kundi, Michael |
author_sort | Kundi, Michael |
collection | PubMed |
description | There is an ongoing debate regarding how and when an agent’s or determinant’s impact can be interpreted as causation with respect to some target disease. The so-called criteria of causation, originating from the seminal work of Sir Austin Bradford Hill and Mervyn Susser, are often schematically applied disregarding the fact that they were meant neither as criteria nor as a checklist for attributing to a hazard the potential of disease causation. Furthermore, there is a tendency to misinterpret the lack of evidence for causation as evidence for lack of a causal relation. There are no criteria in the strict sense for the assessment of evidence concerning an agent’s or determinant’s propensity to cause a disease, nor are there criteria to dismiss the notion of causation. Rather, there is a discursive process of conjecture and refutation. In this commentary, I propose a dialogue approach for the assessment of an agent or determinant. Starting from epidemiologic evidence, four issues need to be addressed: temporal relation, association, environmental equivalence, and population equivalence. If there are no valid counterarguments, a factor is attributed the potential of disease causation. More often than not, there will be insufficient evidence from epidemiologic studies. In these cases, other evidence can be used instead that increases or decreases confidence in a factor being causally related to a disease. Even though every verdict of causation is provisional, action must not be postponed until better evidence is available if our present knowledge appears to demand immediate measures for health protection. |
format | Text |
id | pubmed-1513293 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2006 |
publisher | National Institute of Environmental Health Sciences |
record_format | MEDLINE/PubMed |
spelling | pubmed-15132932006-07-26 Causality and the Interpretation of Epidemiologic Evidence Kundi, Michael Environ Health Perspect Commentaries & Reviews There is an ongoing debate regarding how and when an agent’s or determinant’s impact can be interpreted as causation with respect to some target disease. The so-called criteria of causation, originating from the seminal work of Sir Austin Bradford Hill and Mervyn Susser, are often schematically applied disregarding the fact that they were meant neither as criteria nor as a checklist for attributing to a hazard the potential of disease causation. Furthermore, there is a tendency to misinterpret the lack of evidence for causation as evidence for lack of a causal relation. There are no criteria in the strict sense for the assessment of evidence concerning an agent’s or determinant’s propensity to cause a disease, nor are there criteria to dismiss the notion of causation. Rather, there is a discursive process of conjecture and refutation. In this commentary, I propose a dialogue approach for the assessment of an agent or determinant. Starting from epidemiologic evidence, four issues need to be addressed: temporal relation, association, environmental equivalence, and population equivalence. If there are no valid counterarguments, a factor is attributed the potential of disease causation. More often than not, there will be insufficient evidence from epidemiologic studies. In these cases, other evidence can be used instead that increases or decreases confidence in a factor being causally related to a disease. Even though every verdict of causation is provisional, action must not be postponed until better evidence is available if our present knowledge appears to demand immediate measures for health protection. National Institute of Environmental Health Sciences 2006-07 2006-03-27 /pmc/articles/PMC1513293/ /pubmed/16835045 http://dx.doi.org/10.1289/ehp.8297 Text en http://creativecommons.org/publicdomain/mark/1.0/ Publication of EHP lies in the public domain and is therefore without copyright. All text from EHP may be reprinted freely. Use of materials published in EHP should be acknowledged (for example, ?Reproduced with permission from Environmental Health Perspectives?); pertinent reference information should be provided for the article from which the material was reproduced. Articles from EHP, especially the News section, may contain photographs or illustrations copyrighted by other commercial organizations or individuals that may not be used without obtaining prior approval from the holder of the copyright. |
spellingShingle | Commentaries & Reviews Kundi, Michael Causality and the Interpretation of Epidemiologic Evidence |
title | Causality and the Interpretation of Epidemiologic Evidence |
title_full | Causality and the Interpretation of Epidemiologic Evidence |
title_fullStr | Causality and the Interpretation of Epidemiologic Evidence |
title_full_unstemmed | Causality and the Interpretation of Epidemiologic Evidence |
title_short | Causality and the Interpretation of Epidemiologic Evidence |
title_sort | causality and the interpretation of epidemiologic evidence |
topic | Commentaries & Reviews |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1513293/ https://www.ncbi.nlm.nih.gov/pubmed/16835045 http://dx.doi.org/10.1289/ehp.8297 |
work_keys_str_mv | AT kundimichael causalityandtheinterpretationofepidemiologicevidence |