(7.30am to 8:30am)
There are 9 early morning session. Three (JM Anto; A Wilcox and J Schroeder; K Katsouyanni, J Schwartz and HR Guo) are organised by the ISEE Student and New Researcher Network Committee. Three refer to the evaluation of low level population exposures in environmental epidemiology and to the precautionary principle (D Savitz, Y-C Hong, P Grandjean). Three are on research methods (I Hertz-Picciotto, N Pearce, B Ritz).
Wednesday 14, September, 2011
Prof. Josep-Maria Antó, Centre for Research in Environmental Epidemiology, Barcelona, Spain.
Classics in environmental epidemiology: the Barcelona soy bean outbreak
(organised by the ISEE Student and New Researcher Network Committee)
Perhaps you've heard about the soybean asthma epidemics in Barcelona and how the causes of the epidemics were identified? It is a story of how epidemiological research may sometimes become a thriller! Move back to the 1980s, Barcelona doing the first steps of democracy and competing for the Olympic Games. We were just a bunch of young epidemiologists designing health information systems. A letter to the Lancet drew attention to a series of asthma outbreaks in the city with a consequent collapse of emergency departments, and suggested a possible relation to air pollution. We had to investigate this, and do it quick! The epidemiological approach and leadership allowed a cooperative research group to progress step-by-step, from the identification and description of epidemics to the demonstration of the causes and their prevention. When you are at the ISEE conference, look towards the port of Barcelona from the Montjuic Mountain. You can see the tall silos where the cause of the epidemics, soybeans, were being unloaded. Perhaps you may even see a ship unloading soybeans. Don’t worry, there is no fear of asthma epidemics, these silos have filters that prevent dust contamination of soybeans over the city. That was the result of our research, at that time innovative, nowadays a classic that has also provided the cause to unexplained asthma epidemics in other ports. Or perhaps, simply one more example of epidemiological research leading to effective preventive action!
Antó JM, Sunyer J, Reed CE, Sabrià J, Martínez F, Morell F, Codina R, Rodríguez-Roisín R, Rodrigo MJ, Roca J, et al. Preventing asthma epidemics due to soybeans by dust-control measures. N Engl J Med. 1993 Dec 9;329(24):1760-3.
Antó JM, Sunyer J, Rodriguez-Roisin R, Suarez-Cervera M, Vazquez L. Community outbreaks of asthma associated with inhalation of soybean dust. Toxicoepidemiological Committee. N Engl J Med. 1989 Apr 27;320(17):1097-102.
Sunyer J, Antó JM, Rodrigo MJ, Morell F. Case-control study of serum immunoglobulin-E antibodies reactive with soybean in epidemic asthma. Lancet. 1989 Jan 28;1(8631):179-82.
Prof. David Savitz, Brown University, Providence, RI, USA:.
Determining when epidemiology can (and cannot) help to assess small effects of environmental exposures
Questions asked of environmental epidemiology by policy makers and the public often demand a level of precision that is at or beyond the limit of what we can provide. Distinguishing between no effect and a subtle effect requires precise measurement of exposure and outcome in large populations with essentially no confounding. Obvious examples are lead and neurodevelopment in the range of <10 ug/dl, electromagnetic fields and childhood leukemia, and indoor radon and lung cancer. Policy evaluation requires careful integration of modelling, mechanistic evidence, and (imperfect) epidemiology that can help to put a bound on the range of possibilities. New epidemiologic investigations should be undertaken only when they are demonstrably capable of contributing to a resolution at the boundary of our current understanding.
Prof. Irva Hertz-Picciotto, University of California, Davis, Ca, USA.
Gene x environment interaction: Do we fail to identify influential environmental determinants of health by ignoring genes?
Despite a common perception of the importance of both environmental and genetic factors in the aetiology of most diseases, there are relatively few robust, replicated gene–environment interactions in the epidemiological literature. Furthermore methods for the evaluation of GxE interactions are still being developed. Two distinct perspectives on geneXenvironment interactions have been voiced in epidemiology circles. One argument for studying such interactions is an enhanced power to identify associations of a health outcome with both the gene polymorphism and the environmental exposure, as compared with separate studies examining marginal effects for each factor separately. On the other hand, it is widely assumed, either explicitly, or implicitly based on actual practice of researchers, that pursuit of interactions should be limited to exposures and/or genes that show an overall (marginal) effect in a population. The wisdom in each of these contradictory views hinges on the state of nature, namely, the degree to which underlying interactions actually occur even when marginal associations are unremarkable. This session will discuss geneXenvironment interactions, whether current strategies have been adequate to identify these relationships, and results of some simulations designed to identify what sets of parameter values are compatible, for given sample sizes, with the two alternatives: "marginal association first," vs. "interactions regardless.
Thursday 15, September, 2011
Dr Jane Schroeder, Science Editor, Environmental Health Perspectives, DHHS, NIH, NIEHS, Morrisville, NC, USA and Dr. Allen Wilcox, Editor-in-Chief, Epidemiology, NIEHS, RTP, NC, USA.
Writing and publishing an environmental epidemiology paper
(organised by the ISEE Student and New Researcher Network Committee)
Have you wondered over what you might do to make your paper more appealing to a journal? Are you curious about what happens to your paper once it gets to a journal? Have you puzzled over how to respond to reviewers' comments, or editors' requests? Hear two editors discuss the manuscript process from the journal perspective, with time for questions from the audience.
Prof Yun-Chul Hong, Institute of Environmental Medicine, Seoul National University Medical Research Centre, Republic of Korea.
Low level exposure to chemicals such as lead, VOCs, bisphenol A and phthalates in the community. A discussion on health effects, standard levels and regulations.
Epidemiologic studies showed low level exposure to chemicals found in the community are associated with neurobehavioral deterioration in children and pulmonary, cardiovascular and metabolic disorder in adults, particularly in the elderly. However, even very well known chemicals do not have safety guideline or only have old guideline not applicable at the moment to protect susceptible population. The purpose of the session is to review health effects of chemicals such as lead, VOCs, bisphenol A and phthalates and discuss on stardard levels and regulations.
Epidemiologic studies showed low level exposure to chemicals found in the community are associated with neurobehavioral deterioration in children and pulmonary, cardiovascular and metabolic disorder in adults, particularly in the elderly. However, even very well known chemicals do not have safety guideline or only have old guideline not applicable at the moment to protect susceptible population. The purpose of the session is to review health effects of chemicals such as lead, VOCs, bisphenol A and phthalates and discuss on stardard levels and regulations.
Prof. Neil Pearce, London School of Hygiene & Tropical Medicine, London, UK
Why we should all be Bayesians (and often are without knowing it)
Most epidemiologists write their methods and results sections as frequentists and their introduction and discussion sections as Bayesians. In their methods and results sections, they "test" their findings as if their data is the only data that exists. In the introduction and discussion, they discuss their findings with regards to their consistency with previous studies, as well as other issues such as biological plausibility. This creates some tensions, e.g. when a small study has findings which are not statistically significant but which are consistent with prior knowledge; or when a study finds statistically significant findings which are inconsistent with prior knowledge. thus, in practice, almost all epidemiologists profess to be frequentists, but in practice are qualitative Bayesians. In some (but not all) instances, things can be made clearer if we also formally include Bayesian methods in the methods and results sections of our paper, i.e. if we act as quantitative as well as qualitative Bayesians.
Friday 16, September, 2011
Prof. Klea Katsouyanni, University of Athens, Greece; Prof. Joel Schwartz, Harvard School of Public Health, Boston, MA, USA and Prof. How-ran Guo, National Cheng Kung University, Taiwan.
Grant Writing and Funding Mechanisms for New Investigators
(organised by the ISEE Student and New Researcher Network Committee )
Funding mechanisms in the EU, USA and Taiwan, with a bottom-up approach, addressing particularly the needs of young researchers, helping them to consolidate their independence or participate and learn in a different research environment will be presented and discussed. Important points to take into account when writing a grant, those which make a difference for the Reviewers, will be highlighted and explained.
Prof. Philippe Grandjean, University of Southern Denmark, Odense, Denmark.
Is environmental epidemiology precautionary?
Environmental epidemiology has traditionally focused on “significant” associations and ignored the other extreme of the confidence interval. As the precautionary principle requires documentation on the potential worst-case scenario, is environmental epidemiology anti-precautionary, and - if yes – what can be done about it?
Grandjean P. Seven deadly sins of environmental epidemiology and the virtues of precaution. Epidemiology 2008; 19: 158-62.
Prof Beate Ritz, Department of Epidemiology, School of Public Health, UCLA, CA, USA.
How to be an epidemiologist in large collaborations with toxicologists, geneticists and clinicians, and how to feed information and ideas back and fourth between these fields.
Over the past 15 years, my team at UCLA participated in several center grants focusing on neurodegenerative diseases in which the explicit challenge was to integrate population-based epidemiology studies with basic science approaches ranging from molecular genetics and toxicology in cells, flies, fish and mice to clinical translational projects that can be readily applied to improve disease outcome in patient populations. The specific challenges included developing exposure assessment tools that were specific enough to allow comparisons to lab based experiments and to assess how clinical human phenotypes of neuro-degeneration parallel and can be studied in genetic and toxin induced animal models. I will present an example collaboration and highlight how we can bridge some disconnects between disciplines to inform our human observational studies and create a richer scientific environment for epidemiologists.
