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Vinyl Chloride


Janet Gray, Ph.D.
Janet Gray, Ph.D.

As author of our 2008 and 2010 State of the Evidence reports, Dr. Gray drives the science behind all our work.

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Dichloro-diphenyl-trichloroethane (DDT/DDE)

CATEGORY*: IARC probable carcinogen, NTP reasonably anticipated carcinogen, Endocrine disruptor

FOUND IN: Banned in many countries, still used for malaria control in 17 countries, persists in the environment even where it is not used

THE GIST: Rachel Carson made DDT famous in 1961 with the publication of Silent Spring, a groundbreaking book that spurred the environmental movement—and the passage of important legislation to regulate environmental toxicants. Because of Carson’s work, the United States banned DDT in 1972. The world followed suit—and the chemical was banned for agricultural use under the Stockholm Convention. But it continues to be used in Africa to control malaria. In spite of the ban, the chemical remains in our systems.

State of the Evidence on Dichloro-diphenyl-trichloroethane (DDT/DDE)

DDT was the first widely used synthetic pesticide. It is credited on the one hand with the eradication of malaria in the United States and Europe and on the other with long-term devastating effects on reproductive success in wildlife and with adverse health effects in humans (Beard, 2006). Banned in most countries for agricultural use, DDT is still used for malaria control in many countries, especially in sub-Saharan Africa (WHO, 2007).


Since DDT is banned, there is little we can do besides ensure that similar chemicals are not allowed on the market in the future.

Join the Breast Cancer Fund in advocating for responsible chemical regulations >

Because of its continued use and its persistence in the environment, DDT is found worldwide. Most animals, including humans, ingest DDT-contaminated foods and retain the chemical and its main metabolite, DDE. Substantial concentrations of DDT and DDE are still found in the body fat of humans and animals as well as in human breast milk and placenta, even in areas where it has not been used for a long time (Rogan, 2007; Shen, 2007; Zheng, 1999).

Epidemiological data are mixed regarding the effects of DDT/DDE on breast cancer risk (Brody, 2007). For example, one study from the Long Island Breast Cancer Study Project did not find an association between DDT/DDE (or polychlorinated biphenyls, PCBs) and breast cancer (Gammon, 2002). However, like many such studies that did not find reliable connections between DDT or DDE levels and risk for breast cancer, this project measured contaminant levels near the time of breast cancer diagnosis, without regard to possible exposures during critical early periods of breast development, and did not consider the effect of chemical mixtures nor assess key metabolites. As we now know, exposures to toxic chemicals during critical periods of mammary tissue development may lead to effects on breast cancer rates that are not observed when exposures take place exclusively or primarily in adulthood (Cohn, 2011).

Two critical studies that examined early life (prenatal and childhood) exposures to DDT have demonstrated a clear association between exposures to DDT andincreased risk for developing breast cancer (Cohn, 2007, 2015).


This graph, taken from a 2011 study, demonstrates that DDT exposure early in life is associated with an increased risk for breast cancer. Women and girls exposed to high levels of DDT before under age 7 were more likely to receive a breast cancer diagnosis later in life. Reprinted from Reproductive Toxicology, Volume 31, Issue 3, Cohn BA, Developmental and environmental origins of breast cancer: DDT as a case study, Pages 302–311, Copyright (2011), with permission from Elsevier.

The first study explored women’s estimated DDT levels based on aggregate data from their year of birth (to ascertain historic exposures to DDT levels), as well as blood DDT levels at the time the women gave birth to their first children. Researchers then followed the women over the next two decades, noting cases when women either were diagnosed with breast cancer (invasive or non-invasive) before the age 50, or had died from breast cancer before the age of 50. Results show that exposure to DDT during childhood and early adolescence (younger than age 14) was associated with a fivefold increase in risk of developing breast cancer before the age of 50. The younger the women were during the period of heavy DDT use (1945 to 1972), the greater the effect. At the time of the study, the authors noted, “Many U.S. women heavily exposed to DDT in childhood have not yet reached age 50. The public health significance of DDT exposure in early life may be large” (Cohn, 2007).

The second study was a case-control 54-year follow-up of 9,300 daughters in the Child Health and Development  Studies pregnancy cohort. Maternal blood samples, drawn within one-three data post-delivery, were analyzed for levels of DDT and its major metabolite, DDE. Levels of maternal chemicals were compared for daughters who developed breast cancer before the age of 52 and those who did not. Higher maternal DDT levels were associated with an almost 4-fold increase in occurrence of breast cacner in their daughters (Cohn, 2015).

Supporting the premise that exposures to DDT are associated with increased risk of breast cancer is a recent review comparing the association between disease risk and DDT use in developed countries, where DDT has been banned for several decades, and in developing countries, where DDT use is still prevalent. The association between DDT levels and breast cancer was much stronger in developing countries, where women of the age to be diagnosed with breast cancer also would have been exposed to DDT during critical periods of development (Shakeel, 2010).

Laboratory studies have found that, in addition to being directly genotoxic or carcinogenic (Canales-Aguirre, 2011), the estrogen-like form of DDT enhances the growth of estrogen-receptor-positive (ER+) mammary tumors (Robison, 1985; Scribner, 1981; Uppala, 2005). ER+ tumors are the most common type of breast cancer. The percentage of breast tumors in the United States that are ER+ rose from 73 percent in 1973 to 78 percent in 1992. This is the period when women who were young girls during the highest use of DDT in the 1950s were reaching the age that post-menopausal breast cancer begins to be diagnosed (Pujol, 1994). Another study, looking at chemical levels in breast fat tissue, did not find an association of DDT/DDE with ER+ tumors. However, data from this study indicated a statistically significant association of higher concentrations of these compounds in breast tissue with tumors that were more aggressive and that had poorer prognoses (Woolcott, 2001).


*For chemicals that have been shown to be carcinogens, we provide classifications from two authoritative bodies: the International Agency for Research on Cancer (IARC, an international body) and the National Toxicology Program (NTP, a division of the U.S. Department of Health and Human Services). We have categorized endocrine-disrupting compounds where the body of peer-reviewed research indicates a strong foundation for doing so.