Breasts

by Florence Williams

  By turning vegan for three days, I avoided meats and cheeses wrapped in plastic. I also knew I might drive my levels down by not eating animals that absorb chemicals from their food and water. The higher up the food chain, the more nasties you’ll find. Large marine mammals are probably the most polluted creatures on earth. Regardless of how many chemicals I avoided, I lost three pounds.

  So how did our body burdens measure up? We compared my levels to those of other adults in the Silent Spring Institute/Breast Cancer Fund’s five-family study, as well as to the much larger CDC database. We also compared Annabel’s levels to those found in the BCERC study of hundreds of other six- to eight-year-old girls.

  For BPA, my before level, as measured in urine, was 5.10 nanograms/milliliter (ng/mL), or parts per billion. That level vaulted me just into the upper quarter of the American range (U.S. levels are, incidentally, twice those of Canada). My after-detox level was 0.80, a drop of 85 percent! Most BPA we consume only lasts about half a day in our bodies, so three days of plastic avoidance, fresh food, and veganism really worked. Annabel’s levels went from 0.80 to 0.65, a drop of 18 percent. Annabel didn’t have any soda during the before phase, which is perhaps why her levels started where mine ended. Interestingly, though, her levels dropped lower than mine during detox, maybe because of my polycarbonate glasses or some other mysterious exposure. Our detox BPA values beat those for most of the other families in the study, but we were unable to eliminate our exposure altogether. “You weren’t able to go to zero, and that’s consistent with other data out there,” said Fred vom Saal, a biologist at the University of Missouri who specializes in BPA research. “We need to find out more about where this stuff is used.”

  My high before level is still considered plenty safe by the EPA. My level, in fact, fell about four hundred times lower than the agency’s magic danger number. That should be reassuring, but vom Saal warned me against feeling smug. He and others argue that the EPA safe dose is woefully out of date, based only on a few thirty-yearold toxicity studies and not on more current research of “low-dose” effects on animal endocrine systems. In fact, vom Saal told me that my initial level of 5.10 is “getting toward the red zone in terms of being related to metabolic abnormalities [in animals]. Anything you can do to lower your exposures would be good,” he intoned. Vom Saal’s lab is currently investigating low-dose BPA exposure and urethra disorders. Guess I’ll be rethinking those refried beans.

  For triclosan, we got similarly spectacular detox action. The cutting-board chemical, triclosan is also added to soaps and other products as a disinfectant. Lunder’s organization, Environmental Working Group, has sniffed it out in everything from toothpastes to deodorants to children’s toys to shower curtains. Despite its dubious benefits, the “microbicide” has been a flat-out marketing success, appearing in 76 percent of commercial soaps. Unfortunately, it’s also been shown to disrupt thyroid hormones in frogs and rats.

  In humans, triclosan can be absorbed through the mouth and intestines, as well as through skin. It accumulates in fat and doesn’t exit the body as fast as phthalates or BPA. The median level in U.S. children is 9.8 and in adult women, 12.0. In the BCERC group of girls, the median level was 7.2. Annabel’s before level was considerably lower than average, 3.7, but mine came in at a whopping 141.0 after I amped up my daily hygiene routine with supermarket toothpaste, bubble bath, moisturizer, deodorant, and soap. Annabel joined me in the florid, floral bath. After detox a week later, she brought her levels down 48 percent, and I brought mine down 99 percent, to 1.3 (my underarms went au naturel and I used “natural” products on my teeth and skin). By tweaking a few of my habits over one week, I went from over ten times the mean to one-tenth of it. Still, why couldn’t my ascetic ways zero it out? Probably because triclosan is now found in drinking water and food all around us.

  Another notable chemical group we tested was phthalates. There are many types of phthalates, and each has its own molecular weight and function in commercial products. Typically, the phthalates are measured by their metabolites, or what the molecules look like after circulating and exiting the body (again in urine). For example, one called MBZP, which is used to soften plastics, can be found off-gassing in car interiors. Another, MBP, is a breakdown metabolite of dibutyl phthalates, which, according to the CDC, are used in industrial solvents, adhesives, printing inks, pharmaceutical coatings, pesticides, and as additives in nail polish and cosmetics. Once these enter your body through your mouth or skin, half of them will be gone within 24 hours, at least until the next time you moisturize or eat. A memo released by the U.S. Consumer Products Safety Commission states that dibutyl phthalates “have become ubiquitous in the environment, and can now be found in food, water and air.” Considered an “anti-androgen,” MBP has been associated with genital abnormalities in rats and humans, decreased testosterone levels in men, and unusual mammary growth in male rats, among other problems.

  The median daily level of MBP in U.S. adult females is 28.3 ng/ mL. Hold your hat: my before level was 375, or triple even the highest reported percentiles of all Americans measured by the CDC. But hold your hat one more time, and keep it off in tribute to one girl tested by the CDC: an eight-year-old Mexican American who logged in at staggering 101,000. Ruthann Rudel thinks this girl’s parents should be notified, but that is not currently the policy of the CDC, especially when there is no clear clinical protocol for treating it, as there is for lead or mercury poisoning. “I want to help her, because I’m a mom and because this is a very high level,” said Rudel.

  Even after detox, my levels dropped to 63, still more than double the U.S. median. Rudel was stumped. “Both your levels were way higher than anyone else in the study,” she said. Did I use nail polish remover right before detox? (I had.) Did I take medications? (Yes, for low thyroid.) Was I spending too much time with my printer? (Perhaps.) But Annabel’s levels were also strangely high, finishing even above mine at 80 ng/mL, or double the median for girls her age as measured in the BCERC study. This is weird and, I’ll admit, a little disconcerting. I have no idea why her levels were unusually high. Was she being exposed through food packaging in the school cafeteria? Was her toenail polish that potent? Is it because of the sunscreen I slathered on her for soccer practice? Then there was her school bus. While I was biking everywhere, she was sitting on vinyl seats.

  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 tric
losan 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 wh
o 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.