ArticleEnvironment & health (Washington, D.C.)2026
Early Life Exposure to PFOS or F‑53B is Associated with Increased Asthma Susceptibility in Offspring and Alterations in the Pulmonary Barrier, Immune Function, and Gut Microbiota.
Article in Environment & health (Washington, D.C.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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12 authors.
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Abstract
As perfluorooctanesulfonate (PFOS) is phased out, its alternative, 6:2 chlorinated polyfluorinated ether sulfonate (F-53B), has been widely used in China. However, the health risks associated with F-53B exposure, particularly its potential effects on offspring respiratory outcomes, remain largely unclear. We therefore investigated whether gestational and lactational exposures to PFOS or F-53B alter early lung development and influence asthma susceptibility in offspring. Pregnant mice were exposed to PFOS or F-53B at a dose relevant to the human tolerable daily intake of PFOS during gestation and lactation, and maternal-fetal distribution was quantified by ultraperformance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) at embryonic day 18.5. Both PFOS and F-53B efficiently crossed the placenta and accumulated in the fetal lungs. Following ovalbumin sensitization and challenge, offspring from exposed dams showed increased airway inflammatory pathology and goblet cell hyperplasia, along with higher bronchoalveolar lavage protein and elevated pulmonary
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