The inflammation and oxidative status of rat lung tissue following smoke/vapor exposure via E-cigarette, cigarette, and waterpipe

Background

Tobacco smoking is a major worldwide health issue that contributes to millions of deaths annually. Electronic cigarettes (E-cigarettes) are also harmful. Smoke/vapor from E-cigarettes and tobacco products consists of free radicals and other toxic substances. Tissue damage in smokers, such as lungs, is highly observed and is linked to oxidative damage and inflammation.

Methods

The inflammation and oxidative status of rat lung tissues was examined following whole-body smoke/vapor exposure via E-cigarette, cigarette, and waterpipe for 2 h daily, 5 days per week for 8 weeks.

Results

Lung tissue damage was higher in cigarettes and waterpipe groups compared to the E-cigarette group. Collectively, there was a significant increase (p < 0.05) in the mRNA expression of pro-inflammatory mediators (TNF-α, NF-κB, IL-1β) with the exception of IL-1β in the E-cigarettes group. As for the anti-inflammatory mediators (Nrf2 and IL-10), a significant reduction (p < 0.05) of mRNA expression was observed with the exception of Nrf2 in the E-cigarette group. As for IL-6, there was a significant increase in its mRNA expression (p < 0.05) in the cigarette and waterpipe groups. There was also a significant decrease (p < 0.05) in the antioxidant activity of all antioxidants tested (GPx, SOD, and CAT) in all groups with the exception of SOD in the cigarette group.

Conclusion

Smoke/vapor administered via E-cigarette, cigarette, and waterpipe elicits inflammation and oxidative stress in rat lungs that is accompanied by histopathological changes.