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Breast Cancer Res. 2019 Aug 20;21(1):96. doi: 10.1186/s13058-019-1168-2.

Environmental exposures during windows of susceptibility for breast cancer: a framework for prevention research.

Author information

1
Department of Epidemiology, Mailman School of Public Health, Columbia University, 722 West 168th Street, Room 1611, New York, NY, 10032, USA.
2
Department of Epidemiology, Fielding School of Public Health, University of California, 650 Charles E. Young Drive South, CHS 71-254, Los Angeles, CA, 90095, USA.
3
Silent Spring Institute, 320 Nevada St., Newton, MA, 02460, USA.
4
Department of Preventive Medicine and Biostatistics, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road A-1039F, Bethesda, MD, 20814, USA.
5
Department of Cancer Biology, Beckman Research Institute of City of Hope, 1450 E. Duarte Road, Duarte, CA, 91010, USA.
6
Pioneer Valley Life Sciences Institute and Department of Veterinary & Animal Sciences, University of Massachusetts Amherst, 661 North Pleasant St., Amherst, MA, 01003, USA.
7
Department of Population Health Sciences and the Carbone Cancer Center, School of Medicine and Public Health, University of Wisconsin-Madison, 610 Walnut St., WARF Room 605, Madison, WI, 53726, USA.
8
Departments of Oncology and Biochemistry & Molecular Biology, Georgetown University Medical Center, E411 New Research Building, Washington, DC, 20057, USA.
9
Departments of Medicine, Pediatrics, Environmental Health Sciences; Vagelos College of Physicians and Surgeons, Mailman School of Public Health, Columbia University, PH8E-101B, 630 W. 168th St, New York, NY, 10032, USA.
10
Department of Population Sciences, Beckman Research Institute of City of Hope, 1450 E. Duarte Road, 1500 E. Duarte Road, Duarte, CA, 91010, USA.
11
Department of Communication, University of Delaware, 250 Pearson Hall, 125 Academy St, Newark, DE, 19716, USA.
12
Department of Population Health Sciences and Carbone Cancer Center, School of Medicine and Public Health, University of Wisconsin-Madison, 610 Walnut St., WARF Room 307, Madison, WI, 53726, USA. trentham@wisc.edu.

Abstract

BACKGROUND:

The long time from exposure to potentially harmful chemicals until breast cancer occurrence poses challenges for designing etiologic studies and for implementing successful prevention programs. Growing evidence from animal and human studies indicates that distinct time periods of heightened susceptibility to endocrine disruptors exist throughout the life course. The influence of environmental chemicals on breast cancer risk may be greater during several windows of susceptibility (WOS) in a woman's life, including prenatal development, puberty, pregnancy, and the menopausal transition. These time windows are considered as specific periods of susceptibility for breast cancer because significant structural and functional changes occur in the mammary gland, as well as alterations in the mammary micro-environment and hormone signaling that may influence risk. Breast cancer research focused on these breast cancer WOS will accelerate understanding of disease etiology and prevention.

MAIN TEXT:

Despite the plausible heightened mechanistic influences of environmental chemicals on breast cancer risk during time periods of change in the mammary gland's structure and function, most human studies of environmental chemicals are not focused on specific WOS. This article reviews studies conducted over the past few decades that have specifically addressed the effect of environmental chemicals and metals on breast cancer risk during at least one of these WOS. In addition to summarizing the broader evidence-base specific to WOS, we include discussion of the NIH-funded Breast Cancer and the Environment Research Program (BCERP) which included population-based and basic science research focused on specific WOS to evaluate associations between breast cancer risk and particular classes of endocrine-disrupting chemicals-including polycyclic aromatic hydrocarbons, perfluorinated compounds, polybrominated diphenyl ethers, and phenols-and metals. We outline ways in which ongoing transdisciplinary BCERP projects incorporate animal research and human epidemiologic studies in close partnership with community organizations and communication scientists to identify research priorities and effectively translate evidence-based findings to the public and policy makers.

CONCLUSIONS:

An integrative model of breast cancer research is needed to determine the impact and mechanisms of action of endocrine disruptors at different WOS. By focusing on environmental chemical exposure during specific WOS, scientists and their community partners may identify when prevention efforts are likely to be most effective.

KEYWORDS:

Breast neoplasms; Environment; Menopause; Pregnancy; Puberty

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