Raising Elijah

For the sake of the narrative, let’s go with Elijah’s account, on the grounds that mothers shouldn’t publish tales about their children when the facts are in dispute. So, during the years in which I was obliviously ignoring my son’s desire for a haircut (Why didn’t you just ask me?), he was often perceived as a girl.

Thereafter, no one called him sweetheart or honey anymore. It was all buddy, pal, guy, or dude. The sing-songy voice previously used to deliver a greeting—by everyone from the waitress to the lumberyard guy—dropped an octave. And the Hey there, Mr. Man came with demands for an NBA-style slap-me-five.

A more perceptive mother might have noticed the transgender mistake much sooner and taken steps to correct it. But my other child is a daughter. I was accustomed to hearing a beaming, melodic good morning, sweetie when an adult addressed one of my kids. I thought—oblivious again—that’s just how adults talked to small children. I didn’t realize there were different salutations for girls and boys.

In hindsight, I don’t know why I was so surprised at this discovery. Everything else about childhood is an exercise in extreme gender stereotyping, the likes of which one seldom encounters in adult life. The most conservative of men—the upholders of tradition and the defenders of unfettered capitalism—sit next to me on airplanes dressed in shirts of pale pink, a shade that not even the most unconventional parents would consider for their infant sons.

Along with color limits, the rules for decorative elements on little boys’ clothes are unwaveringly strict. Bees are allowable motifs—but not butterflies. Camouflage-style vines are okay, as are palm trees and anything jungle-y, but flowers are out, and fruits are questionable. A pumpkin hat for a boy is fine, but not a strawberry hat. Bananas are okay, especially if gorillas are holding them. Peapods and root vegetables are fine. Cherries, not fine. Suns, moons, comets: ja. Rainbows, nein. Mammals are permitted. Birds are taboo. Unless it’s archaeopteryx. All dinosaurs are acceptable. At one point, my personal mission was to find, in the bins of gently used children’s clothing at our local consignment shop, something in Elijah’s size that was not festooned with weaponry, a combustion engine, or a large, predatory animal. I rarely succeeded.

Toys, especially the figurative kind, seem even more polarized, as though they had been soaked in great vats of steroidal hormones before hitting the retail shelves. Over here, futuristic, muscle-bound robo-guys with no discernible ecological connections. They’re all about power. Over there, coy, glittery princess fairies who occupy monarchal kingdoms with pollination systems (flowers and butterflies) but where the rules of democracy and science don’t apply. For girls, it’s all magical thinking.

I’ve heard many parents of boy/girl families say that childrearing has convinced them that sex differences in behavior and learning are hardwired. If by this image, we mean “innately predisposed,” I’m not so convinced. My kids enjoyed childhoods that were, for all intents and purposes, commercial free, and in the early years, I can’t say that I noticed a lot of differences. In fact, Faith and Elijah followed strikingly similar pathways of development: both sat up on their six-month birthdays, spoke their first words before they crawled, and didn’t walk until fifteen months. Until Faith was five and Elijah two, when we lived in relative isolation in the cabin—with woods and spongy swaths of cattails for a playground—my kids showed roughly equivalent interests in books, balls, dolls, music, art, trains, frogs, dinosaurs, dance, and outdoor exploration. And it was Faith, not Elijah, who got in trouble for shoving during nursery school sing-alongs.

Maybe, of the two, Elijah showed a greater early interest in throwing and catching—and that explains his greater interest in sports now. Maybe Faith possessed the deeper congenital need to squish things—and that explains her greater interest in baking projects. That’s possible. But it’s equally likely that their various proclivities were differentially encouraged (or ignored) by teachers, peers, and probably—in ways that we can’t even see—by Jeff and me. Certainly, Faith’s early curiosity about cooking was nurtured along by a family friend of ours who was willing to spend hours with her in the kitchen. Faith also seems to possess an unusually keen palate, with a remarkable ability to discern subtle tastes and smells. Is this an inborn olfactory talent? Or did two years of breastfeeding, with its banquet of different flavors, help create it?

Because we are sensitive to accusations of preferential treatment, bias, or unfairness, these accidental factors—especially the ones involving the influence of birth order—tend to get left out of the stories that parents create to explain the origins of their children’s temperaments, learning styles, and talents. Instead, we cobble together a narrative from selective memories that serves to highlight the foreordained nature of it all. I do this, too. When, after a soccer game, someone told me that Elijah seemed to have a natural love of the game, I heard myself say, “Well, you know, his very first word was ball.”

If, on the other hand, by asserting that sex differences are hardwired, we simply mean, “organized as if by permanent electrical connection,” I wouldn’t argue. Developmental pathways laid down in early childhood—however the wiring occurs—can become destiny. As neuroscientist Lise Eliot points out, infant brains are so malleable that any inborn differences between boys and girls—and she believes they are real but small—can easily become magnified when reinforced by gender stereotypes.

Here’s one more tale from the family annals at our house: When Elijah was three, he found a handsaw that Jeff had left, in a violation of all child safety standards ever drafted, lying on the porch. Without the permission or knowledge of anyone, Elijah spirited the tool away, stashing it under the mattress of a futon couch in my office. (This part of the story we reconstructed after the fact.) A few days later, while I was in the kitchen working on dinner, Elijah announced with a sigh that he was feeling a little tired and wished to lie down for a while. Could he go in my office?

Okay, said the oblivious mother, who, a full five minutes later, thought, Wait, that doesn’t sound right, and decided to check on him. He was not there. The mattress of the futon couch was askew, and the door to the backyard was wide open. Stepping outside, I spied my son high up in the magnolia tree.

Here was the dilemma. A gotcha reaction on my part would likely trigger a panic reaction on his part. I could easily imagine the various horrible consequences of that. But ignoring the scene wasn’t an option either. So, employing some stealthy moves of my own, I crept to within catching distance but stayed out of sight. Then I waited. A few sawed branches fell around me. And then, finally, down came Elijah. Slowly. Shimmying along the gnarly trunk, limb by limb, holding on to the tree with one hand, clutching a big shiny saw with the other. During his descent, he hummed to himself. I held my breath. Once his feet were back on earth, he surveyed the scene. And there was mom!

So in the family treasury of stories—which is how we come to understand who we are—what is the message of this one? Is it about Elijah’s innate attraction to tools and weapons? Or to secrecy and adventure? Is it evidence of a male attraction to danger? Is it about how Faith had never ever done anything like that when she was his age and how boys are so different from girls when it comes to impulse control?

Or is it about two semi-exhausted, semi-distracted parents who unwittingly created the opportunity for a premeditated heist in ways that had not happened with our daughter because 1. we weren’t yet engaged in home construction projects when she was small; and 2. we had only one kid, not two, to keep track of when she was his age?

Endocrinology concerns itself with the hormonal messages that fly, like fleet-footed Mercury, through the bloodstream from the Mount Olympus of the glands to the lowly cells of the body. Those bearing receptors that can bind a particular hormone are the intended readers of its message.

Actually, glands both send and receive hormonal messages, and some brain cells act like glands—which is why, all together, the brain’s neurons and the body’s glands are collectively known as the neuroendocrine system. Inside the center of the brain, for instance, sits the throne-shaped hypothalamus, supreme governor of sexual maturation. You cannot grow up without a hypothalamus. More specifically, you cannot grow up without the assistance of its gonad-stimulating neurons (of which there are only about 1,000). At about the end of the first decade of life for girls—a little later for boys—these sleeping neurons wake up and begin drizzling into the blood gonadotrophin-releasing hormone, and, when received and amplified by the pituitary gland, that’s the sound of a gavel coming down: Childhood is adjourned; puberty is now coming into session.

But new research shows that the hypothalamus itself is studded with receptors of all sorts. Some of these respond to hormonal messages produced by glands located elsewhere in the body. Some respond to chemical cues—enzymes and neurotransmitters—produced by neurons and glial cells located elsewhere in the brain. And, in turn, these far-flung brain cells are the receivers of messages streaming in from everywhere.

Some of these incoming signals encourage the slumbering neurons of the hypothalamus to remain quiescent. (Melatonin, which conveys information about light levels in the environment, has this effect.) And some of them encourage arousal. (Leptin, a hormone that reports to the brain on the status of the body’s fat reserves, has this effect but, all by itself, is not able to trigger puberty. Kisspeptin, a protein produced by neurons in the forebrain, appears to be a necessary conspirator.) When the balance of permissive signals finally exceeds the balance of inhibitory ones, the gonadotrophin-releasing neurons of the hypothalamus break dormancy and begin directing the work of pubertal onset. Sitting, as it does, downstream of a whole nexus of chemical cues, the hypothalamus turns out to be less a prime mover than a messenger itself.

There is also infant puberty. Those two words come as a surprise to many people, including the parents of infants. But it’s real, and it’s normal. Both boys and girls come into this world with wide-awake hypothalamic neurons, actively secreting gonadotropin-releasing hormone. In response, the testicles or ovaries of newborns produce sex hormones—testosterone or estrogen. New parents often notice the startling effects. Red, puffy genitals. Acne. Swollen nipples. These traits recede and disappear entirely by nine months. (Newborn boys experience a peak of testosterone at three months.)

During infant puberty, sex hormones help organize the neurological system—as they will a second time during adolescent puberty. In boys, the release of gonadotropin-releasing hormone in infancy may play a role in masculinizing the brain and almost certainly assists with testicular maturation. In both sexes, infant puberty seems to prepare the brain for its job in adult life as the regulator of sex hormones.

After a few brief months, this whole system is switched off and remains latent until adolescent puberty. And that’s the endocrinological definition of being a kid: childhood is a hormonal hiatus between two puberties, made possible by a temporary inhibition of the hypothalamus—through an unknown mechanism.

The chemicals known as endocrine disruptors—like the chemicals known as neurotoxicants—have the power to alter developmental pathways during childhood. About 200 endocrine disruptors have been identified so far. They include certain pesticides, plastics, detergents, flame retardants, air pollutants, dioxins, PCBs, and heavy metals, including cadmium and lead.

Because the brain itself is organized under the influence of hormones, endocrine disruptors and neurotoxicants are overlapping identities. Any chemical, for example, that disrupts the activity of thyroid hormones—which act as wilderness guides for trekking fetal neurons—can bring ruin to the brain. But for our purposes here, we focus on that subset of endocrine disruptors with the potential to interfere with the hormones that oversee the creation of the reproductive system.

Endocrine disruptors, like neurotoxicants, are not screened or regulated as a group. No single federal agency is tasked with the job of monitoring all chemicals with the power to mimic or otherwise interfere with the flow of hormones. Of the many chemicals flagged as possible disruptors of sexual development, three are currently receiving sustained attention by researchers and are the subjects of intense, contested debate: bisphenol A, phthalates, and atrazine. The first two are ingredients of plastic, and the third is an herbicide. All are produced in high volume, and human exposure to all three is widespread—indeed, both bisphenol A and phthalates are considered ubiquitous in the environment and in people.

More specifically, 93 percent of Americans have measurable levels of bisphenol A in their urine, according to the Centers for Disease Control, which keeps track of these things. Researchers at the Columbia Center for Children’s Environmental Health—the folks who put air monitors on pregnant women—found phthalates in virtually all personal air samples, as mentioned in Chapter 1. The Centers for Disease Control also found universal exposure to phthalates among Americans of all ages, with the highest levels in children. Its presence in human amniotic fluid and umbilical cord blood indicates that prenatal exposures are more than hypothetical. And, according to researchers at the National Institute for Environmental Health Sciences, 60 percent of Americans are exposed, mostly through drinking water, to atrazine, the second most common pesticide used in the United States.

At more than 8 billion pounds per year, bisphenol A has one of the largest productions of any chemical in commerce. It is a single chemical compound, and its primary purpose is for the manufacture of plastic: Bisphenol A molecules strung together make the polymer called polycarbonate. Bisphenol A is also used in epoxy resins that coat the inside of food and beverage cans, as dental sealant, and in printer inks and coated paper, such as that used for cash register receipts.

As an endocrine disruptor, bisphenol A is an estrogen mimic and behaves like a forged document. In the mammalian body, it can attach to the estrogen receptor and so elicit the sorts of cellular responses that are triggered by real estrogen (albeit far more weakly). Its talent at faking out the endocrine system is not a new discovery. Indeed, the affinity of bisphenol A for estrogen receptors was demonstrated in 1936. But before it could be widely marketed as a pharmaceutical hormone, a stronger synthetic estrogen took its place—the infamous DES, diethylstilbestrol. Stripped of its career as a synthetic hormone, bisphenol A languished in chemistry labs until it was repurposed as the building block for polycarbonate.

Thus, its innate ability to act like an estrogen is not in dispute. It’s known to shed from plastic bottles and can linings into the food and beverages contained therein, especially when heated—as when a bottle of breast milk or formula is warmed in a pan of water. No one disputes that fact either. Where the contested accusations fly is over exposure estimates and the risks of harm from those exposures, especially for infants and children. Uncertainties swirl around questions such as, How quickly does the liver send bisphenol A to the kidneys?; and, Is there enough to cause harm? Various state and federal agencies are pondering these data gaps. Meanwhile, in 2010, over the objections of the American Chemistry Council, the Canadian government declared bisphenol A a toxic substance.

Phthalates and atrazine bring a more furtive approach to endocrine disruption. Their methods of inflicting damage are not through mimicry. Phthalates, as you’ll recall, are a big family of chemicals with lots of uses. They turn up in the cosmetics department (as ingredients in perfumes, lotions, aftershave, nail polish, shampoo), in the home improvement section (vinyl flooring, shower curtains, wallpaper, garden hoses), and in children’s outerwear (e.g., Curious George raincoats), but, most covertly, in our food. Some, but not all, of these many phthalates are reproductive toxicants. Instead of copying sex hormones, phthalates cut their supply lines, most notably during the production of testosterone and insulin-like factor 3. (In spite of its unsexy name, insulin-like factor 3 is as much an elixir of manhood as its famous friend, testosterone. More on both these hormones momentarily.) The end result, in many animal studies, is demasculinization. And in rats, exposure to phthalates during prenatal life can trigger testicular cancer in later life.

In spite of elegant research that has revealed the vulnerability of the developing male reproductive tract to damage from phthalates, many uncertainties remain. Marmoset testicles, for example, appear less sensitive to phthalate-induced injury than rat testicles owing to hardwired differences in the speed at which they can metabolize phthalate esters. Are human baby boys more like rats? Or marmosets? And, given that we are exposed to mixtures of phthalates of many different molecular weights, how do we tease apart the effects of one from the other? And given that we are almost all exposed on a daily basis to both phthalates and bisphenol A, how might they interact within the bodies of pregnant women? Within the testicles of baby boys? In 2008, Congress banned the use of six phthalates in nipples, pacifiers, teething rings, and toys that might be mouthed. This legislation, while welcome, does not address the exposures during pregnancy.

As for atrazine, its game is to trick the body into making more of its own estrogen. We are all, male or female, yin-yang creatures with mixtures of male and female sex hormones coursing through our bloodstreams. Our genetic sex determines the balance of the two. To make a sex hormone, you start with cholesterol and, like twisting a sausage-shaped balloon into a poodle, amend the molecule to make testosterone. A few more manipulations and, voilà, estrogen. In laboratory studies, atrazine enhances the production of an enzyme called aromatase, which is used by the body to convert testosterone into estrogen. Aromatase is the balloon twister. The more aromatase, the faster the conversion. The end result is higher estrogen levels. Less yang, more yin. (Aromatase inhibitors, by contrast, are chemotherapeutic agents used as a treatment for some estrogen-positive breast cancers.)

In experiments with developing tadpoles, atrazine has feminizing effects—of the most dramatic sort. Male tadpoles exposed at key moments in development turn into fully functional, egg-laying female frogs. In female lab animals, atrazine also interferes with hormones from the pituitary gland, whose job it is to deliver messages from the hypothalamus to the ovaries. Given these effects—and observations from other labs about atrazine’s ability to alter mammary gland architecture in female rodents—questions have been raised about atrazine’s potential to alter the pathways of breast development in girls. There are many uncertainties. What is the message of frogs and rats for humans? Is there a safe threshold level below which exposure effects are negligible? And what should parents of young children do between now and when scientists secure conclusive answers?

At this writing, the EPA is, not for the first time, reviewing the health effects of low-level atrazine exposure with an eye toward understanding its possible developmental effects. In 2006, in spite of the remaining uncertainties, atrazine was banned for use in the European Union.

Attending scientific meetings on environmental threats to reproductive health would surely be an unsettling experience for any mother of young children, biologist or not. From the program of one such conference, here are the titles of some of the presentations I saw: “Prenatal Exposures and Male Reproductive Disorders,” “Urogenital Birth Defects in Newborns,” “Postnatal Life Events That Determine Adult Male Reproductive Function,” “Early Postnatal Environmental Contaminant Exposures and Reproductive Health Effects in the Female,” “Male Mediated Developmental Toxicity,” and “Alterations in Puberty.”

Surely, what makes these topics so profoundly disturbing is the juxtaposition of something public, noxious, and invasive (chemical contaminants) with something that verily defines the words private, innocent, and off-limits (the reproductive organs of infants and children). We are talking here about threats to that part of my children that I am charged, above all else, with safeguarding: their sexuality, their fertility, their connection to future generations, and thus to the abiding, ongoingness of life itself. These are the body parts about which the necessary motherly refrain is This is private. This is just for you. No one else is allowed to touch you there.

And yet, at the same time, there is something, for me, almost liberating about these PowerPoint presentations, with all their micrographs and diagrams and statistical confidence intervals. And that’s because, in their exploration of the evidence linking exposure to endocrine-disrupting chemicals with impaired reproductive health and fertility, they create a forum about an issue for which we have no other language. The data bear witness. They offer vocabulary words that, however stilted or icky, allow us to see that the development of our children’s reproductive tracts (icky words) is jeopardized by insufficiently protective chemical policies. And protection is what I am charged as a parent with providing.

“Altered Semen Quality in Relation to Urinary Concentrations of Phthalate Monoester and Oxidative Metabolites.” “Phthalate Ester-induced Gubernacular Lesions Are Associated with Reduced INSL3 Gene Expression in the Fetal Rat Testis.”

You can go to medical and scientific meetings about asthma, and hear from the experts the latest evidence on its causes and triggers—its possible relationships to diesel exhaust, phthalates, climate change, or pet dander. And you can then go home and talk about the rising rates of childhood asthma with whomever you please. You can attend any number of seminars and workshops on autism and the changing diagnostic criteria for attention disorders. And then you can join advocacy groups, such as the Learning and Developmental Disorders Initiative, and continue the conversation. By contrast, it’s very difficult to talk openly about, for example, gubernacular lesions. Outside of endocrinology seminars, there is precious little discourse on the topic.

A few years ago, I wrote a commissioned report on the falling age of puberty in girls and had the opportunity to present the findings at public meetings, including a Congressional briefing. I had never before entertained so many questions posed in whispers. On the way to the bathroom, in the hallway, while I was putting on my coat and hailing a cab, audience members approached me, one by one and whispered to me their stories and questions. This included at least one EPA official whose adopted seven-year-old daughter was developing breasts and what, he whispered into my ear, did I know about early puberty among foreign-born adoptees? (There’s a small body of literature on this very question, actually.)

Until week five of pregnancy, boys and girls have the same genital tract. Then, the genes associated with the embryo’s genetic sex awaken and spur the production of hormones that guide the reproductive tract along one of two very different directions, male or female. Of the two, the development of the male tract is more intricate and involves considerably more steps. Whereas the female version hews closely to the original template, the male genitalia, when finished, is an elaborate piece of engineering that barely resembles the five-week-old unisex prototype that was its starting point.

Testosterone plays a starring role in much of the design work and subcontracts the rest. After triggering the production of a second hormone to direct the development of the prostate gland, the penis, and the scrotum, testosterone goes to work overseeing the construction of the transportation system along which—someday—sperm will travel. Thus, a continuous pipeline is laid from the interior of each testicle to the tip of the penis. But this ductwork doesn’t take the direct route. Instead, it heads north, into the pelvic cavity, loops over the pubic bone, skirts along the bladder, finally turns south and shoots forward again, making a complete loop-the-loop. This circular arrangement allows various glands to contribute the liquid portion of the semen. Meanwhile, inside the testicles, squadrons of cells begin creating a well-organized center for sperm production, much of which will be devoted to nurturing the sperm cells after their creation. Like glial cells to neurons, a whole support team is needed for every sperm cell. Although not required until after puberty, the infrastructure for spermatogenesis is laid down during fetal life.

The testicles begin their development high inside the body, near the kidneys. Installing them within their permanent home outside the body involves a two-part, carefully orchestrated procession. During part one, a suite of hormones, including allimportant insulin-like factor 3, guides the testicles from the kidneys to a base camp in the pelvis. Then, near the end of pregnancy, like a mountain climb run backwards, the testicles begin their final descent into the scrotal sacs.

Quite a lot of male hormones are required to carry out all of the above. Exposures to chemicals that interfere with the production of these hormones, block their messages, or destroy the cells where they are made can jeopardize the whole process. The result can be a developmental disruption with the (icky and stilted) name, testicular dysgenesis syndrome. It can manifest as a range of smaller and larger alterations, including a collection of four conditions that sometimes occur in isolation but more often cluster and which seem to have a common cause: namely, abnormal development of the testicles in prenatal life due to insufficient levels of male hormones to choreograph the show. Two of these conditions—hypospadias and cryptorchidism—are birth defects visible in the delivery room; another two—testicular cancer and low sperm count—do not show up until adulthood.

Hypospadias occurs when the opening of the penis is located somewhere along the shaft rather than at the tip. Its incidence in some geographic areas has more than doubled since the 1970s. As with autism, some, but not all, of this apparent increase is attributable to greater awareness and changing diagnostic criteria.

Cryptorchidism is the medical term for undescended testicle. It is a word I rather like. Hidden orchid is the image conjured up by its etymology . . . except that orchids were named for their resemblance to testicles and not the other way around. But the poetry of the word belies the unhappiness of the condition. Its prevalence in some parts of the industrial world appears to be increasing, and, along with hypospadias, cryptorchidism is a risk factor for low sperm count and testicular cancer. In men diagnosed with an undescended testicle, the risk of developing a later testicular tumor increases significantly, a pattern that suggests that testicular cancer has its roots in fetal development.

Testicular cancer is now the leading cancer among young men. Its incidence in the United States has doubled since the 1960s. During the same period, sperm counts and semen quality have declined, along with testosterone levels. Due to changing methodologies for ascertaining sperm quantity and quality, many uncertainties surround these historical time trends. However, there are some striking contemporary geographic patterns that persist even with rigorously standardized data collection. These are correlative patterns that offer no proof but do provide clues for further inquiry. Men from rural Missouri, for example, have half the number of moving sperm than do men in urban Minnesota. They also have higher pesticide exposures. In Sweden, a group of men whose mothers had higher PCB levels had elevated rates of testicular cancer. In Taiwan, the sons of mothers who had unknowingly consumed PCB-contaminated rice oil while pregnant grew up into men with smaller penises and larger numbers of sperm abnormalities, as compared to unexposed counterparts.

Testicular dysgenesis syndrome has its origins in many places. Family history—and, thus, heredity—contributes to the risk for cryptorchidism, as does preterm birth, low birth weight, alcohol consumption during pregnancy, and maternal smoking. But, in addition to the indirect evidence for environmental harm gathered from the above human studies, an impressive and growing body of evidence from the lab bench and from the field strongly implicates endocrine-disrupting chemicals as actors in the story.

Wildlife observations of male animals offer striking parallels to patterns seen in human men. In a series of now-famous field studies, for example, zoologists in Florida demonstrated that the failure of alligator reproduction in Lake Apopka is attributable to infertility among the males who had abnormally small penises, low testosterone levels, and high estrogens. They were further able to show that the contamination of the lake with pesticide was the likely cause of the reproductive anomalies among male alligators. Uncontaminated alligator eggs painted with pesticide—at concentrations replicating that found in the water—produced male alligators with reproductive deficits identical to those seen in males born in the lake.

In the club of the demasculinated, alligators are not alone. Field biologists report reproductive anomalies in male mammals as well. They involve species up and down the food chain—including the big, fierce guys that are often emblazoned on clothes for little boys. In addition to pesticide-exposed panthers with undescended testicles, they include frogs with eggs inside their testicles and many species of hermaphroditic fish, from Mississippi sturgeon to Canada whitefish.

From experimental studies in lab animals, researchers have shown that insufficient testosterone can induce all four different manifestations of testicular dysgenesis. As described above, testosterone has many executive functions in male reproductive development—from formation of the urethra to oversight of testicular descent and, in adult life, management of sperm production. Within the developing testicle, testosterone is produced by a specialized group called Leydig cells. These cells are also the main targets of phthalate interference. When they gain entry to the inner chambers of the Leydig cells, phthalates alter the production of enzymes and proteins that guide the transport of cholesterol—testosterone’s starting point. Phthalates also disable genes that oversee the production of insulin-like factor 3, which, together with testosterone, is the GIS system for the traveling testicle during its journey to the bottom of the scrotum.

Along with these findings, lab bench researchers also discovered that inadequate testosterone during the time the fetal testes are developing can result in an externally visible mark: shortened anogenital distance. This is a new finding—and links to specific abnormalities included in the testicular dysgenesis syndrome are just being discovered—but it looks like short male anogenital distance will turn out to be one of the earliest and easiest to identify markers of this syndrome.

Basically, a shorter anogenital distance means that a male newborn possesses a smaller perineum—which is the name for that springy expanse of skin and muscle that extends between the anus and the base of the penis (and in females, to the vaginal opening). All mammals possess perineums, although it’s a body part you’ve probably not given much thought to—let alone worried if yours was bigger, smaller, thicker, thinner, perkier, or plainer than everybody else’s. Exception: A woman in childbirth thinks about her perineum once every thirty seconds or so because she’s attempting to push the baby past it. Delivery without perineal ripping is a core skill of midwifery. Obstetricians bring a less artisanal approach to perineums and are more likely to slice through one (episiotomy) to speed the baby’s arrival and sew it back up after the fact. Among the people truly attuned to their anogenital distances are mothers with stitches in their perineums.

To the business at hand: In mammal species, including us, males have longer perineums—greater anogenital distances—than females (about 50 percent greater, on average). In rodents, male perineums are fully twice as long. An anogenital distance in a male that resembles that of a female is an easy-to-spot sign that testosterone production during fetal development has been inadequate. Male rodents exposed to anti-androgenic chemicals, including phthalates, have shorter perineums. The greater the disruption to testosterone production, the more feminized the perineum.

With the lab discovery that anogenital distance is a sensitive and verifiable measure of endocrine disruption—and is visible and measureable at birth—attention turned once again to human studies, and researchers began comparing anogenital distances among various cohorts of baby boys. So far, the findings include these: boys with shorter perineums have a higher prevalence of undescended testicles and smaller penises. Boys whose mothers had the highest body burdens of phthalates had the shortest perineums. About one in four U.S. women is believed to have phthalate levels in her body high enough to reduce the anogenital distance in their sons.

Of the many oversights—okay, mistakes—I’ve made as a mother, one of my bigger ones involves bedtime. As in, I failed to establish one. A night owl by nature, I always resented the lights-out directive that, every evening of my own childhood, extinguished the fun just as the groove was really getting groovy. Quite possibly, that’s why, as a parent, I have a hard time shouldering the job of making people go to bed.

Of my two kids, Faith is better suited to the accidental policy of Oh, wow, look at the time; what are you still doing up? which is what passes for rule of law in my household. Elijah, on the other hand, would probably prefer the comforting routine of nine o’clock Taps. He often has to remind me—sometimes during a very exciting part of the book!—that he needs to go to sleep now.

In saying this, I’m not intending to present myself as some kind of cool, bohemian mom. I’m now convinced—a dozen years into parenting—that shirking bedtime enforcement duties is truly not a good thing. There is a price to pay at the breakfast table when every night is a slumber party, and I would bet that a big part of the morning crabbiness quotient in our house originates from my own adolescent immaturity around going to bed at a decent hour. In a self-evaluation of my parental skills, I would give myself an A- on Encouragement of Healthy Eating Habits and a D+ on Bedtime. Had I a parenting do-over, I would handle things differently.

Having botched the whole notion of enforced bedtimes, I also seem to have missed the lesson on how to carry off a brisk yet loving tucking-in ceremony. Jeff or I still lie down with each of our kids every night and stay with them until they sink below the surface of sleep. No amount of systems theory can dress this up as an efficient practice. Nevertheless, in this one regard, I have few regrets.

Lying on a narrow bed in the dark with an elbow jutting into my ribs, I allow phone calls to go unanswered, dishes to remain unwashed, and essays to lack concluding paragraphs. With some exaggeration, I could say that the priceless benefit of sharing with my children the vulnerable moments before sleep is that I get to hear what’s really on their minds—the confessions, fears, and existential questions that don’t emerge in the light of day. In truth, this happens only occasionally. More typically, Faith recounts, with reportorial accuracy, the whole arc of the day’s events, and Elijah provides, with fantastical flourishes, a play-byplay account of the recess hour’s soccer game. In these nightly recitations, I still learn a lot about the worlds my children occupy and have created for themselves.

Of the two, Elijah’s world is more mysterious to me. How is it possible—I sometimes ask myself while half listening in the dark to yet another explanation of how a player can be offside if he receives the ball on a free kick but not from a corner kick or a goal kick—that Jeff and I gave birth to this child? Neither my artist husband nor I hold the remotest interest in organized team sports. (My personal approach to all games involving flying objects basically derives from dodge ball: duck.) And yet I now stay up late (okay, even later) to memorize the names and faces on Elijah’s stack of sports cards and study the soccer rulebook so I can impress him by asking informed questions. And, after school, I practice kicking balls, so he can practice goalkeeping.

He gives me lots of credit for these efforts. Elijah and I adore each other in big, bewildering, and complicated ways. All things treasured by my son are sources of delight for me—including those that, sans Elijah, I would scarcely notice. I suspect that this animation of formerly ignored things (who knew I had a special talent for air hockey?) is one of the unseen joys of parenting that is imperceptible to non-parents. I certainly didn’t know about it.

My relationship with Faith requires less translation. Because we jog together a couple of times a week, I actually have a more straightforward athletic partnership with my daughter than with my son. And running side by side along country roads offers us plenty of time for reportage. At age twelve, Faith’s ear for dialogue is as keen as when, in preschool, she referred to herself in the third person. Since I myself occupy a narrative world, I’m on familiar ground while listening to her serialized accounts.

Accordingly, my nighttime ritual with Faith is less an attempt to decode the contents of her heart than it is an enduring act of physical affection. Curled next to me in the dark, she continues her daily news updates while I finger-comb her hair and breathe her in. By contrast, in the upright, daytime world, privacy is now the watchword. The bedroom door stays shut. The forgotten towel is handed over the top of the unfurled shower curtain. The needed roll of toilet paper is passed through a crack in the bathroom door. I’m getting dressed. Stay out.

Not really, if only because so much female reproductive anatomy is hidden from view. Instead, researchers use another metric to identify possible environmental influences on reproductive development: age at onset of puberty. Among U.S. girls, it’s falling—and at a speed far faster than genetics alone can explain and in ways that increased body fat can’t entirely account for. Various lines of evidence—laid out below—point to environmental endocrine disruption as one of several contributing causes.

It would be easy to say that early puberty is to girls as testicular dysgenesis syndrome is to boys. That’s not quite right, though. While both are signs of increased risk, we don’t know if boys are reaching sexual maturity sooner or later than in generations past. Far fewer data are available for boys. (Some researchers do allege that pubertal age is also shifting for boys as well. Maybe. Not yet convinced, I’m awaiting the results of ongoing studies.) By contrast, we just happen to have a rich collection of pubertal data for girls that dates back a hundred years—possibly because assessing breast development and onset of menstruation in pubescent girls is a more culturally acceptable topic of study than, say, assessing penile diameter and scrotal volume of pubescent boys.

A more principled explanation would be that the well-established connection between early sexual maturation and breast cancer risk has made urgent the examination of female pubertal timing and its determinants. All things being equal, early blooming girls—those whose first periods arrive before age twelve—are more vulnerable to breast cancer after menopause and, as breast cancer patients, are more likely to be diagnosed with an aggressive tumor. Conversely, for each year menstruation is delayed, the risk of breast cancer declines by 5 to 20 percent. A first period at age 16 or over decreases breast cancer risk by 50 percent compared with a first period at age 11.

The mechanism by which early puberty makes a breast cancer diagnosis in later life more likely—and possibly more fatal—is not entirely clear, but two aspects appear to be significant. First, early puberty is associated with increased lifetime exposure to estrogens. Second, early puberty opens wide the window of time between first period and first pregnancy, an interval that is considered critical for breast cancer risk. The shorter that vulnerable time span, the better. In either case, it’s clear from the breast cancer literature that identifying the causes of early puberty in girls—and intervening to eliminate them—is a meaningful place to begin a program of breast cancer prevention for our daughters.

From the fields of psychology and anthropology comes this interesting gender discrepancy: Early-maturing boys tend to be treated as leaders by their peers and teachers and are admired, whereas early-maturing girls are more likely than their lateblooming counterparts to be scorned, harassed, and subject to multiple forms of victimization, including violence. From this body of research, I conclude that the culture in which my children live projects esteem onto boys entering manhood and, onto girls becoming women, sexual objectification.

Indeed, early puberty in girls is associated with a number of startling problems, which reads like a list of every bad thing that can happen to a teenager. Girls who are the first in their cohort of friends to develop breasts report more negative feelings about themselves and suffer more from anxiety. Early-maturing girls are more likely to experience depression, eating disorders, and suicide attempts. They are more prone to early drug abuse, early smoking and alcohol use, and early sexual initiation, which itself is linked to a greater number of lifetime partners. They are overrepresented in the criminal record and underrepresented at college commencement ceremonies.

In the late 1990s, a noisy debate on early puberty spilled out of the corridors of clinical practice. It began when a group of pediatric endocrinologists, protective of their patients, recommended lowering the age at which puberty should be considered precocious (an official medical condition) to spare younger girls invasive diagnostic work-ups and drastic hormonal interventions to arrest puberty’s progression. They argued that the existing standards were out of date with today’s trends. These standards, which had long ago set the age of precocious puberty at eight, now automatically categorized 14 percent of U.S. girls as abnormal.

Public health researchers countered that what had become the norm was not necessarily normal. Or good. And changing the definition of abnormal didn’t make it so. Moreover, referring to redefinitions as “updates” made those rightfully concerned about the downward shift in pubertal timing seem somehow out of touch, like elderly aunts who still insist on handwritten RSVPs in an Internet age. Nevertheless, those advocating for change won the argument. In 1999, the cut-off age for precocious puberty was pushed back from eight to seven for white girls and from seven to six for black girls.

Narrowing the definition of precocious has normalized early puberty. Yet, I’m sympathetic with the compassionate impulse behind this revision. As its proponents point out, most earlyblooming girls have no underlying medical problem in need of treatment. And trend is not destiny. In spite of the extra stress they endure, plenty of early-maturing girls develop into happy, high-achieving adults. Indeed, it’s not clear if the very real psychosocial problems faced by early-maturing girls carry over into later life. One large-scale study finds little evidence that early-maturing girls become troubled adults, although they do apparently continue to suffer from significantly higher rates of depression. Other studies do report persistent differences: Early-maturing girls perform less well in school and are less likely to finish college.

But there are no data to show that temporarily halting precocious puberty with injections of hormones—an extreme act of endocrine disruption to be sure—spares girls the various risks that come with early maturation, including the elevated risk for breast cancer. Offering these girls social and psychological support may prove a more effective and compassionate approach than offering them syringes of synthetic anti-estrogens. As always, knowing when to intervene in the life of a child—and with what tools—is a vexing decision.

Meanwhile, caught up in an argument about the normalcy or not of third graders wearing bras, we are avoiding another question: Why are we willing to dream up radical interventions for girls growing breasts and not for our systems of chemical regulation?

In all female mammals, including humans, sexual maturation is a trait that responds to cues from the external environment (availability of food, mates, and shelter) as well as from the internal environment (presence of body fat; absence of infectious diseases). Both must be favorable for successful reproduction, which, in female mammals, requires an immense commitment of calories and nutrients as resources are diverted to the tasks of making babies, giving birth, and making milk. Among white-tail deer—a species I once studied intensely—yearlings and even spring fawns can become sexually mature by the fall mating season if food is plentiful. If it is not, a doe won’t go through puberty until age two or older.

Against this backdrop, the falling age of puberty in girls—a trend that was set in motion more than a century ago and is still underway now—looks like an extension of a natural process: Girls developed the ability to reproduce at younger and younger ages in response to less disease and plentiful calories. Between the mid-nineteenth and mid-twentieth centuries, the age of pubertal advent dropped steadily—about three months every decade. This downward trend was temporarily interrupted during the Great Depression, when malnutrition increased—along with the average pubertal age of girls. When good times returned, pubertal age resumed its slow descent.

The trends of the last fifty years, however, are more complicated. The tempo of advancing puberty has gathered abrupt speed. The different milestones of puberty—breast development and first menstrual period, for example—that were once tightly coupled to each other have become less connected. And puberty is not just starting earlier; it’s also unrolling more slowly and thus lasting longer. Moreover, these changes are seen in thinner girls as well as in chubbier girls. Such trends suggest that girls’ endocrine systems are being subtly rewired by stimuli other than good health and sufficient food.

The procession of events occurs roughly as follows. After their long nap, the gonadotropin-releasing neurons of the hypothalamus re-awaken, like so many electrical Sleeping Beauties, and activate a hormonal circuit that, in turn, arouses the ovaries, which begin secreting estrogen. The result is breast development and, eventually, onset of menstruation. A second signaling pathway, also originating in the hypothalamus, stimulates the adrenal glands atop the kidneys, which begin androgen production. The result is pubic hair, underarm hair, acne, and oily skin. These two signaling circuits appear to operate independently of each other. (For most girls, breasts appear before pubic hair.) The arrival of menstruation—menarche—is a late-stage event. Following on its heels is the arrival of ovulation, which signals the attainment of fertility and, thus, the end of puberty. Ovulation—the release of the first egg from the ovary—typically follows the first menstrual period by about a year, and the first menstrual period follows breast budding by about two years.

Along the way, under the direction of sex hormones, the pelvis widens, fat accumulates, the vagina lengthens, the uterus inflates, and the folds of the vulva blanch from red to pink. Peaking just before the first menstrual period, a pubertal growth spurt takes the girl to her final adult height, while estrogen ossifies the ends of her long bones. She is now as tall as she’ll ever be. The brain is also transformed during puberty. New neuronal connections sprout and elaborate, and older pathways are pruned away. New synapses form. Others disappear. White matter increases in volume; gray matter decreases. In both males and females, pubertal resculpting of the brain’s circuitry is believed to make possible the emergence of abstract thinking, values, autonomy, adult social behaviors, and the capacity to consider alternative points of view. The brain also gains efficiency, becoming faster in its processing.

But speed and the development of higher order thought does not come without a price: During the course of sexual maturation, the brain loses plasticity. As a result, after puberty, the ability to learn complex new skills declines dramatically. Playing a musical instrument. Riding a bicycle. Mastering a sport. Acquiring a new language. The prepubertal brains of children are far better equipped for these tasks than the less moldable brains of adults. Indeed, after puberty, one cannot learn to speak a foreign language without an accent. It’s simply no longer possible. C’est la vie.

Moreover, the risk-taking parts of the brain develop sooner, under the direction of pubertal hormones, than the control centers of the brain. These facts raise for me some questions. If our daughters now have fewer years of cognitive flexibility remaining to them, is accelerated sexual development diminishing their full intellectual, musical, and athletic potential? And if female puberty is starting sooner and unscrolling over a longer number of years, are our daughters now experiencing a more prolonged disconnect between the development of risk-taking and the development of good judgment?

When Faith and I read Little Women together, the following sentence jumped out at me—

Don’t try to make me grow up before my time, Meg: it’s hard enough to have you change all of a sudden; let me be a little girl as long as I can.

Jo—the headstrong, creative-writing tomboy—speaks these words to her older, vainer sister, Meg. At this point in the novel, Jo is fifteen. Meg is sixteen. In 1868, when Little Women was first published, sixteen was the approximate average age for onset of menarche among U.S. girls. By the turn of the century, average U.S. menarchal age had fallen to 14.2 years. By the mid-twentieth century, it was thirteen. Since then, the age at which U.S. girls experience their first period has continued to decline but at rates that differ markedly among racial and ethnic groups. Among U.S. white girls, the average menarchal age has fallen only slightly over the past half-century and now stands at 12.6 years. Among U.S. black girls, average menarchal age is 12.1 years, and the ongoing rate of decline is somewhat swifter, as it is among Mexican American girls.

The more troubling story, though, is what’s happening with the age of breast budding, which has fallen far more rapidly than the age of menarche. This discovery came as a surprise. In the early 1960s, two British pediatricians who had studied the pubertal development of 192 girls in an English orphanage had announced that the mean onset of breast development was 11.2. (Yes, I, too, wonder about their methodologies.) Detailed and meticulously gathered, their data became the basis for what is considered normal puberty.

By the 1990s, many pediatricians suspected that most U.S. girls were experiencing breast development considerably earlier than eleven, and a large study was launched. Published in 1997, the results astonished everyone. The mean age of breast development was about 9.8 for U.S. white girls and 8.8 for black girls. About half of all girls showed signs of breast development by their tenth birthdays, with 14 percent attaining breast development between their eighth and ninth birthdays. Other researchers also discovered that onset of breast budding and onset of menarche were not as tightly coupled to each other in years past. In other words, breast development and menarche are occurring earlier and earlier in the lives of U.S. girls, but the age of breast budding is falling more rapidly than the age of menarche.

In 2009, these findings were replicated in Denmark, where, over a period of fifteen years, average age at onset of breast development fell by a full year—from 10.9 years old (in 1991–1993) to 9.9 (in 2006–2008). During that same interval, age at onset of menarche fell by only a few months. Soon after, a 2010 study in the United States documented a continued drop in pubertal onset, with even more girls starting breast development at age seven and eight than in the 1997 study. In this most recent survey, 10 percent of white girls started breast development at seven years old, along with 23 percent of black girls, 15 percent of Hispanic girls, and 2 percent of Asian girls.

The overall trend, then, is this: U.S. girls get their first periods, on average, a few months earlier than did girls forty years ago. But they get their breasts, on average, nearly two years earlier—closer to age nine than to age eleven, with a sizeable minority sprouting breasts far earlier than that. In the time span between my pubertal life and my daughter’s, the childhoods of U.S. girls have been significantly shortened. And, as with testicular dysgenesis syndrome, discourse about the lived experience of these pubertal time shifts is difficult. Silence surrounds the topic.

In 1971, I was in the sixth grade when I first noticed an achy lump behind my nipple that could only mean that I was growing breasts. According to the historical data, this discovery, at age 11.5, made my initiation into puberty a little later than average for the times. Average is exactly how I experienced this event in real life. I was more or less in the middle of the pack of girls who, one by one, were taken by our mothers to the undergarment outfitter—in the downtown department store with the squeaky floor—to be equipped with bras. By the end of sixth grade, most of us had made that trip.

Two years later, I awoke on a predawn December morning to a different ache, and the toilet swirled with blood. This time, I was outfitted from my mother’s personal stash of feminine hygiene products. Afterwards, I pretended to fall back asleep, while mom herself sat at the foot of my bed, wordlessly patting my leg. I hoped she wouldn’t leave; I wasn’t ready for all this blood. She stayed, and the gray air lightened toward sunrise. At 13.3 years old, I was on the late side of average for menarche.

Heredity clearly plays a role in setting the pace of sexual maturation. Mothers and daughters exhibit similarities in pubertal timing and tempo. Tellingly, identical twin sisters show greater correlation in pubertal onset than do fraternal twins. Nevertheless, genetics can’t explain racial and ethnic differences nor the decline in age over time. Menarche, for example, occurs far earlier in U.S. black girls than among black South African girls from well-off families—or among black girls in Cameroon or Kenya. Moreover, a century ago, U.S. black girls actually entered puberty significantly later than U.S. white girls.

With its multitude of signaling pathways, the instrument that controls pubertal timing is, by its very intricacy, vulnerable to perturbation. Several factors appear able to alter the regulation of the hypothalamus and could thereby hasten the onset of puberty in girls. Premature birth is one. Low birth weight is another. Both are endocrine-altering events that, through unknown pathways, dramatically increase the chance that a girl will develop pubic hair before the age of seven. It’s likely that alterations in insulin levels, which affect adrenal gland functioning, are the underlying mechanism. Low birth weight and prematurity are on the rise within the United States, and, as noted in earlier chapters, the risks for being born too early or too small may themselves be influenced by chemical exposures of the mother (among other important factors). Along with phthalates, PCBs, and air pollution, atrazine appears on the list of chemicals with demonstrable links to shorter pregnancy and lower birth weights.

In addition, overweight and obesity are almost surely playing a role in driving down the age of puberty in girls and may also help explain the racial disparities. Multiple lines of evidence argue for a connection. First, obesity, which has tripled in prevalence among children over the past three decades, dramatically alters levels of hormones to which the hypothalamus is known to be responsive, including insulin and leptin. Second, the trend of increasing body mass for U.S. girls coincides with the trend for earlier puberty. Third, a higher percentage of black girls are obese, and, as a group, black girls also reach puberty sooner than white girls. And, most directly, several large, carefully designed studies show that, as a group, chubby girls develop breasts sooner than lean girls.

And yet, there are equally compelling reasons to believe that the increased fatness of U.S. girls is not the whole story behind the falling age of puberty. In the 2009 Danish study, downward trends in the average age of breast budding persisted even after taking increasing body weight into account. A 2009 study of Chinese girls likewise documented a decline in age of onset for breast development for which obesity was not the complete explanation.

Within the United States, the association between body mass and early puberty, so clearly documented among white girls, is not so apparent for black girls: Even after adjusting for body mass, black girls still have earlier onset puberty, and they also have decreased insulin sensitivity (meaning that more insulin is needed to transport blood glucose into body tissues). These racial disparities suggest an alternative hypothesis: The falling age of puberty is not a direct consequence of increasing fatness itself but may be a result of increasing insulin resistance (for which type 2 diabetes is another potential consequence).

Physical inactivity—quite apart from obesity—may also be playing a role. Exercise is clearly protective against early puberty—but through pathways that are not clearly understood. Strenuous physical training may inhibit the puberty-stimulating neurons of the hypothalamus. As a group, bedridden girls have earlier than average puberties, while female athletes have later puberties. Admittedly, teasing apart the effects of thinness from the effects of exercise is difficult. Girls with anorexia tend to have delayed puberties, as do ballet dancers and runners—but so do elite swimmers and ice skaters, who are typically less lean.

Psychosocial stress is also an endocrine disruptor that acts to hasten pubertal onset—perhaps through adrenal release of cortisol to which the hypothalamus is responsive. Trauma, family dysfunction, and father–daughter relationships all seem to play a role. Conflict and stress within families are consistently associated with early puberty. So is the tragedy of sexual abuse. Absence of a biological father—with or without the presence of a stepfather or other unrelated adult male—has been linked to earlier breast development in a number of studies. No one knows why, although many have speculated. (Do girls living with biological fathers receive pheromones that inhibit puberty, perhaps as an evolutionary mechanism to prevent incest?) Conversely, the presence of siblings in the household lowers the risk of early puberty. So does household crowding: Age of puberty goes up when the number of bedrooms in the house goes down.

Evidence strongly indicates that exposures to endocrine-disrupting chemicals also are playing a role in accelerating puberty in girls. A multidisciplinary expert panel co-sponsored by two different federal agencies in 2008 concluded just that. And a close review of that evidence implicates some of the same suspects fingered in the testicular dysgenesis story.

Well-designed prospective human studies are understandably scarce. Nobody is purposefully exposing cohorts of baby girls to endocrine-disrupting substances and then monitoring their various pathways to puberty. Thus, many human studies try to make sense of accidents that involved the inadvertent exposure of children to chemical toxicants. For example, in 1973, brominated flame retardants (polybrominated biphenyls) were mistakenly added to cattle feed in Michigan. As a result, a cohort of 327 girls were exposed as fetuses or infants when their pregnant or lactating mothers ate beef and milk from the poisoned cows. Researchers enrolled these girls—now middle-aged women—in a long-term study that documented, among other things, that those exposed to the highest levels of flame retardants in early life began menstruating up to a year earlier than girls with less exposure.

Another type of human study measures background levels of hormones and hormonally active agents within the bodies of girls and women within the general population. In the urine of U.S. girls six to eight years old, for example, researchers have identified a wide spectrum of hormonally active agents, including phthalates and bisphenol A. These results confirm that exposures of young girls to ubiquitous environmental endocrine disruptors are, well, ubiquitous.

The authors of the 2009 Danish study, which documents a decline in the age of breast development among the girls of Copenhagen, did not attempt to measure endocrine disruptors in the bodies of their young subjects. They did, however, measure blood levels of two different reproductive hormones that serve as the intermediary messengers between the hypothalamus and the ovaries. Follicle-stimulating hormone and luteinizing hormone oversee the estrogen production that, in turn, is needed for breast development. The levels of these two naturally occurring hormones in the 2006–2008 cohort were no higher than in the 1991–1993 cohort. The investigators surmised that external estrogenic factors may be acting in concert with the body’s own sex hormones to explain the hastening pace of breast development in Denmark.

Supporting the thin, provocative body of evidence from human studies is a fat, more conclusive body of evidence from animal studies. All together, controlled animal experiments show that exposure to environmental estrogens in early life accelerates the pace of sexual development—through a variety of mechanisms and at doses similar to background levels to which human children are routinely exposed. Precocious puberty in lab animals can be induced via exposure to synthetic estrogens either pre-natally or shortly after birth.

The evidence is especially damning for bisphenol A. In female rats, prenatal and early life exposures can trigger early onset of sexual maturation, especially breast development. At concentrations just slightly greater than what U.S. federal agencies consider safe, exposures altered hormonal signals from the hypothalamus and so reprogrammed sexual development—which is to say that while the exposures to bisphenol A were temporary, the effects were permanent, and rats so exposed entered puberty sooner.

When a progress report on risk factors for early puberty was recently released by a breast cancer organization, I received a communiqué. The final paragraph contained a list of steps that parents can take. The first one was help daughters maintain healthy weight.

My daughter belongs to the world now, with its water cycles, air currents, and food chains. She spends her days in a school full of equipment and furniture that no doubt contain flame retardants. She rides home on a diesel-powered bus. She flies around town on her bicycle—or scooter or skateboard—to flute lessons, piano lessons, the public library, passing by pesticidetreated fields and lawns as she goes. She accepts invitations to sleepovers that involve fingernail polish. She signs up for cooking classes and brings home the leftovers in plastic containers. She scours thrift stores for funky bargains. I don’t always know what they’re made of. And when we lie together in the dark at the end of the day, I’m aware that under her skin somewhere lies a wide-awake hormonal network that is receiving incoming signals—from tonight’s dinner; from the chemicals in her shampoo; from the agricultural practices of the county; from the coal plant across the lake; from her father, brother, and me. This much I know: Her body is the medium for a much larger message.

New research shows that bisphenol A is released from burning plastic. It drifts in the wind and attaches to inhalable particles. So don’t give me any more shopping tips and Web sites to consult. Instead, give me federal regulations that assess chemicals for their ability to alter puberty before they are allowed access to the marketplace. Give me a functioning endocrinescreening program, with validated protocols, as mandated by 1996 legislation. Give me chemical reform based on the precautionary principle.

I can stand at the base of a tree in case my saw-wielding son falls out of it, but I can’t place myself between 200 known or suspected endocrine-disrupting chemicals and the body of my daughter. I can’t stop the wind from blowing.

The moment when the waxy smoke balloons up from the red-tipped wicks into the sudden darkness, and the mother of the birthday child realizes that there will never again in this house be a four-year-old boy. Or a seven-year-old girl. Or a six-year-old boy. Or a nine-year-old girl. Or an eight-year-old boy. Or an eleven-year-old girl.

To be sad about birthday cakes is to lament the speed at which the earth circles the sun, which is a helpless, silly sort of sadness. It doesn’t last long. Especially now that the lights are on again and before you is a laughing child—boy or girl—in possession of manners and psychomotor skills, who is doling out cake and ice cream to the neighbor kids and hamming it up for the camera.

And, unbeknownst to him or her, that very sentence was also my unspoken wish, delivered just seconds earlier, as the mighty exhale blew out the flames that number the years already gone by. It’s the same wish for every cake: Oh, let them grow up. Let them find out. Let it go on.