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Environmental estrogen exposures alter molecular signaling in immune cells that promote the development of childhood asthma
Summary
Chemicals that mimic estrogen, like BPA and BPS found in plastics, may change the way immune cells behave at a molecular level, potentially making kids more prone to developing asthma. In lab tests on human immune cells, these estrogen-like compounds altered key signaling pathways that control immune function, suggesting one way everyday exposure to plastics-related chemicals could contribute to rising asthma rates. While this early research was done in cells rather than in people, it adds to concerns about how common chemical exposures might shape our children's health.
Environmental estrogens (EEs) are associated with an increased prevalence of asthma. These epigenetic alterations of the immune cells may explain the multigenerational effects on asthma development. We hypothesized that exposure to immune cells enhances allergic sensitization by initiating signaling in these cells. Human T cell lines (TIB-152, CCL-119) were exposed to varying concentrations of estradiol, bisphenol A, bisphenol S, or bisphenol A + estradiol. H3K27me3, phosphorylations of EZH2 (pEZH2), AKT (pAKT), and phosphatidylinositide 3-kinase (pPI3K) were assessed. pAKT and pPI3K were decreased in response to some of the concentrations of these exposures in both cell lines. It is likely that EEs exposure to immune cells is one of the factors in the increase in the prevalence of asthma.