Exposure to air pollution increases the risk of cardiometabolic diseases. Inhaling air pollution, initiates inflammation, oxidative stress, and receptor activation, which in turn increases the risk of cardiovascular disease (CVD). Although the underlying mechanisms are largely unknown, altered gene expression may be involved in mediating the effects of air pollution on CVD risk. Already before birth, mothers’ exposure to air pollution is associated with foetal growth restriction and low birth weight, which may be caused by epigenetic changes and altered gene expression. In fact, air pollution may have a larger effect on gene expression in children than in adults. In this project, we will investigate the association between air pollution exposure during pregnancy and gene expression in cord blood in ALSPAC. Moreover, we aim to do pathway analyses to get insight into pathways that are associated with air pollution prenatally, and to investigate if the pathways involved have any associations with birth weight and cardiometabolic risk factors such as blood lipids. This work will be a part of the LongITools project, and we aim to do similar analyses in other cohorts, including Generation R (9-year old children) and in the Rotterdam study (adults, 40-100 years). By comparing findings between the different cohorts, we can get insight into biological pathways associated with air pollution throughout the life course.