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Evaluating Inflammatory Gene Expression Linked to Chronic Obstructive Pulmonary Disease in Workers of the
Vahid Babaei1, Azadeh Ashtarinezhad2, Maryam Torshabi3
1Pharmaceutical Sciences Research Center Shahid Beheshti University of Medical Sciences Tehran Iran.
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 t-tests, ANCOVA, and GraphPad Prism 8.
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.
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