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Quoted from Living Downstream:

With a focus on breast cancer, let’s look at the evidence of harm for three chemicals: DDT, PCBs, and atrazine.

In 1976, four years after DDT was banned, researchers reported that women with breast cancer had significantly higher levels of DDE (dichloro diphenyl dichloroethylene) and PCBs in their tumors than in the surrounding healthy tissues of their breasts. (DDT is metabolized in the human body into DDE, a chemical that acts like estrogen.) The study was small but the finding provocative because DDT and PCBs were already linked to breast cancer in rodents.

Other studies followed. Some showed an association between breast cancer and residues of pesticides or PCBs. Some did not. In 1993—seventeen years after the first study—the biochemist Mary Wolff and her colleagues conducted the first carefully designed, major study on this issue. They analyzed DDE and PCB levels in the stored blood specimens of 14,290 New York City women who had attended a mammography screening clinic. On average, they reported, the blood of breast cancer patients contained 35 percent more DDE than that of healthy women, but PCB levels were only slightly higher. The most stunning discovery was that the women with the highest DDE levels in their blood were four times more likely to have breast cancer than the women with the lowest levels. The authors concluded that residues of DDE “are strongly associated with breast cancer risk.”

[…]

They [breast cancer activists] pointed out that pesticide use in the United States had doubled since Rachel Carson wrote Silent Spring and that women born in the United States between 1947 and 1958 had almost three times the rate of breast cancer that their great-grandmothers had when they were the same age. […]

Studies were funded and papers published. Yet the results were maddeningly inconsistent. For every finding of a positive association, another showed no association or yielded a complicated picture. One study found that African American women with breast cancer showed more past exposure to PCBs than their counterparts without breast cancer. Mysteriously, however, the trend for white women went in the opposite direction: the highest levels of blood PCBs tended to occur in women without the disease. The largest and best-designed investigation within this suite of studies, published in the New England Journal of Medicine in 1997, found no association at all between risk of breast cancer and blood levels of PCBs and DDT. Interpretation of these contradictory results sparked considerable debate, but the majority opinion within the scientific community was that women with breast cancer, as a group, do not appear to have higher body burdens of DDE and PCBs than women without breast cancer.

Some researchers found these results reassuring. Others worried that these studies had not considered the underlying genetic differences among women nor taken into account the timing of exposure. What if, they asked, some genetic subgroups were more susceptible to environmentally induced breast cancers than others? Furthermore, most studies had measured levels of DDE or PCBs in adult women—after much of their residues had been eliminated from the body and the chemicals themselves long banned. What if contemporary measures do not accurately reflect historical exposures? What if the important variable is DDT exposure during childhood or adolescence—when the developing breast is most vulnerable? Animal studies clearly demonstrate the importance of toxic exposures that occur in early life when the breast is most sensitive to damage.

[…]

As described in a paper published in 2007, Barbara Cohn and her colleagues at the University of California unearthed medical records and banked blood samples of women who had visited a clinic between 1959 and 1967 to seek routine prenatal care. Knowing that DDT came on the market in 1945, Cohn was able to calculate how old each woman was when she was first exposed to DDT. And she was also able to trace these women and learn their current breast cancer status. The results were clarifying: Women exposed to DDT after age 14—those born in 1931 or before—showed no association between exposure to DDT and breast cancer. But among women exposed to DDT when they were younger than 14, a significant relationship existed: women with high DDT levels were five times more likely to be diagnosed with breast cancer by age 50 than those with the lowest levels. In other words, this study showed a fivefold increase in breast cancer risk among women who had experienced high exposures to DDT before puberty but not in women so exposed after their breasts had already developed. Thanks to hundreds of test tubes that stood silently in the back of a freezer in Oakland, California for a half century, and thanks to breast cancer activists who insisted that environment studies go forward, we now know that DDT exposure in childhood can significantly increase breast cancer risk in adulthood. And we gained this knowledge nearly forty years after DDT was banned.

Meanwhile, other researchers went to work categorizing women genetically. They looked closely at women who had inherited a variation of CYP1A1, a gene that is involved in metabolizing hormones and that is known to be influenced by PCB exposure. About 10-15 percent of white women in the United States are thought have the variant gene. The proportion of black women who have it is not yet known. When data on women with the variant gene were examined in isolation, a picture began to emerge: women who possessed both the genetic variation as well as a high PCB body burden had an elevated rate of breast cancer. Indeed, their rate of breast cancer was two to three times higher than that of women with lower levels and without this genetic trait. The evidence to date now supports an association between breast cancer and PCB exposure for subpopulations of women who have inherited this particular genetic variation. And we gained this knowledge nearly thirty years after PCBs were banned.  

The story of atrazine today is much like the story of DDT and PCBs as it was told decades ago. Worrisome findings followed by equivocal ones. Inconsistencies. Contradictions. Balls of confusion. The difference is that atrazine is not banned. It is the second most abundantly used pesticide in the United States, and its manufacturer plays an aggressive role in defending its product. A proven endocrine disruptor, atrazine causes breast cancer in one strain of rat. Some argue that it does so by a mechanism not relevant to humans. The human studies themselves are inconclusive and, while a few show possible associations, most do not report a link between adult exposure to atrazine and breast cancer. However, no human studies have looked at early-life exposures to atrazine, which is when atrazine exerts its strongest effects in lab animals. A 2009 study called for an investigation into how atrazine might be affecting the pace and tempo of sexual maturation in girls. (Early puberty is, by itself, a known risk factor for breast cancer.) Other human studies have found suggestive evidence for an association between atrazine exposures and several other cancers, including lymphoma and cancer of the prostate, ovary, testes, and brain. There is also suggestive evidence for unique toxicities arising from mixtures of atrazine with other farm chemicals. Laboratory studies report possible synergistic effects: among invertebrate animals, atrazine induces an enzyme that makes a second pesticide, chlorpyrifos, more toxic. In this way, exposure to one contaminant can turn another into a more powerful poison. Are these results applicable to humans? It’s not yet clear.

By 1994, the evidence against atrazine was troubling enough that the U.S. Environmental Protection Agency (EPA) initiated a special review of its registration. Nine years passed. Meanwhile, across the Atlantic, regulators in Europe announced the results of their own review: atrazine was banned throughout the European Union. Finally, in 2003, the EPA announced its decision: continued use of atrazine was approved. This was an intensely controversial decision. One researcher pointed out in disgust that DDT was abolished on the basis of less evidence than we now had for atrazine.

Steingraber, Sandra. Living Downstream: An Ecologist’s Personal Investigation of Cancer and the Environment (p. 11-16). Da Capo Press. Kindle Edition.

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