Air pollutants contribute to epithelial barrier dysfunction and allergic diseases

Abstract

Air pollution is a global problem associated with various health conditions, causing elevated rates of morbidity and mortality. Major sources of air pollutants include industrial emissions, traffic-related pollutants, and household biomass combustion, in addition to indoor pollutants from chemicals and tobacco. Various types of air pollutants originate from both human activities and natural sources. These include particulate matter, pollen, greenhouse gases, and other harmful gases. Air pollution is linked to allergic diseases, including atopic dermatitis, allergic rhinitis, allergic conjunctivitis, food allergy, and bronchial asthma. These pollutants lead to epithelial barrier dysfunction, dysbiosis, and immune dysregulation. In addition, climate change and global warming may contribute to the exacerbation and the development of allergic diseases related to air pollutants. Epigenetic changes associated with air pollutants have also been connected to the onset of allergic diseases. Furthermore, these changes can be passed down through subsequent generations, causing a higher prevalence of allergic diseases in offspring. Modulation of the aryl hydrocarbon receptor could be a valuable strategy for alleviating air pollutant-induced epidermal barrier dysfunction and atopic dermatitis. A more effective approach to preventing allergic diseases triggered by air pollutants is to reduce exposure to them. Implementing public policies aimed at safeguarding individuals from air pollutant exposure may prove to be the most efficient solution. A pressing need exists for global policy initiatives that prioritize efforts to reduce the production of air pollutants.