Molecular and environmental factors affecting respiratory health: from preschool children exposed to e-waste to patients with COPD

This thesis addresses two major health concerns: understanding the pathogenesis of COPD and gaining insight into the impact of environmental pollution on children's respiratory health. In the COPD-focused studies, we identified disease-specific genes in the nasal epithelium that mirror those in the lower airway, suggesting that nasal brushing could serve as an accessible diagnostic tool. Findings further showed that alveolar type 2 (AT2) cells initiate repair by differentiating into type 1 cells, although this process may be hindered by the disease environment. DNA methylation changes were found to affect genes crucial for epithelial cell differentiation and lipid and surfactant metabolism, providing new insights into COPD's underlying molecular mechanisms. The second part investigated the health effects of environmental pollution on children in e-waste recycling areas. Results demonstrated that exposure to polycyclic aromatic hydrocarbons (PAHs) and lead (Pb) significantly impacted immune and respiratory health. Elevated PAH exposure was associated with increased AhR and NLRP3 expression, leading to higher cytokine levels. The combined effects of PAHs and Pb were linked to lower lung function, mediated by reduced urinary PGE2 levels. These findings emphasize the urgent need for stricter e-waste recycling regulations and protective measures for vulnerable children while highlighting promising biomarkers and therapeutic targets for COPD and environmental health monitoring.