DOCSLIB.ORG

Redalyc.Causality and the Interpretation of Epidemiologic Evidence

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Redalyc.Causality and the Interpretation of Epidemiologic Evidence Ciência & Saúde Coletiva ISSN: 1413-8123 [email protected] Associação Brasileira de Pós-Graduação em Saúde Coletiva Brasil Kundi, Michael Causality and the interpretation of epidemiologic evidence Ciência & Saúde Coletiva, vol. 12, núm. 2, março-abril, 2007, pp. 419-128 Associação Brasileira de Pós-Graduação em Saúde Coletiva Rio de Janeiro, Brasil Available in: http://www.redalyc.org/articulo.oa?id=63012215 How to cite Complete issue Scientific Information System More information about this article Network of Scientific Journals from Latin America, the Caribbean, Spain and Portugal Journal's homepage in redalyc.org Non-profit academic project, developed under the open access initiative 419 REVISÃO REVISION REVISÃO Causality and the interpretation of epidemiologic evidence * Causalidade e interpretação de evidência epidemiológica Michael Kundi 1 Abstract There is an ongoing debate regarding Resumo Existe um debate atual sobre como e how and when an agent’s or determinant’s impact quando o impacto provocado por agente ou deter- can be interpreted as causation with respect to minante pode ser interpretado como causa de uma some target disease. The criteria of causation, orig- doença. O chamado “critério de causação”, origi- inating from the seminal work of Sir Austin Brad- nário do trabalho seminal de Austin Bradford Hill ford Hill and Mervyn Susser, are often schemati- e Mervyn Susser, frequentemente é aplicado de cally applied and, furthermore, there is a tenden- forma esquemática e há uma tendência a inter- cy to misinterpret the lack of evidence for causa- pretar erradamente a falta de evidência de causas tion as evidence for lack of a causal relation. There como evidência de falta de relação causal. Não are no criteria for the assessment of evidence con- existem critérios para avaliação de evidência no cerning an agent’s or determinant’s propensity to que diz respeito à propensão de um agente ou de- cause a disease, nor are there criteria to dismiss terminante causar uma doença, nem para descar- the notion of causation. In this commentary, I pro- tar a noção de causação. Neste comentário, pro- pose a dialogue approach for the assessment of an ponho uma aproximação dialógica para a avalia- * This article was originally agent or determinant. Starting from epidemiologic ção de um agente ou determinante. Começando published by the journal evidence, four issues need to be addressed: tempo- com evidência epidemiológica, quatro itens neces- Environmental Health ral relation, association, environmental equiva- sitam ser abordados: relação temporal, associação, Perspectives 114:969–974 (2006). doi:10.1289/ehp. lence, and population equivalence. If there are no equivalência ambiental e equivalência populaci- 8297 available via http:// valid counterarguments, a factor is attributed the onal. Se não há contra-argumentos, a um fator é dx.doi.org/ [Online 27 potential of disease causation. More often, there atribuído o potencial de causação. Na maioria dos March 2006] and is part of the scientific collaboration will be insufficient evidence from epidemiologic casos, há insuficiente evidência a partir de estu- between Rev C S Col and studies. In these cases, other evidence can be used dos epidemiológicos. Nesses casos, outra evidên- EHP . The author declares he that increases or decreases confidence in a factor cia que aumenta ou diminui a confiança num fa- has no competing financial interests. Received 8 May being causally related to a disease. Even though tor relacionado à doença pode ser usada. No en- 2005; accepted 27 March every verdict of causation is provisional, action tanto, qualquer veredito de causação é provisório 2006. must not be postponed if our present knowledge e uma ação não pode ser adiada sob pretexto de 1 Institute of Environmental Health, Center for Public appears to demand immediate measures for health encontrar melhor evidência, quando nosso estado Health, Medical University protection. de conhecimento mostrar que é preciso tomar me- of Vienna. Kinderspitalgasse Key words Causality, Epidemiology didas imediatas para proteção da saúde. 15, 1095. Vienna Austria. michael.kundi@meduniwien. Palavras-chave Causalidade, Epidemiologia ac.at. 420 Kundi, M. Kundi, The principle of causality, so deeply embedded Defining cause and causality in humans’ minds that it has been thought of as immediately evident, is the very foundation not The most advanced sciences, physics and chem- only of all three monotheistic world religions but istry, have altogether abandoned the concepts of also of the first staggering steps of science [de ni- cause and effect. These terms are no longer used hilo nihil (nothing can be born of nothing) 1. in these sciences. Newton had already replaced Hume 2 was the first to note that there is no logi- cause and effect with functional relationships; cal foundation in the assumption that if in the however, to make himself understood to his con- past every event has had a cause, this will also be temporaries, in the third book of his Principia the case in the future and, furthermore, that what (1726) he spoke about causes (especially to de- we perceive in daily life as well as in science is only fend his position of what can be called a minimal a sequence of events but not cause and effect. Al- sufficient cause). Nevertheless, “cause and effect” though Hume deeply believed in the truth of the remained terms used in physics, somewhat anach- principle of causality, he pointed to the role of ronistically, especially for scholarly purposes un- the human mind in constructing reality and the til the end of the 19th century. Mach 7, alluding to futility of scientifically proving its validity. Kant 3, Hume, stressed the psychological nature of these as he became acquainted with Hume’s thoughts, concepts and pointed out that “in nature there is was awakened from his metaphysical slumber, or no cause and no effect” and that these concepts so he kept saying, and set out to solve the prob- are results of an economical processing of per- lem of how Newton’s physics, which he thought ceptions by the human mind. of as eternally true, could be possible in the face The notion that diseases have natural causes of Hume’s demonstration that it cannot be in- and are not God’s punishments or trials or curses ferred from experience. of malicious beings or results of supernatural The Copernican turn in Kant’s reasoning was forces has not even fully penetrated Western cul- to imply the principle of causality from the as- ture, let alone become the prevailing view world- sumption that it is among the conditions of ev- wide. Despite its metaphysical character, the eti- ery experience. Indeed, if A is a necessary condi- ologic axiom that every disease has an endoge- tion of B, then B is a suffi- cient condition of A. nous and/or exogenous cause was extremely suc- Hence, if for every experience we make (B) it is a cessful and is still the foundation of scientific precondition that everything has a cause (A), then medicine. However, what actually “causes” a dis- from the fact that we do have experiences (B), it ease has from the very beginning been a matter follows that everything has a cause (A). Howev- of controversy. Indeed, a single clinical phenom- er, to make this a logically coherent theory, Kant enon can have quite different “causes,” and one had to sacrifice “objective knowledge”—that is, “cause” can have quite different clinical conse- the Ding an sich (the “thing in itself”) remains quences (Table 1). These facts are not consistent incomprehensible for the human mind. For more with the original concept of causation, which than 100 years, the philosophy of science circled states that a cause is an object that is followed by around either the assumptions or the (untoward) another, and where all objects similar to the first consequences of Kant’s solution. When in 1905 are followed by objects similar to the second 2. Not Einstein published his special theory of relativity even for infectious diseases does this (strong) con- and his theory of the interaction of electrons and cept of causation hold. (Hume gave several “def- light 4,5 , the very foundation of Kant’s philosophy initions” of a cause, among these also what has was called into question: the universal truth of been called the counterfactual approach, dis- Newton’s mechanics 6 and the validity of the de- cussed below.) terministic concept. How, then, should cause and causation be These considerations not only profoundly defined? In a review of definitions of “causation” changed modern science but also resulted in an in epidemiologic literature, Parascandola and open-ended controversy within epistemology. Weed 8 delineated five categories. However, all of And last but not least, epidemiology and the in- these definitions (summarized in Table 1) have terpretation of epidemiologic evidence are deep- severe deficits. Not totally unexpected, the defi- ly connected to these fundamental considerations nitions found in the literature are insufficient to about the nature of human knowledge. provide a basis for the notion of disease causa- 421 Ciência & Saúde Coletiva, 12(2):419-428, 2007 12(2):419-428, Coletiva, Saúde & Ciência Table 1 Definitions of causation from the epidemiologic literature (modified from Parascandola and Weed 2001). Definition Main criticism A cause is something that produces or creates an effect. Tautological because “ production” and “creation” are synonyms of “causation” A cause is a condition without which the affect cannot Only very few diseases could then have a cause a occur. A cause is a condition with which the affect must occur. Again, only few diseases could then have a cause b A cause is made up of several components, no single Introduces unnecessary complexity in cases of simple one of which is sufficient of its own, which taken dose response and in cases of interaction between together must lead to the effect.
Load more

Recommended publications
  • Judging the Evidence 2018 Contents World Cancer Research Fund Network 3 1
    Judging the evidence 2018 Contents World Cancer Research Fund Network 3 1. Introduction 5 2. Randomised controlled trials 6 3. Epidemiological evidence 6 3.1 Cohort studies 9 3.2 Case-control studies 10 3.3 Other study designs 10 4. Meta-analysis 11 5. Experimental evidence 16 5.1 Human studies 16 5.2 Live animal models 16 5.3 In vitro studies 17 6. Methods of assessment 17 6.1 Foods, drinks and nutrients 17 6.2 Nutrition status 18 6.3 Physical activity 19 6.4 Cancer outcomes 20 7. Evidence collated for the Continuous Update Project 21 8. The grading criteria 22 8.1 Context for using the criteria 26 8.2 Food-based approach 27 8.3 CUP matrices 28 8.4 Levels and types of judgement 29 9. Conclusions 29 Acknowledgements 30 Abbreviations 34 Glossary 35 References 39 Our Cancer Prevention Recommendations 42 WORLD CANCER RESEARCH FUND NETWORK Our Vision We want to live in a world where no one develops a preventable cancer. Our Mission We champion the latest and most authoritative scientific research from around the world on cancer prevention and survival through diet, weight and physical activity, so that we can help people make informed choices to reduce their cancer risk. As a network, we influence policy at the highest level and are trusted advisors to governments and to other official bodies from around the world. Our Network World Cancer Research Fund International is a not-for-profit organisation that leads and unifies a network of cancer charities with a global reach, dedicated to the prevention of cancer through diet, weight and physical activity.
    [Show full text]
  • Could Low Grade Bacterial Infection Contribute to Low Back Pain? a Systematic Review
    Urquhart et al. BMC Medicine (2015) 13:13 DOI 10.1186/s12916-015-0267-x RESEARCH ARTICLE Open Access Could low grade bacterial infection contribute to low back pain? A systematic review Donna M Urquhart1*, Yiliang Zheng1, Allen C Cheng1, Jeffrey V Rosenfeld2,3, Patrick Chan2,3, Susan Liew2,4, Sultana Monira Hussain1 and Flavia M Cicuttini1 Abstract Background: Recently, there has been both immense interest and controversy regarding a randomised, controlled trial which showed antibiotics to be effective in the treatment of chronic low back pain (disc herniation with Modic Type 1 change). While this research has the potential to result in a paradigm shift in the treatment of low back pain, several questions remain unanswered. This systematic review aims to address these questions by examining the role of bacteria in low back pain and the relationship between bacteria and Modic change. Methods: We conducted electronic searches of MEDLINE and EMBASE and included studies that examined the relationship between bacteria and back pain or Modic change. Studies were rated based on their methodological quality, a best-evidence synthesis was used to summarise the results, and Bradford Hill’s criteria were used to assess the evidence for causation. Results: Eleven studies were identified. The median (range) age and percentage of female participants was 44.7 (41–46.4) years and 41.5% (27–59%), respectively, and in 7 of the 11 studies participants were diagnosed with disc herniation. Nine studies examined the presence of bacteria in spinal disc material and all identified bacteria, with the pooled estimate of the proportion with positive samples being 34%.
    [Show full text]
  • Building a Better Mousetrap: Patenting Biotechnology in the European
    THE BRADFORD HILL CRITERIA: THE FORGOTTEN PREDICATE Dr. Frank C. Woodside, III* & Allison G. Davis** Table of Contents I. INTRODUCTION ....................................................................... 104 II. EPIDEMIOLOGY, DAUBERT, AND ESTABLISHING ASSOCIATION .................................................................... 107 A. Background on the Field of Epidemiology ...................... 107 B. Establishing Association .................................................. 108 C. Daubert and Its Progeny .................................................. 111 III. CAUSATION: THE NINE CRITERIA .................................... 112 A. Strength of Association ................................................... 113 B. Consistency ...................................................................... 114 C. Specificity of the Association .......................................... 116 * Frank C. Woodside, III is of counsel to the law firm of Dinsmore & Shohl. Dr. Woodside is a nationally-known trial lawyer representing manufacturers of pharmaceutical and medical devices, chemicals and flavorings, as well as producers of consumer products. Over a period of more than 40 years, he has tried 80-plus cases to verdict or judgment, serving as primary trial counsel in medical malpractice, product liability, and mass tort cases. Dr. Woodside’s clients include Fortune 500 companies, health care providers, and hospitals. His background to practice Medicine and Surgery for nearly 40 years affords him added knowledge and insight he uses to his
    [Show full text]
  • Does Sufficient Evidence Exist to Support a Causal Association Between Vitamin D Status and Cardiovascular Disease Risk?
    Nutrients 2014, 6, 3403-3430; doi:10.3390/nu6093403 OPEN ACCESS nutrients ISSN 2072-6643 www.mdpi.com/journal/nutrients Review Does Sufficient Evidence Exist to Support a Causal Association between Vitamin D Status and Cardiovascular Disease Risk? An Assessment Using Hill’s Criteria for Causality Patricia G. Weyland 1,*, William B. Grant 2 and Jill Howie-Esquivel 1 1 Department of Physiological Nursing, School of Nursing, University of California, San Francisco (UCSF), #2 Koret Way Box 0610, San Francisco, CA 94143, USA; E-Mail: [email protected] 2 Sunlight, Nutrition, and Health Research Center, P.O. Box 641603, San Francisco, CA 94164-1603, USA; E-Mail: [email protected] * Author to whom correspondence should be addressed; E-Mail: [email protected]; Tel.: +1-831-420-7324. Received: 22 May 2014; in revised form: 31 July 2014 / Accepted: 18 August 2014 / Published: 2 September 2014 Abstract: Serum 25-hydroxyvitamin D (25(OH)D) levels have been found to be inversely associated with both prevalent and incident cardiovascular disease (CVD) risk factors; dyslipidemia, hypertension and diabetes mellitus. This review looks for evidence of a causal association between low 25(OH)D levels and increased CVD risk. We evaluated journal articles in light of Hill’s criteria for causality in a biological system. The results of our assessment are as follows. Strength of association: many randomized controlled trials (RCTs), prospective and cross-sectional studies found statistically significant inverse associations between 25(OH)D levels and CVD risk factors. Consistency of observed association: most studies found statistically significant inverse associations between 25(OH)D levels and CVD risk factors in various populations, locations and circumstances.
    [Show full text]
  • Bradford Hill Criteria for Causal Inference Based on a Presentation at the 2015 ANZEA Conference
    Bradford Hill Criteria for Causal Inference Based on a presentation at the 2015 ANZEA Conference Julian​ King Director,​ Julian King & Associates – a member of the Kinnect Group www.julianking.co.nz​ | www.kinnect.co.nz 2015 We think we’re good at determining causality, but we suck at it One​ of the great At​ one level, this is an Unfortunately,​ though, the challenges in evaluation is everyday, common sense way we are wired does not determining whether the task. As a species we’ve predispose us to logical results we’re seeing are been making judgments thinking. We are inclined because of the program about causation for a to be led astray by all sorts we’re evaluating, some million years or so. of biases and heuristics. other influences out there in the big world, or random chance. The​ Kinnect Group www.kinnect.co.nz 2 Along came logic Eventually,​ after a very long time, we evolved into philosophers who invented formal logic. Thanks to scientific method, our species has recently triumphed to the extent that we now have cars that drive themselves and flying drones that deliver pizza (don’t confuse this with progress – we still suck at ethics but that’s a story for another day). 3 But we’re still not great at causation Over​ time, the rocket But​ deep down we’re still Such​ a rigid view is not science for dealing with biased, heuristical beings much use in the real causation has become and not very good at world, where there are all more sophisticated – a thinking things through.
    [Show full text]
  • 9. Causal Inference*
    9. Causal inference* The desire to act on the results of epidemiologic studies frequently encounters vexing difficulties in obtaining definitive guides for action. Weighing epidemiologic evidence in forming judgments about causation. "The world is richer in associations than meanings, and it is the part of wisdom to differentiate the two." — John Barth, novelist. "Who knows, asked Robert Browning, but the world may end tonight? True, but on available evidence most of us make ready to commute on the 8.30 next day." — A. B. Hill Historical perspective Our understanding of causation is so much a part of our daily lives that it is easy to forget that the nature of causation is a central topic in the philosophy of science and that in particular, concepts of disease causation have changed dramatically over time. In our research and clinical practice, we largely act with confidence that 21st century science has liberated us from the misconceptions of the past, and that the truths of today will lead us surely to the truths of tomorrow. However, it is a useful corrective to observe that we are not the first generation to have thought this way. In the 1950s, medical and other scientists had achieved such progress that, according to Dubos (1965:163), most clinicians, public health officers, epidemiologists, and microbiologists could proclaim that the conquest of infectious diseases had been achieved. Deans and faculties began the practice of appointing, as chairs of medical microbiology, biochemists and geneticists who were not interested in the mechanisms of infectious processes. As infectious disease epidemiology continues to surge in popularity, we can only shake our heads in disbelief at the shortsightedness of medical and public health institutions in dismantling their capabilities to study and control infectious diseases, whose epidemics have repeatedly decimated populations and even changed the course of history.
    [Show full text]
  • Epidemiological Causation Criteria
    Slide 1 © 2003 By Default! EpidemiologicalEpidemiological CausationCausation CriteriaCriteria James R. Coughlin, Ph.D. Coughlin & Associates Laguna Niguel, California [email protected] www.jrcoughlin-associates.com Meat Industry Research Conference Chicago, IL October 23, 2007 A Free sample background from www.awesomebackgrounds.com Slide 2 © 2003 By Default! DiscussionDiscussion TopicsTopics 1. Types of epidemiologic studies 2. Epidemiologic science and the media 3. Bradford Hill’s “Causation Criteria” 4. Statistical considerations 5.5. QuestionsQuestions toto askask whenwhen reviewingreviewing anan epidemiologicepidemiologic studystudy A Free sample background from www.awesomebackgrounds.com Slide 3 © 2003 By Default! Epidemiology Defined • Epi (upon) = demos (people) + ology (study of) • Historical - the study of epidemics of infectious disease • Modern - the study of the distribution and determinants of health and disease frequency in human populations • Epidemiology looks for patterns of disease (time, place, personal characteristics) A Free sample background from www.awesomebackgrounds.com Slide 4 © 2003 By Default! A Free sample background from www.awesomebackgrounds.com Slide 5 © 2003 By Default! A Free sample background from www.awesomebackgrounds.com Slide 6 © 2003 By Default! A Free sample background from www.awesomebackgrounds.com Slide 7 © 2003 By Default! A Free sample background from www.awesomebackgrounds.com Slide 8 © 2003 By Default! A Free sample background from www.awesomebackgrounds.com Slide 9 © 2003 By Default! Epidemiologic Science and the Media • Dramatically increased interest in health over the past decade • What we eat…or don’t eat…is always being linked to various diseases, especially obesity and cancer • Anxiety-provoking media headlines – • “Carcinogen-of-the-month” being the most scary to consumers • Dietary epi studies always seem to be contradicting each other • Lots of nutrition nonsense and “food faddism” out there • U.S.
    [Show full text]
  • Sedentary Behaviour and Adiposity in Youth: a Systematic Review of Reviews and Analysis of Causality Stuart J.H
    Biddle et al. International Journal of Behavioral Nutrition and Physical Activity (2017) 14:43 DOI 10.1186/s12966-017-0497-8 REVIEW Open Access Sedentary behaviour and adiposity in youth: a systematic review of reviews and analysis of causality Stuart J.H. Biddle1,2*, Enrique García Bengoechea1,3 and Glen Wiesner1 Abstract Background: Sedentary behaviour (sitting time) has becoming a very popular topic for research and translation since early studies on TV viewing in children in the 1980s. The most studied area for sedentary behaviour health outcomes has been adiposity in young people. However, the literature is replete with inconsistencies. Methods: We conducted a systematic review of systematic reviews and meta-analyses to provide a comprehensive analysis of evidence and state-of-the-art synthesis on whether sedentary behaviours are associated with adiposity in young people, and to what extent any association can be considered ‘causal’. Searches yielded 29 systematic reviews of over 450 separate papers. We analysed results by observational (cross-sectional and longitudinal) and intervention designs. Results: Small associations were reported for screen time and adiposity from cross-sectional evidence, but associations were less consistent from longitudinal studies. Studies using objective accelerometer measures of sedentary behaviour yielded null associations. Most studies assessed BMI/BMI-z. Interventions to reduce sedentary behaviour produced modest effects for weight status and adiposity. Accounting for effects from sedentary behaviour reduction alone is difficult as many interventions included additional changes in behaviour, such as physical activity and dietary intake. Analysis of causality guided by the classic Bradford Hill criteria concluded that there is no evidence for a causal association between sedentary behaviour and adiposity in youth, although a small dose-response association exists.
    [Show full text]
  • Terron Canedo, Nuria (2017) Mirnas in Equine Sarcoids: Identification and Profiling of Mirnas in Equine Fibroblasts and BPV-1 Transformed Equine Fibroblasts
    Terron Canedo, Nuria (2017) miRNAs in equine sarcoids: Identification and profiling of miRNAs in equine fibroblasts and BPV-1 transformed equine fibroblasts. PhD thesis. https://theses.gla.ac.uk/8130/ Copyright and moral rights for this work are retained by the author A copy can be downloaded for personal non-commercial research or study, without prior permission or charge This work cannot be reproduced or quoted extensively from without first obtaining permission in writing from the author The content must not be changed in any way or sold commercially in any format or medium without the formal permission of the author When referring to this work, full bibliographic details including the author, title, awarding institution and date of the thesis must be given Enlighten: Theses https://theses.gla.ac.uk/ [email protected] Title Page miRNAs in equine sarcoids: Identification and profiling of miRNAs in equine fibroblasts and BPV- 1 transformed equine fibroblasts Dr Nuria Terrón Canedo September 2016 This thesis is submitted to the University of Glasgow in accordance with the requirements for the degree of Doctor in Philosophy in the School of Veterinary Medicine. © Nuria Terrón Canedo Author’s declaration: I declare that the work carried out in this thesis is original and it was carried out by either myself or with the appropriate acknowledgements. Exceptions to this have been the miRCURY LNA™ microRNA Array 7th Gen (performed by an external company, Exiqon A/S, Vedbeck, Denmark), high throughput sequencing (performed by Miss Julie Galbraith at Glasgow Polyomics, University of Glasgow) and several parts of the bioinformatic analysis such as set-up of the miRDeep 2.0.
    [Show full text]
  • A Weight of Evidence Approach to Causal Inference
    Journal of Clinical Epidemiology 62 (2009) 270e277 A weight of evidence approach to causal inference Gerard Swaena,*, Ludovic van Amelsvoortb aEpidemiology Department, the Dow Chemical Company, The Netherlands bEpidemiology Department, School for Public health and Primary Care (CAPHRI), Maastricht University, The Netherlands Accepted 24 June 2008 Abstract Objective: The Bradford Hill criteria are the best available criteria for causal inference. However, there is no information on how the criteria should be weighed and they cannot be combined into one probability estimate for causality. Our objective is to provide an empirical basis for weighing the Bradford Hill criteria and to develop a transparent method to estimate the probability for causality. Study Design and Setting: All 159 agents classified by International Agency for Research of Cancer as category 1 or 2A carcinogens were evaluated by applying the nine Bradford Hill criteria. Discriminant analysis was used to estimate the weights for each of the nine Bradford Hill criteria. Results: The discriminant analysis yielded weights for the nine causality criteria. These weights were used to combine the nine criteria into one overall assessment of the probability that an association is causal. The criteria strength, consistency of the association and exper- imental evidence were the three criteria with the largest impact. The model correctly predicted 130 of the 159 (81.8%) agents. Conclusion: The proposed approach enables using the Bradford Hill criteria in a quantitative manner resulting in a probability estimate of the probability that an association is causal. Ó 2008 Published by Elsevier Inc. Keywords: Causal inference; Bradford Hill criteria; Epidemiology; Risk assessment; Methodology; Epistemology 1.
    [Show full text]
  • Sudden Infant Death Syndrome: the Bradford Hill Criteria and the Evaluation of the Thyroxine Deficiency Hypothesis Harold D
    Sudden Infant Death Syndrome: The Bradford Hill Criteria and the Evaluation of the Thyroxine Deficiency Hypothesis Harold D. Foster, B.Sc, Ph.D.1 Abstract less likely to occur in industrial states, but was In the United States, SID Sis approximately found most often in those states with soils that twice as common in infants in the Pacific and contained elevated levels of selenium, calcium, Mountain Regions as in the Atlantic States. These strontium and sodium. In contrast, states with spatial differences appear unlikely to be due to soils that were very high in mercury, the selenium chance and their analysis ought to provide antagonist, had depressed SIDS mortality rates. insights into the etiology of this syndrome. A data Stepwise multiple regression was then conducted bank was developed, therefore, from published for each year and for the entire five-year period government and academic sources that contained using those data that had correlated with SIDS 132 incidence and/or prevalence and/or mortality mortality, either negatively or positively at the p patterns for 84 disorders and diseases, including < 0.001 level. In all six regressions, male recruit SIDS mortality for each of the years 1983 to 1987 goiter was the first independent variable to enter and for the period as a whole. This bank also the initial equation; where it could explain contained information on the spatial distribution between 57.4 percent and 42.2 percent of the of 221 environmental variables, including a wide SIDS variance. range of climatic and geo chemical data and On the basis of these analyses and a review of information on air and water pollutants and a the literature, it is suggested that the fundamental variety of industrial, commercial and agricultural cause of SIDS may be a maternal iodine activities.
    [Show full text]
  • The Environment and Disease: Association Or Causation?
    Observational Studies 6 (2020) 1-9 Submitted 1965; Published reprinted, 1/20 The environment and disease: association or causation? Sir Austin Bradford Hill Editor's Note: Sir Austin Bradford Hill was Professor of Medical Statistics, University of London, United Kingdom. This article was originally published in the Proceedings of the Royal Society of Medicine, May 1965, 58, 295-300. This paper is reprinted with permission of the copyright holder, Sage Publications. New comments by the following researchers follow: Peter Armitage; Mike Baiocchi; Samantha Kleinberg; James O'Malley; Chris Phillips and Joel Greenhouse; Kenneth Rothman; Herb Smith; Tyler VanderWeele; Noel Weiss; and William Yeaton. Among the objects of this newly founded Section of Occupational Medicine are: first, `to provide a means, not readily afforded elsewhere, whereby physicians and surgeons with a special knowledge of the relationship between sickness and injury and conditions of work may discuss their problems, not only with each other, but also with colleagues in other fields, by holding joint meetings with other Sections of the Society'; and second, `to make available information about the physical, chemical and psychological hazards of occupation, and in particular about those that are rare or not easily recognized'. At this first meeting of the Section and before, with however laudable intentions, we set about instructing our colleagues in other fields, it will be proper to consider a problem fundamental to our own. How in the first place do we detect these relationships between sickness, injury and conditions of work? How do we determine what are physical, chemical and psychological hazards of occupation, and in particular those that are rare and not easily recognised? There are, of course, instances in which we can reasonably answer these questions from the general body of medical knowledge.
    [Show full text]