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The Role of the Environment and Occupational Exposures in Chronic Rhinosinusitis
Summary
This review examines how environmental exposures including air pollution, tobacco smoke, occupational chemicals, and microplastics may contribute to chronic sinus inflammation. Researchers found growing evidence that these exposures can trigger or worsen chronic rhinosinusitis by disrupting the nasal microbiome and immune responses. The study highlights microplastics as an emerging factor in respiratory health that warrants further investigation.
PURPOSE OF REVIEW: The purpose of the review is to summarize the current literature and evaluate how different environmental exposures may contribute to the development and course of chronic rhinosinusitis (CRS). The review aims to explore the relationship between host factors and environmental exposures in the pathogenesis of CRS. RECENT FINDINGS: Recent studies have helped establish the role of air pollutants, tobacco smoke, occupational exposures, and microplastics in the pathogenesis of CRS. These exposures have been shown to cause epithelial dysfunction and promote inflammation through different mechanisms and to different degrees. The pathogenesis of CRS is complex and multifactorial, with environmental exposures playing a key role in its onset and exacerbation. Research indicates that pollutants can damage the sinonasal epithelial barrier and disrupt the microbiome, leading to increased inflammation. A deeper understanding of the mechanisms behind this inflammatory process and its link to environmental exposures could enhance strategies for preventing and treating CRS.
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