Environmental Health Perspectives 105, Supplement 1, February 1997

Breast Cancer Risk and Environmental Exposures

Mary S. Wolff and Ainsley Weston

Division of Environmental and Occupational Medicine, Mount Sinai School of Medicine, New York, New York

Abstract
Although environmental contaminants have potential to affect breast cancer risk, explicit environmental links to this disease are limited. The most well-defined environmental risk factors are radiation exposure and alcohol ingestion. Diet is clearly related to the increased incidence of breast cancer in developed countries, but its precise role is not yet established. Recent studies have implicated exposure to organochlorines including DDT as a risk factor for breast cancer in the United States, Finland, Mexico, and Canada. Other investigations have discovered associations between breast cancer risk and exposures to chemical emissions and some occupational exposures. Several points must be considered in evaluating the relationship of environmental exposure to breast cancer. Among these considerations are the mechanism of tumorigenesis, timing of environmental exposure, and genetic modulation of exposure. Epidemiologic and ecologic investigations must take into account the very complex etiology of breast cancer and the knowledge that tumorigenesis can arise from different mechanisms. Thus crucial exposures as well as reproductive events related to breast cancer may occur years before a tumor is evident. Moreover, environmental contaminants may alter reproductive development, directly or indirectly, and thereby affect the course of tumorigenesis. Such alterations include change in gender, change in onset of puberty, and inhibition or promotion of tumor formation. Timing of exposure is therefore important with respect to mechanism and susceptibility. Finally, genetic polymorphisms exist in genes that govern capacity to metabolize environmental contaminants. Higher risk may occur among persons whose enzymes either are more active in the production of procarcinogens or fail to detoxify carcinogenic intermediates formed from chemicals in the environment. -- Environ Health Perspect 105(Suppl 4):891-896 (1997)

Key words: breast cancer, environment, genetic, timing, metabolism

This paper is based on a presentation at the symposium on Mechanisms and Prevention of Environmentally Caused Cancers held 21-25 October 1995 in Santa Fe, New Mexico. Manuscript received at EHP 16 April 1996; accepted 6 August 1996.

Address correspondence to Dr. M.S. Wolff, Mount Sinai School of Medicine, Division of Environmental and Occupational Medicine, Box 1057, 1 Gustave L. Levy Place, New York, NY 10029-6574. Telephone: (212) 241-6173. Fax: (212) 966-0407.

Abbreviations used: DES, diethylstilbestrol; DMBA, dimethylbenzanthracene; DNU, dimethylnitrosourea; NAT, N-acetyl transferase; PAHs, polycyclic aromatic hydrocarbons; PCBs, polychlorinated biphenyls; RFLP, restriction fragment length polymorphism; TCDD, 2,3,7,8-tetrachlorodibenzodioxin.

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Last Update: June 19, 1997