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Airway exposure to microplastics: Potential mechanisms from epithelial barrier damage to the development of allergic rhinitis
Summary
This review summarized the mechanisms by which airborne microplastic exposure triggers allergic rhinitis, identifying pathways including physical and chemical disruption of the airway epithelial barrier, oxidative stress from adsorbed pollutants, and induction of Th2 immune responses and IgE class-switching. The findings support airborne MPs as a novel trigger for upper respiratory allergic disease.
Microplastics, as global pollutants, are widely distributed in the atmosphere and pose a potential threat to human respiratory health. This review summarizes the multiple mechanisms by which airborne microplastic exposure triggers allergic rhinitis (AR). Research indicates that microplastics drive AR progression through several pathways: (1) physical abrasion and chemical toxicity that disrupt the airway epithelial barrier (2) adsorbed pollutants (e.g., PAHs) that induce oxidative stress and inflammation; and (3) induction of a Th2 immune shift and IgE class-switching, leading to immune dysregulation. By integrating evidence from environmental toxicology, immunology, and clinical medicine, this paper elucidates the role of microplastics as an emerging environmental risk factor in AR pathogenesis and proposes multi-dimensional intervention strategies, including barrier repair, pollution control, and immune modulation. We emphasize the urgent need for interdisciplinary research to address the health challenges posed by microplastics and call for collaborative efforts across environmental governance, precision medicine, and public education to mitigate their impact on global public health.
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