Evaluating Inflammatory Gene Expression Linked to Chronic Obstructive Pulmonary Disease in Workers of the Nanoparticle Industries: A Cross-Sectional Study.

Background: Nanoparticles (NPs) are increasingly used in industry for their unique properties. However, prolonged occupational exposure to common NPs like titanium dioxide (TiO₂), zinc oxide (ZnO), silver (Ag), and silica (SiO₂) may trigger systemic inflammation and contribute to chronic obstructive pulmonary disease (COPD). Evidence suggests potential adverse health effects in exposed workers. Aim: Assessment of plasma pro- and anti-inflammatory cytokine levels related to respiratory inflammation in nano-industry workers. Methods: A total of 110 workers from NP-manufacturing facilities were categorized into three exposure groups based on work experience (Group I: < 10 years; Group II: 10-20 years; Group III: 20-30 years; Group IV: control). RT-qPCR was used to quantify IL-4, IL-6, IL-8, and TNF-α expression. Statistical analyses were performed using Results: Exposure to ZnO and TiO₂ NPs significantly upregulated inflammatory cytokines in all exposure groups compared to controls, except for IL-4 in Group I exposed to TiO₂. Ag-NP exposure increased IL-4, IL-6, and TNF-α but reduced IL-8 expression in Group I. Silica exposure in Group I downregulated IL-4 and IL-6, while elevating IL-8 and TNF-α. Cytokine levels were consistently higher in Groups II and III, with Group III exhibiting the greatest elevations for all NP types. Conclusion: Occupational NP exposure correlated with increased systemic cytokine levels, particularly in workers with longer exposure durations. This suggests a potential link between chronic NP exposures and heightened respiratory inflammation, although the absence of clinical diagnostic testing warrants cautious interpretation. Network pharmacology analysis identified pathways involved in NP-related inflammatory responses.