Still she went on growing, and, as a last resource, she put one arm out of the window, and one foot up the chimney, and said to herself, “Now I can do no more, whatever happens. What will become of me?”
— LEWIS CARROLL,
Alice’s Adventures in Wonderland
ON THE AFTERNOON SONYA LUNDER CAME TO VISIT, I was, as usual, madly making after-school snacks for the kids, who are seven and nine. It entailed scooping some dip out of a store-bought plastic container, peeling carrots, and slicing some cheese. The kitchen is where love and guilt—those dual sirens of parenthood—merge at their most intense. It was a fitting place to begin planning a chemical-body-burden experiment. At the heart of the experiment lies one central fact: girls today are getting breasts earlier than ever before.
Lunder works as a senior toxins analyst for the Environmental Working Group. The mother of two small children, she has taken her knowledge of chemicals into realms I never imagined. At the gym where our kids take classes, she noticed the big foam blocks in the “pit” that students land in as they jump off a rope swing. She asked the gymnastics director if the foam was treated with flameretardant chemicals, which are known to slough off and accumulate in human tissues. To his credit, he’d actually considered the question before and told her he tries to get untreated foam. She encouraged him in her friendly Sonya way to keep trying.
In my kitchen, Lunder zeroed right in on the fridge. Even the door’s water dispenser attracted her attention. “You know, the water tubing is probably plastic,” she said. After noting all the plastic-contained food in my fridge—yogurt, juice, cheese, meats—she pointed to a cutting board on the counter. She asked if the original packaging had said “antimicrobial” on it. I shrugged. “If it did, that means it’s embedded with triclosan,” she said. She scrutinized my hand soap gel. I thought she’d be happy, because it was from a leading “green” brand and declared on the bottle that it contained no parabens. “Interesting!” she said, reading the smaller print. “It’s got benzophenone in it! That’s related to a sunscreen chemical linked to endocrine disruption in animals. Why would they put that in your hand soap?” she mused. “It probably keeps the contents from breaking down in UV light.”
Lunder was here to help me prepare for the detox phase of my home experiment, in which I would valiantly try to avoid exposures to chemicals to see if I could reduce my body’s levels of toxins. The experiment, designed with help from both Lunder and Ruthann Rudel, the toxicologist for the Silent Spring Institute, would incorporate a before and an after phase for both me and my seven-yearold daughter, Annabel. We would compare our levels to those of five other American families in a study sponsored by Silent Spring and the Breast Cancer Fund, both nonprofits interested in elucidating the environmental connections to breast cancer. In the first “tox” phase, Annabel and I would live our normal lives, absorbing hidden molecules of plastic from our food and the occasional canned beverage, as well as from shampoo and moisturizers purchased from the supermarket. In other words, for three days, we would be average Americans. Then we would pee into some glass jars and ship them to Canada for testing. A week later, I would enter detox for three days. I would become a vegan, avoid triclosan and plasticizers to the best of my ability, and have my urine retested. I would not drive (to avoid chemicals in the car upholstery and interior) and would only eat food that had never touched plastic. As a testament to just how foreign this is to the American experience, I couldn’t imagine getting Annabel to undergo full detox. It would mean no vehicles, no pizza, no bubble bath. I didn’t have the heart to put her through it. For much of phase two, I’d be on my own.
WHY BOTHER WITH ALL THIS? BLAME IT ON THE GOVERNMENT. For seven years, the National Institute of Environmental Health Sciences (NIEHS) and the National Cancer Institute have joined forces in a $40 million study trying to understand the forces behind early puberty and its link to breast cancer. I’d heard about the effort, called the Breast Cancer and Environment Research Centers (BCERC), and was closely following the results, which fall into three main buckets: chemical exposures, lifestyle (diet and exercise), and social factors (economic status, number of parents in the home, etc.). Data have been coming out of four research hubs across the country, in which a total of 1,500 girls were participating, beginning at the age of six. Already the information shows these girls have some of the highest body burdens of everyday chemicals yet seen. As a group, they also have the youngest breasts ever recorded. I was curious to know how our levels matched up, and what it all meant.
Scientists have known about the relationship between the age of puberty and breast cancer for a long time, ever since they began looking at lifetime estrogen exposures. Then in 1997, Marcia Herman-Giddens, a scientist at the University of North Carolina, published a bombshell of a paper. Her research indicated that girls were developing breasts and sprouting pubic hair one to two years younger than expected, with white girls getting breasts at a mean age of 9.8 years and black girls at 8.8 years (menstruation typically starts two to three years later). Within two years, experts revised the official definition of “precocious puberty” downward, from age eight to seven in white girls and from age seven to six in black girls. Welcome to the new normal.
The age of puberty matters. A 2007 report for the Breast Cancer Fund notes that if puberty can be delayed by one year in girls, thousands of breast cancers could be prevented. Suzanne Fenton, a scientist with the Reproductive Endocrinology Group at NIEHS, went even further. “We think that puberty may be the main driver in the risk of breast cancer,” she told me. If you get your first period before age twelve, your risk of breast cancer is 50 percent higher than if you get it at age sixteen.
Why? It might have to do with hormones. Earlier puberty means an additional few years of estrogen and progesterone flooding the breasts and causing cellular changes. Or it could be that estrogen gets metabolized by the body into some toxic by-products that create free oxygen electrons and can damage DNA. But why would an extra year or two have such a big effect given our long lifetime of ovulating? Another theory is that puberty—with all its inherent cellular instability—causes breasts to be extra vulnerable to carcinogens. If puberty comes earlier, that window of vulnerability is open for longer. The new government-funded research attempts to answer some basic questions: What causes early puberty? Is it something we can possibly manipulate?
I got my first period when I was eleven. Annabel is likely to fall on the early side too, since the magic number is driven partly by genes. At seven, she is the perfect age to examine suspected environmental factors. We’re testing for some of the same chemical candidates investigated in the BCERC study: BPA, phthalates, triclosan, parabens, and flame-retardants, all common substances known to mimic sex hormones or otherwise interfere with their normal coursings through the body.
When I look at Annabel, I see total prepubescence. She sings and twirls around and makes elaborate rooms and nests for her dolls and stuffed animals. She is still drawing figures that are not anatomically endowed. It’s almost inconceivable to imagine that some girls her age are actually wearing bras. To put the data into perspective: by 2011, one-third of black girls between the ages of six and eight were “budding” breasts (that’s actually the technical term) or growing pubic hair, along with 15 percent of Hispanic girls, 10 percent of white girls, and 4 percent of Asian girls. Some of the breast budding is correlated with obesity. We live in the thinnest town in America—Boulder, Colorado—and not many of the mostly white, professional-class kids in Annabel’s elementary school are overweight. Still, the fourth- and fifth-graders are maturing here earlier than they did when I was their age. Today, half of all girls in the United States start popping breasts by their tenth birthday, well ahead of girls of the Brady Bunch era.
If you’re a parent, this should make you nervous. Puberty has got to be one of the strangest and most profound experiences we humans undergo. Breasts and hair appear out of nowhere, voices drop, personalities change. We get hijacked by hormones and taken to another planet. It would all be comical if it didn’t involve teenagers doing so many stupid and hazardous things involving their bodies, high-speed vehicles, and illicit substances, sometimes all at the same time. Girls’ bodies begin to enter an uneasy and public arena of male attention. We probably all remember that exquisite tension between wanting to show off our new breasts and not wanting anyone creepy to notice them.
I started getting breasts around the summer between fifth and sixth grade. That’s when my father gave me a book about girl power. His girlfriend, a librarian, had recommended it. The gist of it was how to say no to boys or men who wanted you to do things you didn’t want to do. I was uncomfortable reading it. I was uncomfortable discussing it with him. I just wanted to think about my new blue Princess phone and calling my girlfriends.
By the next summer, when I was twelve, I had small but shapely little mounds. I was now tall enough to wear some of my mother’s clothes, a rite of passage in itself. She had a designer T-shirt, an incredibly soft, thin weave in orange and green stripes. It must have shrunk in the wash because I don’t think it could have fit both of us. She was a 36D, and I was probably a 28AA. But the shirt fit me, and I claimed it. It was a treasure. Between the thin cotton and the stripes, I knew it made the most of what I had.
That summer I traveled out West with my father and some family friends, including two teenaged boys. I wore the shirt often. One day we hired a guide and some horses and rode out to see some ancient ruins in the Arizona desert. It was a long ride over rough country. On a couple of occasions my horse lagged behind and out of sight of the others. Our guide, a youngish Navajo cowboy, would come galloping back to me, reach out, and give my nearest breast a squeeze. He would roar with laughter and try to do it again. I rued my slow horse, my striped shirt, and my posse for leaving me behind. I goaded that old horse until I finally caught up with the others.
A few months later, in the completely different canyons of New York City, I took a taxi with two friends across town. After we paid our fare, the driver reached back through the open Plexiglas window and groped us as we slid across the seat to the door. That time I cursed him out and slammed the door. Maybe my father’s assertiveness training had gotten through. I was now in the brave new world of boobs.
How many girls have memories like this, or worse? Probably all of us.
It’s hard enough to stand your ground as a preteen. But an eight-year-old is pretty much incapable of it. Little girls aren’t emotionally equipped to handle the challenges of puberty. Teens barely are. Girls with breasts are the targets of teasing and jokes by their peers, and statistically they’re more likely to be victims of sexual assault. Studies have shown that prematurely developed girls are at greater risk of substance abuse, depression, and suicide.
Lately, the advent of earlier puberty has converged with the advent of 3G and 4G video-phone technology. The tragic result, according to pediatrician Sharon Cooper of the University of North Carolina School of Medicine: more cyber-sexual exploitation of very young girls.
WHILE THE DECLINING AGE OF SEXUAL MATURITY IS WORRISOME, it’s important to know that it’s not entirely new. Here’s the general evolutionary scenario: if you can eat more, you can reproduce earlier, resulting in more offspring. And in fact, our ascent out of caves and hovels has meant that the age of sexual maturity in girls has dropped slowly but steadily, about three months per decade, since 1850. The reasons for the change were expected and benevolent: better nutrition and less infectious disease. But does this mean that we’re designed by nature to have babies as early as we possibly can? Not necessarily.
Humans, as we’ve seen, are unusual creatures. One of the ways in which we are unique lies in our prolonged childhood. We take longer to reach sexual maturity than any other primate, meaning we sit around for more time being relatively useless with regard to the propagation of our species. (Chimps, by contrast, become mothers when they’re six to nine years old.) There are good reasons for our dawdling; namely, our bodies and brains are big and grow slowly. The longer we hold off puberty, the taller and stronger we’ll be and the greater the likelihood our offspring will be healthy too. (One of the reasons boys grow taller than girls is that they reach puberty later. The sex hormones that come with puberty, such as estrogen in girls, actually seal the bones from growing more. Sometimes estrogen is given to prepubertal girls by doctors who believe they are growing too tall too soon, which will likely go down as a bad idea in the annals of pediatric medicine.)
Having a long childhood, though, takes a toll on parents and society. Kids need resources, a whopping 13 million calories approximately, before reaching adulthood. For some populations of humans—those with fewer resources—that toll is harder than for others. This may partly explain the great natural variation in age of puberty from eleven or twelve to sixteen. Although girls tend to reach puberty about the same time their mothers did, there’s still a lot of wiggle room.
Here’s where we give another nod to the power of our environment. Breasts are like little antennae, processing information out there in the neighborhood and bringing it home. Among other things, the environment tells breasts when to show up. Evolution designed our bodies to be responsive to all sorts of cues, including the nutritional status of our mothers and even, remarkably, our grandmothers.
Even though genes account for some of the timing of puberty, the environment determines when and how the genes get switched on. When a woman’s prenatal nutrition is good, her baby’s fetal cells program themselves for earlier puberty. When it’s lousy, the opposite occurs. And along the way, there’s still opportunity for course corrections. When poor, once-hungry immigrants move to industrial countries, suddenly encountering “nutritional excess,” the girls’ bodies recalibrate. Adopted Indian girls who move to Sweden as infants, for example, reach puberty uncommonly early. They also gain weight faster than their Scandinavian peers, having been programmed in the womb to store more calories as fat.
Okay, so now we know the age of puberty naturally fluctuates. That doesn’t mean we should shrug it off. The Herman-Giddens data suggest that between the 1970s and the 1990s, the age of puberty dropped much faster than expected. Perhaps the latest oscillation isn’t so “natural” after all.
There’s no doubt modern society, with its overnutrition and better medicine (as well as perhaps its industrial pollutants), has caused the age of sexual maturation to fall. Ironically, though, this same complex modern world means we need more time for what experts call “psycho-social maturation,” or time to figure things out. The human brain takes two decades to mature, especially the prefrontal cortex, which governs self-concept and the control of impulses and reward-seeking. It’s arguably a lot harder to be a young mother now—with all our social and familial fragmentation—than ever before. Evolutionary biologists call this a “mismatch.” Our bodies are responding to one set of determinants, but our brains don’t appear to be catching up.
Our Paleolithic legacy has left us with other mismatches, such as obesity and diabetes. It’s becoming increasingly obvious that our bodies weren’t designed to handle modern, industrial diets. While metabolic diseases have received a lot of attention, the changing age of puberty hasn’t. But it should. Peter Gluckman is a biologist at the University of Auckland in New Zealand and a pioneer in a field known as evolutionary medicine. As he puts it, “For the first time in our evolutionary history, biological puberty in females significantly precedes, rather than being matched to, the age of successful functioning as an adult.”
WHAT EXACTLY IS IT ABOUT OUR MODERN ENVIRONMENT THAT’S driving the age of puberty toward toddlerhood at an ever-increasing pace? The government’s BCERC study posits the broad hypothesis that “chemical, physical and social factors interact with genes” to set breasts on their inflationary course. Many of those factors are new in our human life history. The research is divided into three areas: animal studies, human breast cell studies, and real-life, whole-person studies. It may be our best hope for understanding some of the key unanswered questions behind the mysteries of puberty and breasts.
Although it’s tempting—for both the researchers and people like me—to try to identify a single culprit for early ballooning bosoms, we won’t be easily gratified. One thing seems clear: many factors lead to the complex, multistaged “event” of puberty.
Obesity has long been the leading contender in the earlypuberty sweepstakes. Everyone in the field knows that the percentage of American girls aged six to eleven who are obese more than tripled, to 16 percent, between 1974 and 2006. Nearly a third of girls are now labeled overweight. Although the exact timing of puberty remains wrapped in mystery, the role of fat is partly known. Where there’s fat, there’s also the enzyme aromatase. Aromatase helps convert the building blocks of steroids—cholesterol—into estrogen. Fat has been called “the third ovary” because of its ability to make estrogen. The crude equation is more fat equals more estrogen, and this is true even in men, witness man boobs. Fat also increases levels of leptin, a hormone that tells us when we’re hungry, and also seems to fire up the puberty engine. Leptin levels have been found to be higher in African Americans than in other groups. But fat is not the whole story, not by a long shot. Otherwise, fat babies would be oozing in estrogen, and they’re not. And obese women often have less circulating sex hormones because they don’t ovulate regularly.
Puberty is like an orchestra. The ovaries are the violins. Fat cells are the oboes. We have some sort of internal conductor that tells the parts when to make their music. Some call it a gonadostat— literally, a thermostat for our sex gonads—and it sets our pubertal tempo. Whatever it is, it’s regulated by the hypothalamus in the brain, the director of the symphony, and that in turn responds to all sorts of internal and external cues in the forms of enzymes and hormones.
The BCERC researchers are devoting a lot of time to studying diet and exercise, regularly asking the 1,500 girls what they’re eating and how often they visit playgrounds, play sports, and walk to school. So far, there appears to be some relationship between the amount of fiber in their diet and the age at which they get breasts. The more fiber and vegetables they eat, the later they enter puberty. Another study out of Britain in 2010 found that girls who reached puberty earlier ate more meat than their peers, with the biggest carnivores maturing earliest.
Said Dr. Frank Biro, a pediatrician and coinvestigator of the BCERC study from the University of Cincinnati, “The nutritional factor consistently associated with timing of puberty, in those societies where there are sufficient calories for all members, is fiber. Higher fiber equals later maturation.” This is probably because of the way some genes interact with fat, he says.
Fair enough, but as Biro himself acknowledges, diet alone doesn’t seem to explain the puberty clock. I never totally bought the simplistic fat-triggers-puberty argument. I went through puberty a good year earlier than all of my friends, and I was skinny as a rail and always had been. Doctors and cancer scientists know that plenty of thin girls fall on the early side of the puberty curve.
It turns out that while fat may trigger one pathway to puberty, there are other pathways as well. Some girls get breast buds as their first sign of puberty. It may be months or years before they grow pubic hair or get their periods. Other girls grow pubic hair first, with nary a breast in sight. Pubic hair is influenced more by adrenal hormones than by estrogens. So you might think this means you’re off the hook for breast cancer if you were thin, but, maddeningly, it doesn’t. In fact, thin girls who menstruate early are at slightly higher risk of breast cancer later on than their pudgy peers. In a recent Swedish study, researchers found that women who had fatter bodies during childhood were 27 percent less likely to have breast cancer than women who were leaner as children. I was tall and thin as a fourteen-year-old, and it turns out both of those traits are linked to higher breast cancer risk.
Because of the holes in the obesity theory, I was curious to visit the lab of pediatric endocrinologist Lise Aksglaede in Denmark. Her office at the Rigshospitalet of the University of Copenhagen looks out over the west side of the city and its lakes. She was late for our appointment and came bounding in, breathless, from her hurried bike ride across town. Like nearly one-third of all workers in the city, she bikes to the office every day. And like nearly everyone here, she’s fit, blonde, and peppy. I suspect the fit and peppy parts come from all the biking. According to various happiness indices, the Danes are among the happiest people on earth, despite terrible North Sea weather and a crippling tax code. In her mid-thirties, Aksglaede is still breast-feeding her one-year-old son, chalking her up as another statistical norm; breast-feeding rates in Denmark are double those in the United States.
Wondering whether the American puberty data were really so unusual, she decided to take a closer look at her hometown. She and her colleagues examined almost one thousand girls in 2006 using the exact same protocols as a similar study in 1991. It turned out that the girls—all white and middle class—started budding breasts a full year earlier than they had just fifteen years ago. (The age of menstruation had advanced only about four months.) But the real head-scratcher was that the change in the girls’ body weight was minimal and couldn’t account for the difference. Nearly all the girls were relatively thin, said Aksglaede.
So if fat isn’t setting the puberty clock for these girls, what is?
There are three other leading theories: artificial light, divorce, and highly sexualized media. The light theory hinges on melatonin, a hormone that flows from our pineal gland at the center of our brain to our hypothalamus, telling it to quiet down (the hypothalamus, remember, regulates our gonadostat). We make melatonin in darkness. Women who are blind make more of it, and guess what? They have a lower risk of breast cancer. By contrast, women who work under lights on the night shift at work have a higher risk.
Nighttime light—in the form of computer and TV screens, electric overhead lights, and the ubiquitous hallway night-light—is clearly not something we evolved with. Some researchers speculate these girlhood light exposures could be suppressing natural melatonin levels, and in turn speeding up the gonadostat. Studies have found that girls with precocious puberty have unusually low levels of melatonin, while female athletes have high levels. (Note to self: remove the nightlight from Annabel’s bedroom.) The problem, though, with the light theory is it doesn’t totally explain the difference in just fifteen years in girls in Copenhagen. Presumably, even with their crippling tax code, Danes had plenty of electric lights in 1991.
Let’s look at the divorce theory: it’s been documented that girls not living with a biological father tend to mature earlier. Female elephants do something similar in the absence of a parent. It makes some survival sense that populations under stress would be more desperate to reproduce, even if they can’t raise the next generation in an optimal environment. The absent-father theory could account for my early age at puberty. My parents divorced when I was two. But it couldn’t explain all of today’s girls, because families are actually slightly more stable now than they were two decades ago.
Which leaves us with the boobs-and-sex-all-over-the-media theory. It sounds reasonable, but if girls are becoming more sexualized from a constant stream of media images, their hormone levels would also be rising, and oddly, that’s not happening. While the Copenhagen girls are growing breasts earlier, their bodies are not making any more estrogen than they were in 1991. To Aksglaede, this indicates that the source of estrogen—needed for breast development—must lie somewhere else.
“Our best suggestion is that [the source] is something from outside,” said Aksglaede. “The main discussion is environmental factors.” Specifically, chemicals that mimic hormones, many of which girls are exposed to every day, even in Europe, which is only now just starting to regulate them. Endocrine-disrupting compounds, as we saw in the last chapter, include the much-publicized baby-bottle ingredient BPA, as well as other ingredients in plastics, pesticides, and compounds in cigarettes, among many others.
The BCERC’s Biro agrees, to a point. “Heavier girls are more likely to enter puberty first,” he said, “but something above and beyond that is going on and that’s where it gets really interesting. There are lots of others who believe that chemicals are the major cause. I believe that they are clearly contributing.”
Not all experts are convinced. Dr. Paul Kaplowitz is the man behind revising the clinical age of “precocious puberty” after Herman-Giddens’s groundbreaking study came out in the 1990s. “The environmental puberty hypothesis is interesting,” said Kaplowitz, the chief of endocrinology and diabetes at Children’s National Medical Center in Washington, D.C. “But my position is that we need more information on environmental exposures. I’ve gotten into the habit of asking my patients with early puberty if they’re using hair care products, essential oils, lavender, tea tree oils, and so on. It’s pretty rare for them to say yes. The phthalates and the BPA are plausible. But if external estrogens were really affecting girls, you’d think you’d see more breast development in boys as well. We do see some of that, but I haven’t seen a big increase,” he said.
Biro counters this argument by pointing to studies suggesting that boys are indeed showing signs of unusual estrogen and antiandrogen exposure, such as smaller penis sizes, decreased sperm counts, and shorter distances between the genitals and anus, all of which are considered markers of “feminization.” By some estimates, the once-rare birth defect of undescended testicles in baby boys is increasing in the United States and parts of Europe. In a study of 1,600 babies born between 1997 and 2001, Danes had smaller testicles than the Finns. Scientists know this because they expertly measured “ellipsoidal volume” and found the Danish package lagging at birth. The differences were even more pronounced after three months, with the Finns averaging three times more testicular growth. Researchers went back and tested samples from the babies’ stored blood and their mothers’ breast milk in each country. Danes are known to smoke and drink during pregnancy, but that didn’t seem to explain the genital effects. Then other hormone-monkeying suspects turned up at relevant levels: certain industrial chemicals. As researcher Katharina Main, who works across the hall from Lise Aksglaede at the University of Copenhagen, told me, “It’s higher here. The higher your [chemical] burden … the higher the risk of undescended testes.”
IT’S BEEN WELL DOCUMENTED THAT PUBERTY CAN BE SWAYED BY chemical exposures. Lead and dioxin (a by-product of combustion), for example, are known to delay puberty in both animals and people. The pesticide DDT has been associated with earlier puberty in girls, and PCBs (polychlorinated biphenyls, used as industrial greasers) have been alternately linked in separate studies with both delayed and advanced puberty.
But external culprits are hard to pinpoint. Consider the weird epidemic of precocious puberty in Puerto Rico during the 1980s and 1990s. So many very young girls (under age five) were developing breasts that the government there established the world’s only “early sexual development registry” to record it. The incidence there turned out to be eight out of every thousand girls between 1984 and 1993, eighteen and a half times higher than the incidence in the United States. Why would Puerto Rico be the world’s hot spot for toddler breasts? The cause appeared more geographic than genetic, because Puerto Ricans in the mainland United States had normal development, and the problem was afflicting other ethnic groups living in Puerto Rico as well.
Journalist Orville Schell describes interviewing a Puerto Rican pediatrician and seeing Polaroids of some of these children in 1982:
In the first photo, a four-and-a-half-year-old girl with delicate coffee-colored skin, doelike brown eyes and almost fully developed breasts lies on an examining table. She smiles with a sweet innocence at the camera, seemingly unaware of the dramatic changes that have gone on in her body.
“She had an ovarian cyst,” says Dr. Saenz [de Rodriguez] tersely.
A twelve-year-old boy stands against a white wall looking with blank bewilderment into the camera. He wears a silver crucifix around his neck, which dangles down between two grossly swollen breasts.
“We’ve had to schedule him for surgery,” says Dr. Saenz matter-of-factly. “The emotional stress on him is incredible.”
The children had reportedly eaten school-lunch chicken contaminated with high levels of DES, the same hormone Pat Hunt’s mother took to prevent miscarriage, as we learned in the last chapter. At the time, DES was given to farm animals to make them plumper. When many of Dr. Saenz’s patients stopped eating meat and milk, their symptoms improved. But an investigation—conducted after a considerable delay—turned up only average levels of the growth hormone in more than eight hundred subsequent food samples. Investigators also considered pharmaceutical wastes and agricultural pesticides, both widespread there, but again, there was no obvious evidence. One study did find unusually high levels of phthalates in the blood of girls with early breasts, but there is the lingering possibility that those samples were accidentally cross-contaminated by plastics in the testing laboratory.
Phthalates are a family of molecules used as scent stabilizers in lotions and shampoos, and as common additives in plastics. Concerned over their health effects, the European Union will soon be restricting three types of phthalates from general use in commercial products. California recently banned several phthalates in products sold to the under-three set. Known endocrine disruptors, they’ve been recently linked to genital abnormalities in baby boys and increased “girl play” in toddler boys. It’s possible they may be turbocharging the future breast tissue of young or even unborn girls. One way to find out is to compare the urinary levels of phthalates in girls and see who gets the earliest breasts. (Unfortunately, it’s not enough to simply ask the girls which toys and personal care products they’ve used; companies are not required to list ingredients on their labels. The only reliable way to test exposures is to ask the girls for body fluids.)
The BCERC researchers are measuring girls’ blood and urine for fifty-one chemical substances, including phthalates, BPA, organochlorine pesticides, heavy metals, industrial solvents such as PCBs, and naturally occurring plant-based estrogens such as soy. Nearly all the girls have these substances in their bodies, sometimes in much larger concentrations than what is found in adults. There are also some geographical ticks: Girls in California are endowed with the highest recorded levels of flame-retardants, probably due to that state’s strict flammability standards. Girls in New York City carry more cotinine, a molecule found in cigarettes and secondhand smoke, as well as more 2,5-dichlorophenol, used in mothballs and room deodorizers, while girls in Cincinnati carry more PFOA, a chemical used in making products with Teflon.
The Centers for Disease Control and Prevention (CDC) releases measures of the so-called body burdens of girls every two years as part of its National Health and Nutrition Examination Survey. When the BCERC researchers in Cincinnati studied the values measured in their girls, they found that fully 40 percent of them carried levels of PFOA above the CDC’s last measured ninety-fifth percentile. The researchers are currently trying to determine why the girls had unusually high levels and whether PFOA is linked to early breast development, particularly in thinner girls.
African-American girls in the study bore considerably higher levels of phthalates (the fragrance stabilizer) and parabens (a preservative in personal care products), four times the level found in white and Asian girls. Could this possibly help explain why the proportion of African-American girls who reach puberty at age eight is four times greater than the proportion of white girls? Or why African-American women in their twenties have a nearly 50 percent higher rate of breast cancer than white women of the same age (above age forty, though, the white rate surpasses the African-American rate). Researchers would like to know.
AS I FOUND OUT FROM OUR HOME EXPERIMENT, PHTHALATES ARE everywhere. Since they bind fragrances, they’re often present in our shampoos, soaps, and moisturizers. They are an important ingredient in softening polyvinylchloride (PVC), so they waft out of things like shower curtains, plastic toys, and fake leather. (There’s more fake leather lying around than you think. I had to throw out one of my daughter’s play wallets because it smelled so strongly of chemicals. My son has a belt made out of it, and it’s also common in sneakers. Now I have a radar for “pleather” when I go into box retail stores, and I steer clear.) Phthalates may also be present in sandwich bags and plastic wrap, but it’s hard to know for sure since manufacturers aren’t saying.
A newspaper in Taiwan recently reported that phthalates had been found in food such as baked goods. Apparently it makes them smell good even after many days on the shelf. This put officials in the absurd position of warning consumers not to buy food that smelled fresh.
For the before—or tox—phase of our experiment, I indulged in some very American habits, and Annabel joined me in some of them. For three days, we ate a couple of meals out of cans. (One out of every five U.S. dinners includes a can, according to the Canned Food Alliance.) Refried beans were a favorite. I drank a can of ginger ale at lunch and dinner. I indulged in a professional pedicure (pearly pink), the better for sitting briefly in a cloud of chemicals. We both shampooed and conditioned with “fresh” floral fragrances and used a perfume-y bar of soap. I wore brand-name deodorant, moisturized my body in “deep healing” lotion. I topped it off with a swath of coral lipstick. I felt like a beauty contestant.
As anyone on Celebrity Rehab can attest, detox isn’t nearly as fun as what precedes it. It was very hard to avoid food that had never touched plastic. Coffee beans? Nope. Grapes? Sorry. I rode my bike (because my car interior off-gasses phthalates as well as flame-retardants) to the farmers’ market. Even my bike had plastic handle grips, but there was no helping that. I also wore a helmet made of shatter-proof polycarbonate, rife with BPA. (Yes, there are plenty of beneficial uses for BPA.) My prescription sunglasses are made out of the same, another product that was hard to avoid considering I left my metal frames behind in about 1999. At the market, I perused the farmers’ offerings. Some, like the tomatoes, were displayed in plastic. No tomatoes for me. But beautiful artisanal breads were wrapped in paper bags. I asked the seller where the flour had come from, and if it had touched plastic. This being Boulder, he didn’t look at me like I was a freak. He assured me the flour came straight from the mill in large cloth sacks, the old-fashioned way. I stocked up. I also bought some ridiculously expensive quinoa that came packaged in paper. I eyed some greens, but noticed the seller was serving them with rubber gloves (PVC) and stuffing them into plastic bags (phthalates). I asked him if I could handle my own greens and put them in my own cloth bag. He said sure. Boulder is apparently full of chemically sensitive plastophobes.
I had a good excuse not to do any other shopping: BPA is used to coat thermal paper, the kind used for store receipts and airline boarding passes. Unlike the BPA in polycarbonate water bottles, the BPA in paper isn’t “bound” to other molecules, so it rubs off in relatively high amounts. Although we don’t generally go around eating receipts, Sonya Lunder says the substance easily ends up on dollar bills and our hands.
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 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.
I have to admit, Annabel is not a huge fan of tofu. Or of whole wheat. She’s part of the macaroni-and-cheese generation. I recently heard that children who watch “average” amounts of television will see five thousand commercials, more than half of which are about processed food. The “ad pyramid,” dominated by fats, oils, and sweets, is exactly the opposite of the traditional government-recommended nutrition pyramid (now it’s a nutrition plate). Fortyfour percent of TV ads pitch sugary foods, while 2 percent pitch fruits or vegetables. It gives the term boob-tube a whole new meaning.
But some societal trends are pushing back. The public school system in Boulder recently stopped serving chicken nuggets. It replaced chocolate milk with organic low-fat milk. The cafeteria also switched to using organic, locally grown produce, all under the able tutelage of Ann Cooper, an Alice Waters protégée known as the “Renegade Lunch Lady.” She started a Colorado-based nonprofit called Lunch Lessons to improve school lunches for the sake of things like health and attention spans. “We’re done with Day-Glo orange cheese,” she pronounced, earning my lifelong devotion.
Hoping Cooper would offer some other inspiration for my home cooking, I visited her at the school’s district headquarters. Wearing a white chef’s tunic, she ushered me into a cramped office filled with books. Was Cooper aware of the early puberty or breast cancer research? Not at all. But she’s happy to add it to her arsenal of reasons to improve lunches for eight thousand public school children. It didn’t surprise her that hormone-mimicking chemicals might be messing with our girls’ bodies. Cooper, it turns out, is a DES daughter. She told me she’d been badly affected by the drug her mother took in pregnancy.
Under Cooper’s direction, a gleaming salad bar now holds center stage in the school cafeteria. Back in the kitchen, the spaghetti and tortillas are whole wheat. The rice is brown. Hamburgers are served just once a month. I want to throw my arms around her in gratitude. Surprisingly, though, she said some parents are complaining about the loss of chocolate milk from the lunchroom. If Boulder Valley, with its culture of Buddhist triathletes, can’t improve kids’ diets, I don’t know who can.
I’ve also changed some things in our own house. From our body burden experiments, I’ve learned to avoid scented products when possible. No air fresheners for us. No floral dryer sheets. No lavender shampoos. I don’t want to make it sound like I’m a total killjoy, because that’s not my style. We still use the occasional plastic straw and we still have plastic toys. I refuse to say to my children, Step away from the Lego. I still buy cheese in plastic because I’m not about to buy a cow.
In an ideal, childhood-preserving world, I would banish TV and avoid taking my kids to the grocery store with its eye-level barrage of snack temptations. So I’m working on that, but I’m not an all-or-nothing kind of person. I’m cutting down on canned beverages and foods. I could take a cue from Copenhagen’s Aksglaede, who no longer washes her hair or uses sunscreen with products containing parabens or phthalates. (It’s easier to be a savvy shopper in Denmark because that country requires labeling.) I now often pack my kids’ lunches and snacks in thick glass containers and cloth sacks. This at times makes me feel virtuous, but more often than not, it feels like an exercise in futility. The food, after all, comes right out of a plastic carrot bag, bread bag, or cracker box. Even if I had the patience and fortitude to strap on a bonnet and grow the food myself, my local water supply carries a load of contraceptive and other hormonally active compounds.
In fact, the whole prospect of trying to individually safeguard one’s family from silent endocrine disruptors feels like a folly, because it can’t be done in any meaningful way until the government and chemical companies change the way they test, manufacture, and market these substances.
We can only eat so much quinoa out of a paper bag.
