In a recent study published in the Scientific reports Journal, researchers examined the toxic effects of aerosol exposure from electronic cigarettes (ECs) and conventional cigarette smoke (CS) on mice’s cardiovascular, gastrointestinal, and renal systems.
Study: The toxic effects of electronic cigarette aerosol and cigarette smoke on cardiovascular, gastrointestinal and renal systems in mice. Image Credit: Andrey_Popov/Shutterstock.com
Background
Smoking is a significant health hazard, causing numerous diseases and affecting both smokers and bystanders. CS contains thousands of chemicals, many of which are carcinogens.
With over one billion smokers worldwide, ECs have emerged as a popular alternative to traditional cigarettes in recent years. ECs are nicotine inhalation systems that produce an aerosol mixture of flavoring e-liquids. They have become a multi-billion-dollar industry, but concerns about their safety persist.
While ECs contain 9 to 450 times less harmful compounds than conventional CS, they are not without risks. Nicotine, aroma, volatile organic compounds (VOCs), pyridine, and carbonyl compounds were found in EC aerosols, affecting the respiratory, central nervous, immune, throat, and mouth. EC use is also linked to inflammation, oxidative stress, and hemodynamic imbalance.
Although the harmful effects of smoking on various organs are well-established, the impact of different exposure conditions on the cardiovascular, gastrointestinal, and renal systems is poorly understood.
Therefore, more research is needed to determine EC’s acute and chronic effects and its potential as a smoking cessation tool. To address these knowledge gaps, the present study used male mice to compare the results of ECs and CS on the cardiovascular, gastrointestinal, and renal systems.
About the study
The study used EC1 (mung bean-flavored) and EC2 (watermelon-flavored) closed-pod type ECs with ceramic atomizers and 3% nicotine e-liquids. Forty-eight specific pathogen-free male C57BL/6J mice were purchased from Guangdong Medical Laboratory Animal Centre and kept in a 12-hour light/dark cycle with a room temperature of 22°C.
A Cambridge filter was used to gather aerosol from the EC or primary stream smoke from the CS, and the average amount of nicotine in EC and CS in 30 minutes was measured using ultra-performance liquid chromatography (UPLC).
The mice were placed into six groups, including low and high doses of mung bean-flavored EC aerosol, watermelon-flavored EC aerosol, and CS. They were exposed for ten weeks, five days a week.
Researchers evaluated the effects of CS on cardiac function, blood oxygen saturation, heart rate, mucosal integrity, and histopathological changes in various organs. Cardiac function was assessed using an ultra-high-resolution small animal ultrasound imaging system.
Changes in oral mucosa were observed under a cold light source, and histopathological changes were evaluated in the heart, stomach, duodenum, liver, and kidney using staining techniques. Differentially expressed proteins and their functions were observed through proteomic analysis performed using the Maxquant search engine and gene ontology.
Statistical analysis was performed using GraphPad Prism version eight and standard one-way analysis of variance ANOVA with Tukey’s multiple comparisons tests, with significance set at P < 0.05.
Results
In vivo, cardiac function analysis showed no significant changes in the mice indexes after ten weeks of exposure to EC and CS. However, blood oxygen saturation decreased significantly in the CS group compared to the EC group. Proteomics analysis revealed differentially expressed proteins in the cardiac tissues after ten weeks of exposure.
The common differentially expressed proteins were immunoglobulin heavy constant gamma 2C (Ighg2c) and cysteine-rich protein 2 (Crip2) between EC1 and CS, and NGG1 interacting factor 3-like 1 (Nif3l1), NHL repeat-containing protein 2 (Nhlrc2), and Crip2 between EC2 and CS.
They analyzed the distribution of differentially expressed proteins in the cytoplasm and nucleus in EC1 groups, mitochondria and nucleus in EC2 groups, and the cytoplasm, extracellular, and plasma membrane in CS groups. Most proteins were involved in signal transduction mechanisms, posttranslational modification, protein conversion, and chaperone function.
Using the Sonis standard score, anesthesia with 1% pentobarbital sodium was used to observe oral mucosa alterations under cold light. Scoring criteria included normal mucosa, erythema, severe erythema, ulcers, and ulcer areas between 25% and 50%.
Gastric tissue was observed, with no significant differences between groups. The liver cells were radially distributed, closely structured, and neatly arranged, with clear outlines and stained cytoplasm.
Masson staining showed fibrous septa formed in liver tissues, complete lobule structure, and collagen fiber deposition.
Conclusion
The current investigation suggests that EC aerosols and CS can harm various organ systems. CS appeared to be more harmful in reducing blood oxygen saturation and causing damage to the oral cavity.
Notably, these findings suggested that the differentially expressed protein Crip2 may contribute to the effects of smoking on the heart and cardiovascular systems.
Given the increasing popularity of ECs, it is important to continue researching their potential health risks to inform public health policies and promote safer alternatives for nicotine consumption.
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Xu, A. et al. (2023) “The toxic effects of electronic cigarette aerosol and cigarette smoke on cardiovascular, gastrointestinal and renal systems in mice”, Scientific Reports, 13(1). doi: 10.1038/s41598-023-39201-7. https://www.nature.com/articles/s41598-023-39201-7