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Systematic Review

Is breast cancer a result of epigenetic responses to traffic-related air pollution? A review of the latest evidence

    Debashish Sahay

    Division of Pulmonary, Allergy & Critical Care of Medicine, Department of Medicine, College of Physicians & Surgeons, Columbia University, New York City 10032, NY, USA

    ,
    Mary B Terry

    Department of Epidemiology, Mailman School of Public Health, Columbia University, New York City 10032, NY, USA

    Herbert Irving Comprehensive Cancer Center, Columbia University, New York City 10032, NY, USA

    &
    Rachel Miller

    *Author for correspondence:

    E-mail Address: rlm14@cumc.columbia.edu

    Division of Pulmonary, Allergy & Critical Care of Medicine, Department of Medicine, College of Physicians & Surgeons, Columbia University, New York City 10032, NY, USA

    Herbert Irving Comprehensive Cancer Center, Columbia University, New York City 10032, NY, USA

    Division of Pediatric Allergy, Immunology, & Rheumatology, Department of Pediatrics, College of Physicians & Surgeons, Columbia University, New York City 10032, NY, USA

    Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, New York City 10032, NY, USA

    Published Online:https://doi.org/10.2217/epi-2018-0158

    Environmental toxicants can exert adverse health effects via epigenetic regulation. We conducted a review of studies assessing traffic-related air pollution (TRAP) exposure and breast cancer (BC) risk, and the evidence for epigenetic mediation. 14 epidemiological studies demonstrated associations between TRAP exposure and BC risk, in which a total of 26 comparisons were assessed. 11 of these comparisons reported a positive association; whereas 15 comparisons were negative. Five publications linked TRAP exposure to epigenetic alterations in genes that may be related to BC risk. One animal study provided evidence of TRAP-treatment inducing breast tumorigenesis. Associations between TRAP components polycyclic aromatic hydrocarbons (PAH) and nitrogen dioxide (NO2) and BC risk were more consistent. While evidence for epigenetic regulation remains limited, polycyclic aromatic hydrocarbons (PAH) and nitrogen dioxide (NO2) exposures may alter methylation of breast tumorigenic genes (e.g., EPHB2, LONP1). Future epigenomic studies with environmental measures are needed to interrogate the relationship between TRAP and BC risk.

    Papers of special note have been highlighted as: • of interest; •• of considerable interest

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