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New paper: Prenatal exposure to traffic-related air pollution, the gestational epigenetic clock and risk of early-life allergic sensitization
September 5, 2019
A new paper* by Drs. Stuart Turvey and Michael Kobor has provided proof of concept that a biological marker known as epigenetic gestational age can be used to understand how prenatal exposure to traffic-related air pollution relates to the risk of asthma and allergy in childhood.
Several previous studies have provided support for the idea that a pregnant woman’s exposure to air pollution caused by vehicle traffic can increase her children’s risk of developing health conditions related to allergic sensitization, such as asthma. As with many other early-life exposures, the health effects of air pollution are believed to be mediated at least in part by epigenetic marks – changes to the DNA and to the proteins it’s associated with that act as “dimmer switches”, increasing and decreasing the activity of certain genes. Researchers from the Kobor and Turvey labs tested these ideas by looking at the DNA and environmental exposure history of 145 children from the Canadian Healthy Infant Longitudinal Development (CHILD) Study, of which Dr. Turvey is Co-Director. This subset of the much larger CHILD group was selected to ensure that there were sufficient children with allergic sensitization represented in the study. Thanks to the excellent records collected by the CHILD Study team, prenatal exposure to air pollution was calculated using local readings that were taken near each child’s mother’s address during pregnancy.
The research team used a recently developed biological marker of development, called epigenetic gestational age. There are some locations in the human genome where a type of epigenetic mark called DNA methylation follows predictable enough patterns over time that it can be used as an “epigenetic clock”, a measure of biological age. In adults, differences between actual and epigenetic age are associated with a number of health conditions. Epigenetic gestational age can be calculated at birth, using cells taken from the baby’s umbilical cord, and is thought to reflect developmental maturity.
The study confirmed previous reports that exposure to higher levels of traffic-related air pollution during the first trimester of pregnancy correlated with increased risk of allergic sensitization at one year of age. It also showed for the first time that exposure to this type of air pollution was associated with bigger mismatches between actual and epigenetic gestational age, and also that bigger age mismatches correlated with higher risk of allergic sensitization. A statistical analysis estimated that about 30% of the association between air pollution and allergic sensitization was mediated by differences in epigenetic gestational age; the source of the remaining association is not yet known.
These proof-of-concept findings need to be studied further in bigger groups of children, but are important in demonstrating that epigenetic gestational age can be used to investigate connections between early-life environmental exposures and health conditions. This study also provides additional evidence that early pregnancy is a critical time window when children’s DNA is particularly vulnerable to the effects of air pollution and other adverse environmental exposures. The collaborations enabled by the Social Exposome Cluster will help to further develop these and related research projects aimed at identifying and mitigating harmful early life exposures that adversely affect lifelong mental and physical health.
*"Prenatal exposure to traffic-related air pollution, the gestational epigenetic clock and risk of early-life allergic sensitization". Sbihi H, Jones MJ, MacIsaac JL, Brauer M, Allen RW, Sears MR, Subbarao P, Mandhane PJ, Moraes TJ, Azad MB, Becker AB, Brook JR, Kobor MS, Turvey SE. J Allergy Clin Immunol. 2019 pii: S0091-6749(19)31101-7. doi: 10.1016/j.jaci.2019.07.047.
Article by Dr. Cath Ennis