The DOHaD (Developmental Origins of Health and Disease) hypothesis states that, because of developmental plasticity, in utero and early postnatal stressors can increase chronic disease risk in childhood and later. Alterations of epigenetic marks, impacting on gene expression, are one mechanism that could explain such long-term impact. These hypotheses have so far been tested mostly in animals, and little for atmospheric pollutants, for which animal evidence is scarce.We aim to characterize the impact of environmental exposures on childhood health. Our focus is on two families of pollutants with a highly prevalent and controllable exposure in humans: atmospheric pollutants and specific high-volume non-persistent chemicals (Bisphenol A, other phenols and phthalates). These pollutants are archetypal of modern life pollutants challenging environmental health research. We will set up a new type of mother-child cohort with early recruitment in pregnancy, intense follow-up (including geolocalisation of subjects with GPS combined with fine-scale air pollution modelling), personal exposure monitoring, repeated collection of biological samples. Transcriptomic analysis, non-invasive clinical examinations (Doppler and ultrasound imaging, ECG, early postnatal evaluation of lung function) will bring clues regarding target functions. This observational approach in humans will be supplemented by an animal experiment aiming at characterizing the impact of in utero exposure to traffic-related atmospheric pollutants on foetal development and health in adulthood, and characterizing target functions and organs more finely than the human study can allow.E-DOHaD spans over the whole range of environmental health disciplines, with epidemiologic and toxicologic studies being conducted in parallel to ease comparability and results synthesis. E-DOHaD is expected to have far-reaching implications in environmental health research and for public health.