E-cigarettes have been promoted as a less harmful alternative to traditional cigarettes. Because they do not involve tobacco combustion, many people consider them a safer option for those seeking to reduce or quit conventional cigarette smoking. However, as their popularity continues to grow, so does scientific interest in understanding their potential long-term effects on health.
Several studies have shown that the aerosol generated by these devices contains potentially toxic chemical compounds and substances capable of triggering various cellular events that may contribute to cancer development. Since these products have been on the market for a relatively short period of time, there is still insufficient evidence to fully understand their long-term health consequences.
The Lung: The first line of exposure
Because inhaled aerosol comes into direct contact with the respiratory tract, the lungs are among the organs most exposed to the potential effects of e-cigarettes. Recent research has demonstrated that repeated exposure to these aerosols may induce pulmonary inflammation, disrupt antioxidant mechanisms, and promote oxidative stress, a biological process associated with cellular damage and tissue aging.
In addition, some studies have reported increased levels of inflammatory molecules such as IL-6 and IL-8, as well as alterations in the epithelial cells lining the respiratory tract. Although many of these findings come from experimental studies, they suggest that prolonged exposure to aerosolized compounds may impair the lungs’ ability to maintain normal function.
EVALI: The most commonly associated condition
Concern regarding the respiratory effects of vaping increased considerably in 2019 with the emergence of EVALI (E-cigarette or Vaping Product Use-Associated Lung Injury), a severe pulmonary condition associated with the use of e-cigarettes and vaping products.
Thousands of cases were reported in the United States, including hospitalizations and deaths. Patients developed symptoms such as shortness of breath, persistent cough, chest pain, fever, and severe fatigue. Subsequent investigations identified a strong association with THC-containing products adulterated with vitamin E acetate. Although EVALI does not represent the typical outcome observed in all users, this event demonstrated that certain inhaled substances delivered through vaping devices can cause severe lung injury.
Beyond Addiction: The role of nicotine
One of the compounds of greatest concern to researchers is nicotine. Beyond its well-known addictive properties, nicotine may directly influence biological processes involved in cancer development and progression.
Experimental studies have shown that nicotine can promote tumor cell survival, stimulate proliferation, increase the formation of blood vessels that supply tumors, and facilitate processes associated with invasion and metastasis. Although nicotine is not considered a classical carcinogen, evidence suggests that it may act as a promoter of mechanisms involved in tumor progression.
In addition to these direct effects, nicotine may act in a less obvious but equally important way. Once it enters the body, it stimulates the sympathetic nervous system, which is responsible for the release of hormones such as adrenaline and noradrenaline.
Over the past several decades, numerous studies have revealed that persistent activation of this system may contribute to different stages of cancer development. Among other effects, it may promote chronic inflammation, reduce certain anti-tumor immune responses, stimulate angiogenesis, and increase the ability of cancer cells to migrate and colonize distant tissues.
For this reason, some researchers propose that prolonged nicotine exposure may create a biological environment that favors the growth and progression of certain cancers.
Figure 1. Aerosol components may induce oxidative stress, inflammation, and cellular damage, contributing to respiratory complications and activation of pathways associated with tumor progression.
DNA: Another potential target
Studies conducted in cellular and animal models have found that exposure to e-cigarette aerosol may induce genetic and molecular changes similar to those observed following exposure to tobacco smoke.
Researchers have also described alterations in DNA repair mechanisms, increased oxidative damage, and changes in the expression of genes involved in cancer-related processes. Other investigations have reported epigenetic modifications and a reduced capacity of cells to correct genetic damage, factors that could favor the accumulation of cellular alterations over time.
Although these findings do not by themselves demonstrate that e-cigarettes cause cancer in humans, they do suggest the existence of biologically plausible mechanisms that warrant further investigation.
An important consideration for cancer patients
This issue is particularly relevant for individuals with a history of cancer or those at elevated risk. In many cases, e-cigarettes are perceived as a virtually harmless alternative. While available evidence indicates that exposure to many carcinogenic substances is lower compared with traditional cigarettes, “less harmful” does not necessarily mean “safe.” The absence of combustion reduces certain risks but does not eliminate the potential biological consequences associated with prolonged exposure to nicotine and other compounds present in the inhaled aerosol.
Experts agree that long-term clinical studies are still needed to determine more precisely how prolonged e-cigarette use may influence cancer incidence, disease progression, and responses to cancer therapies.
As research continues to evolve, a better understanding of the biological effects of e-cigarettes will be essential for making informed decisions regarding their use.
This article is intended solely for educational and informational purposes. It is not intended to provide medical advice, diagnosis, or treatment recommendations. Readers should consult qualified healthcare professionals regarding any medical concerns or decisions related to their health.
Main reference:
Mravec, B., Tibensky, M., Horvathova, L., & Babal, P. (2020). E-Cigarettes and Cancer Risk. Cancer prevention research (Philadelphia, Pa.), 13(2), 137–144. https://doi.org/10.1158/1940-6207.CAPR-19-0346
Other references:
Schuller H. M. (2009). Is cancer triggered by altered signalling of nicotinic acetylcholine receptors?. Nature reviews. Cancer, 9(3), 195–205. https://doi.org/10.1038/nrc2590
Lee, H. W., Park, S. H., Weng, M. W., Wang, H. T., Huang, W. C., Lepor, H., Wu, X. R., Chen, L. C., & Tang, M. S. (2018). E-cigarette smoke damages DNA and reduces repair activity in mouse lung, heart, and bladder as well as in human lung and bladder cells. Proceedings of the National Academy of Sciences of the United States of America, 115(7), E1560–E1569. https://doi.org/10.1073/pnas.1718185115
