Some studies show increased breast cancer risk from exposure to xenoestrogens, but few have explored exposures via ambient air, which could impact large populations.
This study explored the association between breast cancer risk and residential exposures to ambient estrogen disruptors among participants in a large cohort study, the California Teachers Study.
Participants consisted of 112,379 women free of breast cancer and living at a California address in 1995/1996. Eleven hazardous air pollutants from the US Environmental Protection Agency 2002 list were identified as estrogen disruptors based on published endocrine disrupting chemical lists and literature review. Census-tract estrogen disruptor air concentrations modeled by the US Environmental Protection Agency in 2002 were assigned to participants’ baseline addresses. Cox proportional hazards models were used to estimate hazard ratios associated with exposure to each estrogen disruptor and a summary measure of nine estrogenic hazardous air pollutants among all participants and selected subgroups, adjusting for age, race/birthplace, socioeconomic status, and known breast cancer risk factors.
Five thousand three hundred sixty-one invasive breast cancer cases were identified between 1995 and 2010. No associations were found between residential exposure to ambient estrogen disruptors and overall breast cancer risk or hormone receptor-positive breast cancer risk, nor among targeted subgroups of participants (pre-/peri-menopausal women, post-menopausal women, never-smokers, non-movers, and never-smoking non-movers). However, elevated risks for hormone receptor-negative tumors were observed for higher exposure to cadmium compounds and possibly inorganic arsenic among never-smoking non-movers.
Long-term, low-dose exposure to ambient cadmium compounds or possibly inorganic arsenic may be a risk factor for breast cancer.
Supplemental Digital Content is available in the text.
From the aCancer Prevention Institute of California, Berkeley, CA; and bDepartment of Health Research and Policy, School of Medicine, Stanford University, Stanford, CA.
Submitted 18 June 2014; accepted 28 January 2015.
This research was supported by funds provided by the Department of Defense office of Congressionally Directed Medical Research Programs (DOD CDMRP), Award #W81XWH-10-1-0134, and by the National Cancer Institute (NCI) Grants R01 CA77398 and K05 CA136967. The collection of cancer incidence data used in this study was supported by the California Department of Public Health as part of the statewide cancer reporting program mandated by California Health and Safety Code Section 103885; the NCI’s Surveillance, Epidemiology, and End Results Program under contract HHSN261201000036C awarded to the Cancer Prevention Institute of California, contract HHSN261201000035C awarded to the University of Southern California, and contract HHSN261201000034C awarded to the Public Health Institute; and the Centers for Disease Control and Prevention’s National Program of Cancer Registries, under agreement #1U58 DP000807-01, awarded to the Public Health Institute. The ideas and opinions expressed herein are those of the author(s), and endorsement by the State of California Department of Public Health, the NCI, and the Centers for Disease Control and Prevention or their Contractors and Subcontractors is not intended nor should be inferred.
Supplemental digital content is available through direct URL citations in the HTML and PDF versions of this article (www.epidem.com). This content is not peer-reviewed or copy-edited; it is the sole responsibility of the authors.
Correspondence: Ruiling Liu, Cancer Prevention Institute of California, 2001 Center Street, Suite 700, Berkeley, CA 94704. E-mail: email@example.com.