For a while, environment could be defined as "everything except genetic". The recent scientific progress show on the contrary that most of the health impacts of environmental pollutions are mediated through genetic and epigenetic mechanisms. It is now impossible to draw an impervious barrier between these two compartments. Environment and genetic, more particularly mutagenesis, are closely linked and this creates a new form of complexity. What is in stake is the definition of a new paradigm to understand the interactions between pollutants exposures and the onset of human diseases. The new paradigm has to encompass the four preceding ones that have guided the development of scientific research in the field of environmental health. The first one was the time of 'poisons' when Pasteur, Koch and the founders of biochemistry and physiology were thinking in terms of "one pollutants for each disease". The second one was of experimental nature with the development of modern toxicology using animal, tissue or cellular models. Then the epidemiology applied to the observational study of chronic diseases in populations emerged in the 50’s. This was the beginning of the understanding of the multifactorial nature of the determinants of many diseases. Thirty years ago, the US National Academy of Sciences promoted the quantitative risk assessment paradigm. Toxicological and epidemiological knowledge could be synthesized through four formal steps: hazard identification, dose-response relationship analysis, human exposure measurement and finally risk characterization. In this presentation, we will show that for each of these steps, recent advances in research challenge the way to assess the health impact of environmental pollutions. Using examples like bisphenol A, chemical-induced obesity, chlordecone and nanoparticles, we will discuss the desirable characteristics of the fifth paradigm that must integrate many disciplines from mathematics to social sciences.


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  • Received: 07 May 2012
  • Accepted: 07 May 2012
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