Several compounds of the phenol family are endocrine disruptors; this family includes compounds with very high exposure prevalence in the general population, such as bisphenols and parabens, and with suggested adverse health effects in animal studies. Adverse respiratory health and overweight represent outcomes with a very high contribution to the burden of disease in childhood and adulthood in our societies; animal experiments suggest that early-life exposure to endocrine disruptors such as phenols (including Bisphenol A and possibly other members of the Bisphenol family) may contribute to the onset of such diseases and act as modulators of metabolic and immune functions. Most former human studies on this topic relied on a cross-sectional design (not allowing to consider all toxicologically relevant exposure windows) or, for the few longitudinal studies, on a very small number of urine samples to assess exposure, disregarding the very high temporal variability of non persistent phenols such as Bisphenol A, and thus leading to strong exposure misclassification in spite of the use of exposure biomarkers. Our project aims at studying the effects of phenols (including bisphenol A and its substitutes) exposure during early life on child growth and respiratory health. The possible role of immunological factors as mediators in any effect of phenols on respiratory health will be characterized. This project relies on SEPAGES platform, an already funded couple-child cohort of pregnant women recruited in the first trimester of pregnancy and followed-up with their child (n=500) during 2 years, with an extensive biobank. Exposure to environmental phenols will be assessed through a novel approach in biomarker-based epidemiology, relying on the (within-subject) pooling of a large number of urinary samples per subjects during pregnancy (around 60 per woman) and in the first year of life (around 15 per newborn), allowing for the first time an accurate estimation of exposure. Respiratory health will be characterized through standardized questionnaires and with objective lung function measures as early as from 2 months of age. Immunological parameters, including detailed quantification of leucocyte cell subsets and functional tests of these cells (in terms of detailed cytokine expression analysis), will be measured in chord and maternal blood samples and considered as a possible intermediate pathway between prenatal exposure to phenols and respiratory health. Prenatal growth will be characterized by three ultrasound measures, and post-natal growth by repeated weight and height growth assessments and impedance measures to evaluate body composition. The feasibility is high given the fact that SEPAGES, the research platform on which the study will rely, is already funded and has been successfully tested via a pilot study; the funding requested will mainly be devoted to exposure assessment, biological assays and epidemiological analyses. In conclusion, SHALCOH main strengths rely on the longitudinal design, the collection of repeated biological samples to assess exposures during pregnancy and early childhood, on the objective assessment of respiratory characteristics by early measures performed by trained clinicians, and on the consideration of intermediate pathways. This project will bring robust evidence regarding the possible impact on public health relevant outcomes (weight, respiratory function) of early life exposure to endocrine disruptors with high exposure prevalence.