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Impact of early environmental and genetic determinants on lung development from infancy to preschool age
Third-party funded project
Project title Impact of early environmental and genetic determinants on lung development from infancy to preschool age
Principal Investigator(s) Frey, Urs Peter
Organisation / Research unit Bereich Kinder- und Jugendheilkunde (Klinik) / Pädiatrie (Frey)
Project start 01.09.2009
Probable end 31.08.2012
Status Completed
Abstract Background: The high prevalence of wheezing disorders in infants and preschool children has become a major health issue. Wheezing disorders can occur as a result of simple viral infections and are mostly episodic and transient in nature, but they may occur recurrently and be an expression of disturbed fetal growth or lung development or the consequence of early allergic bronchial asthma (multi-trigger wheeze). These different phenotypes are clinically often difficult to distinguish in infancy, however, they have different long term outcomes into school age. While genetic risk factors such as parental atopy (allergy) play an important role, environmental factors such as tobacco exposure, Western lifestyle or air pollution are also known risk factors for wheezing disorders in children. Our hypothesis raised in project 3200-052197.97/1, that different mechanisms may be responsible for the impairment of lung growth to those for the impairment of the immune, allergic or inflammatory system, has been recently reinforced in the literature. Many longitudinal studies show that this loss of lung function tracks throughout life, and impaired lung function at a young age is related to chronic respiratory morbidity in old age. This suggests that the determinants of impaired lung growth may be programmed in early life and that these programmers have a sustained impact on long term morbidity with its related burden for the health care system. Evidence that air pollution impairs lung growth has recently been demonstrated in school children. Based on this current cohort, we have recently shown for the first time that prenatal exposure to particulate matter air pollution is similarly related to impaired lung function shortly after birth. These effects are even more dramatic than in older children suggesting a particular vulnerability of fetuses and infants to pollutants. Aims: The aim of the current study is to test whether these lung functional changes at birth persist into school age, and whether there is genetic susceptibility of certain infants to develop impaired lung growth. Methods: In our prospective birth cohort, we have identified a variety of asthma genes in the cord blood which have been related to lung growth, as well as to susceptibility to environmental toxins. We will improve our pre- and postnatal exposure modelling to tobacco and air pollution of all infants according to the Swiss national air pollution monitoring system (NABEL). In this worldwide unique and optimal dataset of 400-500 infants (currently 420 included), we longitudinally measure lung function after birth and at 5-6 yrs and evaluate whether any impairment persist into childhood, are modified by genetic risk factors, atopy, exposure to air pollutants in the preschool age or the prospectively assessed number and type of viral infections during the first year of life. Additionally we will investigate whether infants exposed to pollutants during pregnancy will have higher prevalence allergic sensitisation and/or asthma at early school age. Significance: The consequence of today s air pollution on the fetal lung development has a unknown but potentially very relevant impact on global respiratory health in the future with unpredictable costs. If genetic and physiological mechanisms that lead to impaired lung growth at this early vulnerable phase of lung development are better understood, we will be better able to identify infants at risk and to develop environmental, preventative, and therapeutic strategies for infants and children at risk.
Financed by Swiss National Science Foundation (SNSF)
   

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29/03/2024