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Environmental estrogen exposures alter molecular signaling in immune cells that promote the development of childhood asthma
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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.
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Researchers found that perinatal exposure to the plasticizer bisphenol A (BPA) in mice enhanced allergic asthma development across up to four generations, acting through a molecular pathway involving BRD4, ZDHHC1, and immune-signaling protein STING. Blocking STING in exposed mothers reduced asthma severity in offspring, revealing a transgenerational epigenetic mechanism by which environmental plastic chemicals can program immune dysfunction.
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Bisphenol A (BPA), a chemical found in many plastics, was shown to alter the immune environment within breast tumors and increase lung metastasis in mice. The findings suggest that BPA exposure may worsen cancer outcomes by promoting spread of the disease.
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Researchers analyzed data linking urinary metabolites of DEHP — a phthalate plasticizer (a chemical added to plastics to make them flexible) found in food packaging, medical devices, and household products — to asthma risk, finding that certain asthma subtypes showed heightened vulnerability to these exposures. The results suggest DEHP metabolites may affect immune pathways in asthma through mechanisms distinct from classic inflammatory responses.
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Researchers found tiny plastic particles (microplastics) in the lung mucus of every single child with asthma they tested, and kids with worse-controlled asthma had higher levels of these particles in their airways. Lab experiments on lung tissue models suggested these plastics may trigger harmful cell stress and inflammation, though more research is needed to confirm this actually causes the asthma symptoms rather than just being linked to them. This study is a reminder that the air we breathe, and the plastic particles in it, may be quietly affecting respiratory health, especially in children.
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