Generally speaking, cigarette smoking and exposure to second-hand smoke increase the risk of breast cancer only modestly. However, there are windows of vulnerability during which the harmful effects of cigarette smoke are heightened, including the prenatal period, childhood, and prior to first pregnancy. For example, a number of studies have reported that smoking during the teenage years contributes disproportionately to subsequent breast cancer risk. In addition, cigarette smoking is associated with increased risk of breast cancer-specific death (as well as death from other causes) among breast cancer survivors.
While rates of cigarette smoking have been declining, use of e-cigarettes (vaping) has expanded. This is especially true among teenagers: E-cigarette use was reported by 37% of U.S. 10th-grader in one recent survey. Part of the reason teenagers give for choosing e-cigarettes is the belief that this habit is less harmful than cigarette smoking. Now a new study has reported for the first time that e-cigarette exposure has the potential to increase breast cancer growth and metastasis.

Latest research finds E-cigarettes promote mammary tumor growth

The study referenced above was designed to investigate how E-cigarettes influence tumor development and metastasis in an animal model of breast cancer. The authors hypothesized that E-cigarette exposure can drive breast cancer-monocyte/tumor-associated macrophage (TAM) crosstalk via CCL5 and V-CAM-1 axes in ways that could promote breast cancer. Monocyte subpopulations previously have been shown to be significantly altered by the presence of breast cancer. Furthermore, an auto-regulatory loop between TAMs and cancer cells can be driven by self-reinforcing processes involving CCL5 and V-CAM-1.
In the study, the authors first demonstrated that E-cigarettes promoted the infiltration of circulating monocytes into the mammary fat pads of animals that had been injected with breast cancer cells. E-cigarette exposure also was shown to promote breast cancer cell growth in mammary fat pads, as well as metastatic lung colonization. This was accompanied by increased TAM infiltration, as well as increased breast cancer cell proliferation and reduced apoptosis (programmed cell death).
Secondly, the authors used cell studies to demonstrate that treatment with E-cigarette vapor condensate upregulated expression of CCL5, V-CAM-1, and other tumor-promoting factors in breast cancer cells. A co-culture system designed by the authors showed that E-cigarette vapor condensate and macrophages both independently stimulated breast cancer cell growth and migration via the CCL5/CCR1/CCR5 axis. Furthermore, E-cigarette exposure was found to enhance breast cancer cell survival directly through interaction with infiltrated macrophages during metastasis. The authors conclude that E-cigarettes promote breast cancer growth and metastasis.
Please see our article on the teenage years and young adulthood for more information on protecting our high-risk daughters.