Miljön under fosterstadiet och astma och luftvägsproblem hos barn – risker, orsaker och prediktion.

Background: In Sweden, about 20% of all 1-2-year olds and 24% of all 7-year olds have experienced wheezing and 10% of school age children have been diagnosed with asthma. Exposure to chemicals during fetal development could make some children more vulnerable. Examples supporting this includes studies where high levels of perfluorinated compounds and bisphenols during pregnancy have been associated with increased risk of childhood asthma.

A potential mediator between exposure and outcome is epigenetic modifications (such as altered DNA methylation) which can potentially prime the individual for future development of asthma.

Project goal: The goal of the proposed project is to identify chemical exposures during pregnancy that are associated with increased risk of wheezing and asthma in young children. This will then be extended into studies on possible mechanisms. Our main hypothesis is that high levels of certain chemical exposures during pregnancy will be associated with increased risk of developing asthmatic symptoms at an early age. Our secondary hypothesis is that the underlying mechanism will include epigenetic reprogramming.

Work plan: The project is based on NorthPop– a prospective birth cohort in Västerbotten county, with the goal of recruiting 10’000 pregnant women. The first part will include 300 mother-child pairs where we are using a multifactorial approach to measure chemical pollutants in plasma collected during pregnancy and connect these to early respiratory diseases.

We will also measure DNA methylation in cord blood from the new-born children in order to identify altered patterns. In a planned follow up sample including an additional 700 mother-child pairs we plan to validate our findings and determine how well we can predict asthmatic outcomes.

Significance: Understanding the biological pathways between exposures and asthma development is essential in order to develop public health guidelines and aid in future therapeutic measures. In this proposal, our strategy is to determine the contribution of chemical exposures during pregnancy to early signs of asthma, with an in depth focus on underlying epigenetic mechanisms. Our hope is that this will aid in future efforts to slow down, or reverse, the rising incidence of childhood asthma.