Abstract Background This study aims to enhance our understanding of how heat stress affects barrier dysfunction in airway epithelial cells, potentially influences Chronic Obstructive Pulmonary Disease (COPD) outcomes, and modifies the effects of pollutant exposure. COPD is a primary global health concern, ranking as the 3rd leading cause of death worldwide and the 5th leading cause of chronic disability. This progressive respiratory condition is characterized by persistent airflow limitation with narrowed airways, and various systemic effects beyond the lungs. Environmental factors like air pollution (particulate matter) play a crucial role in the development and progression of COPD. In recent years, there has been growing interest in the impact of heat exposure on COPD, particularly considering projected temperature increases due to climate change. In Birmingham, Alabama, residents of a local superfund site face a legacy of exposure to air pollutants, and the increasing heat stress during summer months that may further exacerbate respiratory illnesses. Methods24 hrs). Tight junction proteins and adherens junction proteins were stained and analyzed using fluorescence microscopy and/or western blotting. Tight junction protein influencing markers- oxidative stress, ERK1/2 signaling were analyzed to outline the pathway associated with TRPV4 expression. Conclusion A smaller size of PM enhances its bioaccumulation at cellular level in lungs leading to increased intracellular stress. We demonstrate that increasing environmental temperatures in combination with PM exposure can disintegrate epithelial cell barrier function. Suppressed cell-cell interactions lead to better penetration and exposure of pollutants to tissue resident cells. This may ultimately contribute to the development or severity of airway diseases like COPD. This abstract is funded by: NIEHS
Singh et al. (Fri,) studied this question.