Abstract
Polycyclic aromatic hydrocarbons (PAHs) from fossil fuels initiate breast cancer in animal models, and in humans a link between PAH exposure and breast cancer risk has been established. In women, it takes approximately two decades for PAH-exposed breast cells to progress to diagnosable breast cancer, and the exposure needs to happen during a time window when breast is vulnerable to PAHs. Further, not everyone exposed to high levels of PAHs develops breast cancer. PAHs are most likely to lead to breast cancer initiation among individuals who were exposed in utero through pregnant mothers to environmental pollutants or maternal obesity or both. These early life exposures are shown to increase daughter's later susceptibility to breast cancer by causing in the daughter (1) an increase in the number of structures in the breast in which breast cancer initiation takes place, (2) a suppression, perhaps epigenetically, in the ability of cells to repair DNA damage caused by PAHs by inhibiting expression of tumor suppressor genes, or (3) a persistent gut dysbiosis, which then impacts immune cells in the tumor microenvironment. Among the early life environmental pollutants that increase breast cancer susceptibility may be volatile aromatic BTEX compounds. Thus, aromatics from fossil fuels are likely to be involved in causing breast cancer, and efforts should be directed toward reducing human exposure to these compounds to prevent breast cancer.