Air pollutants contribute to epithelial barrier dysfunction and allergic diseases.

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.

Cigarette smoke induces distinct histone modifications in lung cells: implications for the pathogenesis of COPD and lung cancer.

Cigarette smoke (CS)-mediated oxidative stress induces several signaling cascades, including kinases, which results in chromatin modifications (histone acetylation/deacetylation and histone methylation/demethylation). We have previously reported that CS induces chromatin remodeling in pro-inflammatory gene promoters; however, the underlying site-specific histone marks formed in histones H3 and H4 during CS exposure in lungs in vivo and in lung cells in vitro, which can either drive gene expression or repression, are not known. We hypothesize that CS exposure in mouse and human bronchial epithelial cells (H292) can cause site-specific posttranslational histone modifications (PTMs) that may play an important role in the pathogenesis of CS-induced chronic lung diseases. We used a bottom-up mass spectrometry approach to identify some potentially novel histone marks, including acetylation, monomethylation, and dimethylation, in specific lysine and arginine residues of histones H3 and H4 in mouse lungs and H292 cells. We found that CS-induced distinct posttranslational histone modification patterns in histone H3 and histone H4 in lung cells, which may be considered as usable biomarkers for CS-induced chronic lung diseases. These identified histone marks (histone H3 and histone H4) may play an important role in the epigenetic state during the pathogenesis of smoking-induced chronic lung diseases, such as chronic obstructive pulmonary disease and lung cancer.