Phthalates Increase the Risk of Allergies Among Children
Phthalates, which are used as plasticizers in plastics, can considerably increase the risk of allergies among children. This was demonstrated by UFZ researchers in conjunction with scientists from the University of Leipzig and the German Cancer Research Center (DKFZ) in a current study published in the Journal of Allergy and Clinical Immunology.
If the mother is particularly heavily exposed to phthalates during pregnancy, there is an increased risk of allergic asthma for the children.
At the outset of the study, the team of UFZ researchers examined the urine of pregnant women from the LINA (lifestyle and environmental factors and their influence on the newborn-allergy-risk) mother-child cohort study and searched for metabolites of phthalates. The concentration level determined in each case was found to correlate with the occurrence of allergic asthma among the children.
In the course of the LINA mother-child cohort study, UFZ scientists investigated the lifestyle and environmental factors of pregnant women and their influence on the allergy risk of infants.
Phthalates turn off regulatory genes
In order to establish precisely what may have been modified, Polte and his team, in collaboration with colleagues from the German Cancer Research Center (DKFZ), took a close look at the genes of the young mice born to exposed mothers. So-called methyl groups were found in the DNA of these genes – and to a greater extent than is usually the case. In the course of this so-called epigenetic modification of the DNA, methyl groups attach themselves to a gene like a kind of padlock and thus prevent its code from being read, meaning that the associated protein cannot be produced.
But which genes cause allergic asthma if they cannot be read? So-called T-helper 2 cells play a central part in the development of allergies. These are kept in check by special opponents (repressors). If a repressor gene cannot be read as a result of being blocked by methyl groups, the T-helper 2 cells that are conducive to the development of allergies are no longer sufficiently inhibited, meaning that an allergy is likely to develop.
From humans to mice and back again
In mice, the researchers were able to prove that a repressor gene that has been switched off due to DNA methylation is responsible for the development of allergic asthma. But does this mechanism also play a part in humans? In order to answer this question, the researchers consulted the LINA cohort once more. They searched for the corresponding gene among the children with allergic asthma and studied the degree of methylation and gene activity. Here, too, it became apparent that the gene was blocked by methyl groups and thus could not be read.
Contacts and sources:
PD Dr. Tobias Polte
Susanne Hufe
Helmholtz Centre For Environmental Research – UFZ
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