Where There is Smoke: An Updated Review of Environmental Contributions to Chronic Rhinosinusitis

The pathogenesis of chronic rhinosinusitis (CRS) is thought to include a complex interaction between environmental exposures and host immune responses that generates a self-perpetuating inflammatory process. As molecular pathways continue to be explored, the impact of environmental exposures on CRS pathogenesis and exacerbation must not be overlooked. This review will explore the association between environmental exposures and CRS, specifically focusing on tobacco smoke, occupational inhalational exposures, air pollution, particulate matter, and wildfire smoke.

Tobacco smoke is associated with increased prevalence of CRS symptoms and formal diagnosis with worse surgical outcomes observed in both adults and children exposed to tobacco smoke. Numerous occupational exposures have been associated with increased sinonasal symptoms, though exposures and disease definitions are often poorly characterized. Pollution and microparticle exposure has been associated with an increased likelihood of CRS diagnosis, as well as increased need for surgery. Last, while wildfire smoke has been attributed to increased hospital and emergency room visits for respiratory-related complaints, no primary research has yet been performed regarding CRS and wildfire smoke, though in-vitro studies support an association.

Population-based studies bolstered by in-vitro mechanistic data support an association between numerous environmental exposures and the onset and severity of CRS.