Breasts (14 page)

Another phthalate metabolite, MEP, was also surprisingly high for me, 654 ng/mL versus the national median of 127. Annabel’s was much lower at 18.2, but pity the young girl in the BCERC study whose level came in at 2,580. Preliminary data suggest MEP may be weakly linked to breast size in the girls. (But that could be due to related exposures in girls who wear a lot of fragrance, since many things in fragrances are estrogenic.) The girls with the highest levels had slightly more advanced breast development. After detox, I brought my level down only 66 percent. This metabolite comes from DEP, which is used in lotions, perfumes, and soaps.

Annabel and I also clocked high levels of other phthalate metabolites called MCPP and MEHHP. The former comes from vinyl gloves, garden hoses, cables, adhesives, and food packaging sealants. The latter can be found in products made with vinyl, including plastic wrap, toys, and consumer products. It has been associated with liver toxicity, decreased testicular weight, and testicular atrophy in rodents fed high doses. I was able to bring my levels for these down 62 to 95 percent, but Annabel only 5 percent, and her levels were higher than those in 95 percent of the girls tested.

For parabens, a whole other class of chemicals added as preservatives
to cosmetics and to food products, I alone showed high levels followed by big drops. Females tend to have levels three to seven times higher than males. The CDC calls them weakly estrogenic and says human health effects are unknown.

What these tests tell us is how stunningly easy it is to get relatively high levels of biologically active chemicals into one’s body. In just a few days of using mainstream toothpaste and deodorant, I scored off the charts for body burdens of triclosan and MBP. The good news is we know how to reduce some of our contaminants through better shopping; the bad news is it’s so hard to do. What if you don’t want to brush your teeth with an endocrine-disrupting pesticide? What if you’d rather not moisturize with printing inks and industrial solvents? Well, unless you have a chemistry lab in your basement, you’re out of luck, because most labels won’t tell you anything. (In the United States, foods, drugs, and cosmetics are exempted from federal reporting requirements.)

One lesson is that the “cleaner” you are—at least by the standards of consumer culture—the more contaminated you are. Another is that these are just a few of many, many biologically active compounds coursing through our bodies. “There are zillions of phthalates,” said Rudel. “There might be some other important commercial ones that are endocrine disrupting. But they’re not tested, so we don’t know.”

Partway into this project, I ran across a publication from the NIEHS. It described a talk given by George Bittner, a professor of neurobiology at the University of Texas, Austin, called “Are Plastics without Estrogen-Active Compounds Possible?” I found the title a stunner. It implies that nearly all of the plastics in our lives
are
estrogenic. And in fact, according to Bittner, that is the case, at least with common kitchen plastics. I gave him a call to learn more.
Bittner and his colleagues chopped up hundreds of products ranging from plastic wrap to soda bottles and storage containers. Then they broke each of them down in a saline solution, and fed the extracts to estrogen-sensitive breast cancer cells. Over 90 percent of the extracts they tested made the cells grow, including many that were BPA-free. “The results were rather striking to us,” said Bittner, who has founded a company to test plastics. “We had not anticipated it. There are hundreds, maybe thousands of chemicals used to make plastic that have estrogenic activity.”

OF COURSE, THE QUESTION EVERY PARENT WANTS ANSWERED IS,
What do all these exposures mean for our breasts and bodies?

Just because a chemical is sitting uninvited in your cells doesn’t mean it’s necessarily doing harm. This is a point the chemical industry loves to make: the amounts of chemicals released into our bloodstreams are so tiny, it’s inconceivable that small quantities of additives from face cream or ATM receipts could be altering our bodies. The industry would prefer that people not even look for these chemicals; what’s the point other than to cause needless anxiety?

These were the standard arguments used for decades to justify the unregulated presence of chemicals in the market. But scientists have two new tools with which to challenge the industry: first, they are using dazzling new technologies to measure small amounts of chemicals never before seen in our bodies; and second, with that advance comes the ability to see how these newfangled molecules could be gumming up biological systems.

Tom Burke, the former director of science for the state of New Jersey, was one of the first people in the country to get his body fluids
tested for the presence of industrial chemicals, and he defends the practice. Now the director of the Risk Sciences and Public Policy Institute at Johns Hopkins, Burke believes that the more people know about what’s coursing through their bodies, the more likely industry will be to adjust the ingredients. “Sometimes the best management is a little sunshine,” he said. Soon it will be as routine for people to test their bodies for these substances as it is to test their blood pressure. “We now know what different blood pressure levels mean and what diseases are associated with them,” he said. “That is also where we are with lead and mercury and where we should be with other substances.”

But we’re not there yet. Just how might our moisturizers and sunscreens be causing earlier breasts? As we’ve seen, many of the molecules in everyday products look like estrogen, with structural rings held together by carbon atoms. It’s possible that these substances are bypassing the body’s normal hormone-making process, attaching directly to estrogen receptors in girls’ breast tissues and switching them on before their time. Or they might be acting as “obesogens,” altering gene expression that governs fat storage (making girls fatter, for example). Nobody yet knows how the molecules might be causing miscues in a growing girl’s body. “What is scary is that we don’t have any idea what the mechanism is. It’s a big black box,” said Aksglaede, the bicycling Danish endocrinologist.

To find out how these substances work in the body, the BCERC researchers are looking at their effects, both singly and when combined, in lab animals, from tissues to cells to genes. Seven years into the study, the lab science is complex and unsettling. For one thing, it’s so new. It used to be that you took a sorry lab rat and dosed him with ever-increasing amounts of a chemical in question. When he keeled over and croaked, you knew you had a toxic effect. Soon
scientists got better at looking for obvious signs of sickness, such as severe weight loss or tumors. Then they started being able to look at DNA, and to changes in DNA caused by toxins. Now, researchers aren’t just looking at DNA mutations, but at how our environment triggers epigenetic changes—how in “normal” DNA, genes can be turned off and on in ways that make lab animals behave differently, reproduce differently, parent differently, metabolize differently, and get sick in much sneakier fashion. They are noticing disturbing effects that would never have been seen in standard toxicity studies.

Some scientists argue that in addition to our genome, we should be mapping our “exposome,” the environmental exposures that change our cell behavior. As we learn more about DNA expression, it’s becoming increasingly apparent that human biological systems depend as much on external cues as on the code itself.

DRS. JOSE AND IRMA RUSSO ARE CONDUCTING SOME OF THE MOST
revealing experiments out of their Breast Cancer Research Laboratory at the Fox Chase Cancer Center in Philadelphia. The Russos met in a lab in Argentina and have hardly stepped outside one since, except to attend conferences, where they are coveted speakers. I first met them at a BCERC conference, and BCERC funds quite a bit of their work. “We wrote an abstract together in medical school,” said Irma. “Our passion for science flourished into romance, and we’ve been talking about the same science ever since.” Both in their sixties, they immigrated nearly forty years ago to work as pathologists at the renowned Michigan Cancer Foundation. They spent nineteen years there studying, among other things, the effects of estrogen on cell growth. Jose is small and trim, with short-cropped copper hair and glasses that seem to cover half his face. Irma is
elegant and warm. Their maternal-nerd combo is perfect for nurturing a lab full of hard-driving international scientists and postdocs. It’s a family affair. Their daughter worked as a tech there during college summers, and Irma makes sure the staff eats well during lunch meetings.

I visited them in their adjoining offices one snowy day in February. The oath of Hippocrates hangs on the wall between photos taken of their lab employees over the years and a few diplomas. Like good couples should, Irma proceeded to tell me about Jose’s groundbreaking research, but she was frequently interrupted by Jose telling me about Irma’s. For example, Irma pioneered using a rat model to study how the breast develops, because she found that rats have mammary glands (even if they have six of them) very similar to human mammary glands. Because breast cells are dividing like mad during puberty, the Russos have found that puberty is a very vulnerable time for these cells to be exposed to possible carcinogens. Their lab work has borne this out, over and over. Jose told me that “window of susceptibility” is a term Irma invented. “Around puberty, if something happens, there’s an impact,” said Jose in his thick accent. Added Irma, “If a girl has X-rays at twelve, she will have cellular damage.”

I thought back to the X-rays I got at exactly that age for minor scoliosis. It seems somehow unfair that in addition to all the other troubles girls face during those tender adolescent years, even their cells are vulnerable.

Examples from the atomic bombs dropped on Hiroshima and Nagasaki are telling. Among girls who were exposed to the fallout, breast cancer rates (as determined decades later) were highest for the girls who were younger than ten when the bombs fell, and also high for girls between ten and twenty. They were lowest for women who
were between twenty and forty. For many women, this would be after pregnancy has protected their breasts and before the increased vulnerability of menopause.

To further explore the unique windows of harm for the mammary gland, the Russos have been dosing their lab animals at different stages of development, from prenatal exposure to prepubertal to later. One of the main chemicals they use to “assault” the rodents is the favorite egg-crusher of Patricia Hunt and one of our most ubiquitous daily-life substances: BPA.

In one particularly revealing experiment, they gave some young, “child-aged” female rats a hit of BPA, a bit higher than what we humans are exposed to everyday, and they left other rats alone. Then they let all the rats grow to early middle age, whereupon they exposed them to a known carcinogen called DMBA. The rats that had been given BPA before puberty grew more mammary tumors, and got them faster, than the control rats. To find out why, the Russos took apart the tumors and analyzed their genes. The BPA-dosed rats had altered DNA expression that supported cancer growth.

Here’s a quick mini-lesson in cancer cell biology. For cancer to do its thing, a number of cellular events have to happen. These events generally fall into two categories: the
promotion
of cell growth (including gene transcription, replication, division, invasion, blood sucking, food gathering, and other delightful habits of a tumor) and the
suppression
of cell death (think of riot police who control unruly mobs, only now they’re on strike). Genes in our bodies control these processes, and they are known, respectively, as oncogenes and tumor suppressor genes.

If we don’t want cancer, we have to coddle our tumor suppressor police. We don’t want them to go on strike, or get sick, or go rogue. This is, tragically, what happens to people who have the mutated
breast cancer genes, BRCA1 and BRCA2. Those are technically suppressor genes, acting as DNA repairmen, and they haven’t been working right in some families for thousands of years. One more recent variant of BRCA2 was traced back to a single “founder mutation” in Iceland in the mid-sixteenth century. It’s a heck of a family legacy; around 80 percent of women born with bad BRCA genes will get breast cancer. The ones who don’t get cancer probably have some other lucky genes to help them compensate, or maybe somehow they manage to skate through their developmental windows without any serious carcinogenic exposures. Women with the BRCA genes are much more likely to get cancer if they were born after 1940 than before, a fact attributed to everything from changing reproductive patterns, to body size, to the rise in the use of synthetic chemicals produced after World War II.

BPA appears to turn off some of our blessed suppressor genes and at the same time turn on the bad tumor promoters, the oncogenes. Some of us can resist these events better than others. Remember, the breast is the body’s only organ that still has to do most of its basic construction well after birth. Therein lies some of our problem. With change comes instability. An organ incredibly responsive to cues both outside and inside our body, breasts are too trusting. That quality served them brilliantly in our evolutionary past, but it has not prepared them well for the modern age.

The Russos found that the rats exposed prepubertally were worse off than even the rats exposed in the womb, reinforcing the idea that the time near puberty, when the organ is growing fast, is the most vulnerable, at least to BPA. Their theory is that in order for breasts to form, there are “mammary progenitor cells” that are actively dividing at this time, and they are particularly responsive to hormonal signals. When their genes get messed up during this
developmental tumult, they’ll have a harder time warding off disaster later in life.

Jose’s not-very-practical take-home message: “Avoid the exposure of young girls to these compounds.”

IF EARLY PUBERTY IS, AS WRITER SANDRA STEINGRABER PUTS IT,
an “ecological disorder,” what’s a mother to do? Is it possible to keep Annabel on the childhood farm a little longer? Larry Kushi, a BCERC scientist and associate director of research at Kaiser Permanente, points to childhood diet as one area over which parents can exert some control. In recent experiments with adolescent rats, a high-fat diet led to inflammation, and later, cancer, in mammary glands. Kushi encourages more whole grains, more vegetables, and less meat. Kushi, the son of macrobiotic food entrepreneurs, is also a fan of tofu, which appears to have some preventative effects as far as early breast budding.