Recurrence and metastasis are the foremost causes of morbidity and mortality for breast cancer (BC). Recent studies have highlighted the critical role of the tumor microenvironment, in particular, because it is related to tumor-associated macrophages (TAMs), in metastasis of BC. TAMs are mainly derived from macrophages that are recruited by C-C motif chemokine ligand 5, which are secreted by cancer cells and cancer-related stromal cells. Although E-cigarettes (E-cigs) were originally proposed as a healthy substitute for conventional cigarette smoking, clinical and experimental evidence has highlighted the potentially lethal effects of this alternative. Several studies have illustrated the immune or macrophage activation and DNA damaging effects of E-cigs. However, the potentially pivotal role of TAM-BC crosstalk during BC progression and metastasis for E-cig vaping has not been explored. This review discussed the significant effect that E-cig use had on the BC tumor microenvironment, which ultimately led to enhanced tumor malignancy and metastasis, with an emphasis on the extent that E-cig uses had on the crosstalk between cancer and immune cells, as well as the potential underlying mechanisms that drive this aggressive phenotype of BC. This review advances our understanding of this matter and provides scientific evidence that could highlight risks associated with vaping and suggest a potential intervention for the treatment of aggressive BCs that present an increased risk of metastasis.