Hypotheses:

In utero particulate matter exposure has been linked to adverse pregnancy outcomes such as low birth weight and intrauterine growth retardation, which in turn have been linked to adult cardiovascular disease and metabolic abnormalities such as obesity, hypertension, insulin resistance and glucose intolerance. These findings suggest that adverse intrauterine conditions that promote reduced birthweight, such as air pollution exposure, may also promote lifelong susceptibility to cardiovascular diseases. Although it is becoming clear that in utero exposure to environmental stressors plays a role in fetal metabolic programming, the mechanisms are still unclear. The investigation of OMICS measurements at different molecular levels provides an insight into the biological pathways involved in the process linking in utero air pollution exposure to early life growth and cardiovascular development.

Aims:

The objective of this project is to derive a molecular pathway linking in utero air pollution exposure to fetal and childhood growth and to study potential consequences on the development of the cardiovascular system. I address four main objectives:

1) The investigation of prenatal and postnatal growth in association with in utero air pollution exposure.

2) The derivation of biomarkers (within in each OMICS level) linking prenatal air pollution exposure to growth trajectories in the first years of life.

3) The identification of common patterns across different OMICS levels (cross-omic analyses) in order to get an insight into the biological pathways involved in the association between in utero air pollution exposure and growth.

4) The investigation of the role of early life growth and the derived OMICS signature in the association between prenatal air pollution exposure and cardiovascular endpoints in childhood and early adulthood.