No Link Between Abortions and Breast Cancer Risk

April 1, 2003

BETHESDA, Maryland-Well-established epidemiological evidence shows that neither an induced nor a recognized spontaneous abortion increases a woman’s risk of breast cancer, a workshop convened by the National Cancer Institute (NCI) concluded after an extensive review of the available scientific data. However, important gaps exist in the understanding of how events prior to and during pregnancy may affect a woman’s risk of malignant breast tumors, and those gaps need to be filled, the workshop’s report added (see Table).

BETHESDA, Maryland—Well-established epidemiological evidence shows that neither an induced nor a recognized spontaneous abortion increases a woman’s risk of breast cancer, a workshop convened by the National Cancer Institute (NCI) concluded after an extensive review of the available scientific data. However, important gaps exist in the understanding of how events prior to and during pregnancy may affect a woman’s risk of malignant breast tumors, and those gaps need to be filled, the workshop’s report added (see Table).

The "Early Reproductive Events and Breast Cancer Workshop" attracted some 120 scientists to assess the state of the evidence regarding breast cancer risk factors associated with pregnancy. At one point, the public meeting was closed so that researchers could present new and unpublished findings.

Epidemiologist Leslie Bernstein, PhD, of the University of Southern California’s Keck School of Medicine, presented the workshop’s findings and recommendations to a joint meeting of NCI’s Board of Scientific Counselors and Board of Scientific Advisors. After hearing her report, the two boards voted unanimously to accept the workshop report.

Federal law requires that an NCI advisory board accept such a report before it can be forwarded to the institute’s director for consideration and action.

The issue of whether induced abortions increase breast cancer risk—which in part stimulated NCI director Andrew C. von Eschenbach, MD, to convene the workshop—drew considerable public attention to the meeting. A few studies have indicated a possible link. However, the workshop rated the evidence "well established" that an abortion, whether induced or spontaneous and recognized by the woman, does not increase the risk of breast cancer. The researchers could not address the issue of all spontaneous abortions because "a large portion of spontaneous abortions are not recognized by women, and it is difficult to record those," Dr. Bernstein said.

Other Epidemiological Findings

Six other epidemiological findings received well-established ratings: (1) Early age at first term birth is related to a lifetime decrease in breast cancer risk; (2) increasing parity is associated with a long-term risk reduction, even when controlling for age at first birth; (3) the additional long-term protective effect of young age at subsequent term pregnancies is not as strong as for the first term pregnancy; (4) a nulliparous woman has approximately the same breast cancer risk as a woman with a first term birth around age 30; (5) breast cancer risk is transiently increased after a term pregnancy; and (6) long-duration lactation provides a small additional risk reduction after consideration of age at, and number of, term pregnancies.

Workshop participants did not find the clinical evidence regarding pregnancy-associated risk factors for breast cancer to be as strong as the epidemiologic literature. They concluded that the "weight of the evidence" favors the idea that a long-lasting decrease in mammographic density follows pregnancy. The workshop found other clinical evidence to be in the category of "suggested from human population studies but speculative." These were that changes in breast histology can be correlated with risk in premenopausal women, and that prolactin, estradiol, and IGF-1 are decreased after pregnancy,

Future Research

Workshop participants recommended that NCI pursue 11 issues in future research aimed at answering questions about pregnancy and breast cancer. These included developing additional animal and treatment models, examining the molecular mechanisms of hormone-induced protection, pursuing descriptive studies about human breast development in order to formulate new hypotheses, pursuing international studies to develop hypotheses for observed international differences in breast cancer risk, developing surrogate markers to identify the risk of breast cancer following pregnancy, and translating knowledge about protective effects of pregnancy into intervention trials with human populations.

The summary report can be found at http://www.nci.nih.gov/cancerinfo/ere-workshop-report.