Ecologist Sandra Steingraber explores the eco-causes of early puberty
Editor’s note: The following is an excerpt from “The Falling Age of Puberty in U.S. Girls: What We Know, What We Need to Know,” written by Sandra Steingraber, Ph.D., and published by the Breast Cancer Fund. In the full report (downloadable here), Steingraber reviews several causes of and contributors to early puberty, including environmental factors.
Over the course of just a few decades, the childhoods of U.S. girls have been significantly shortened. Girls get their first periods, on average, a few months earlier than did girls 40 years ago. But they get their breasts, on average, one to two years earlier. Recent studies show that the advent of breast budding — one of the earliest visible signs of puberty — appears to be arriving earlier and earlier in the lives of U.S. girls. We need to know why.
As a biologist, I’m accustomed to distinguishing cause from consequence and consequence from co-variable. But in the puberty story, so many variables are interwoven and interdependent that, as I began to trace the threads of causality to their beginning points, I sometimes felt as though I were caught in a Mobius strip. For example, obesity raises the risk of early puberty in girls, but weight gain itself is a consequence of early pubertal development. And risks for both obesity and early puberty are raised by being born too small or too soon — risks that are modulated by maternal exposure to certain environmental chemicals during pregnancy. Even as I strove to isolate each variable and discuss its relative importance, I found it necessary to return to particular topics several times and in several different contexts, because the potential influences on puberty are manifold and diverse.
All of the stressors that appear to contribute to early puberty in girls — obesity, television viewing, sedentariness, family dysfunction, preterm birth, formula-feeding, chemical exposures — are higher in poor communities and communities of color where poverty, racism, unemployment, and toxic substance exposures are high and access to nourishing food and safe places to exercise is low. In particular, U.S. black children are disproportionately exposed to physical environmental stressors, and it is also this group that reaches puberty earliest among U.S. girls.
Early puberty poses several risks for girls. It raises the risk for breast cancer and is associated with many high-risk behaviors in later adolescence — such as smoking, drinking, drugs, crime, and unprotected sex — that have potential lifelong consequences. Early-maturing girls are also more likely to suffer violent victimization and psychopathologies such as depression and anxiety. It is not clear whether the social or physiological experience of pubertal change is responsible for these negative outcomes. In either case, interventions that reverse the trend toward ever-earlier puberty in girls are a public health imperative.
What We Know About Environmental Factors
In some respects, the falling age of puberty appears to be part of a natural process: humans, evolving in hunter-gatherer societies, developed the ability to reproduce at younger ages in response to plentiful calories, and subsequent environmental stimuli have simply accelerated that trend. This remains the best explanation for the falling age of menarche (onset of menstruation) in U.S. girls, as well as European girls, from the mid-19th through the mid-20th century. Increasing access to food and less infectious disease lowers menarchal age.
During the last 50 years, however, additional forces seem to have been at work. The evidence suggests that children’s hormonal systems are being altered by various stimuli and that early puberty is the coincidental, non-adaptive outcome.
Chemicals in the environment may indirectly contribute to early puberty by shortening gestation time, lowering birth weight, and increasing risks for obesity and insulin disregulation — all of which, in turn, may increase the risk for early puberty. The extent to which environmental chemicals are contributing to changes in human pubertal development remains largely unknown, but the underlying science is sound and the potential for such effects is real.
Endocrine-disrupting chemicals are substances that disregulate some aspect of the endocrine system. They can exert their effects in a number of ways: by mimicking hormones, blocking their uptake by receptors, altering the rate of their synthesis or secretion, interfering with their metabolism or elimination from the body, or altering the number of hormone receptor sites and thereby making the body more or less sensitive to its own hormonal signals.
Studies from the United States document cases of breast development in children accidentally exposed to estrogen creams used by their mothers, as well as to ointments, hair tonics, or ingested pharmaceuticals. In most cases, symptoms regressed after use discontinued. Likewise, cases of premature pubarche (appearance of pubic hair) in both male and female children have been triggered by passive dermal exposure to testosterone creams used by fathers. In most cases, these products were purchased without a prescription and were advertised for enhancing strength, libido, or athletic performance.
Hormonally active agents are found in many other consumer products as well as in pesticides, packaging, and building materials. Hence, apart from accidental, one-time exposures, children are also exposed continuously to low-level endocrine disruptors in their diets, drinking water, and air supply. Further identification of the endocrine-disrupting chemicals found in the bodies of infants and children — and understanding how their levels vary by race, age, and geography — is necessary but not sufficient for evaluating their impact on pubertal timing. For this, large-scale, prospective, longitudinal studies are required.
Natural and synthetic hormones are still used as growth promoters in the U.S. beef industry. Their impact on pubertal timing of girls who are the consumers of its products remains an unanswered question. In the U.S. dairy industry, recombinant bovine growth hormone has been used to increase milk production since 1993. It is not approved in Canada or the European Union. While there are important objections to the routine use of growth hormones by dairy farmers, the potential for rBGH to lower the average age of puberty in U.S. girls is probably not among them. However, before milk can be eliminated as an environmental determinant in human puberty, much more needs to be known about the potential for its various growth factors to cross the gut wall and interact with human receptor sites.
High blood lead levels are significantly associated with later menarche in U.S. girls. These findings are consistent in animal studies in the lab and with occupational studies of lead workers. Environmental exposure to lead delayed thelarche (breast development), menarche, and pubarche in Mexican-American and black girls. Among white girls, there were lesser delays that were statistically non-significant. Among Mohawk girls, higher lead levels were likewise associated with older age at menarche. Average lead levels among U.S. children have been falling steadily for the past three decades, as lead has been phased out of gasoline, paint, and soldered cans. The possible role of declining blood lead levels in the acceleration of pubertal onset in girls is a question for further study.
A recent California study found that girls born to mothers who smoked a pack or more of cigarettes daily during pregnancy experienced significantly earlier menarche than unexposed girls. Babies born to smoking mothers are, on average, one-half pound lighter at birth than babies born to nonsmoking mothers. Smaller birth size may explain part of this association. It is not the whole story, however, because exposure to passive smoke during early childhood also lowers menarchal age by about four months.
In contrast to the paucity of human data on the posited link between hormonally active chemicals and earlier puberty in girls, there is a wealth of evidence for such a link from experimental studies with laboratory animals and wildlife. All together, the animal data demonstrate that early exposures to environmental estrogens can advance pubertal onset — through a variety of mechanisms and at doses similar to background levels to which humans are routinely exposed. For more details on these studies, see www.ourstolenfuture.com.
What We Can Do
The proximate contributors to pubertal maturation in girls have not all been identified — much basic science, epidemiology, chemical testing and tracking, and biomonitoring remains to be done. However, there is sufficient evidence for the contribution (direct or indirect) of body mass to pubertal timing in girls to support efforts that combat childhood obesity. Any campaign to address this problem should begin with the promotion of breastfeeding. Breast milk safeguards against obesity. At 12 months, breastfed babies are leaner than formula-fed babies, a difference that persists into later childhood. Breastfeeding is most important for children born small for gestational age or premature, for whom rapid weight gain raises additional risks for obesity and early puberty.
For older children, successful battles are being waged at local and regional levels even as national efforts remain mired. A number of school districts around the country have begun working to eliminate sugary, high-calorie foods — and continue doing so without federal funding or support from the school lunch program. Some school-based obesity-prevention programs have already demonstrated an ability to delay menarche. One is Planet Health, a school-based intervention designed to decrease television viewing and consumption of high-fat foods while increasing exercise and consumption of fruit and vegetables. After two school years, sixth- and seventh-grade girls in the Boston area who attended schools randomly selected for this curriculum had lower average body mass indices, lower body fat, higher levels of physical activity, and decreased screen time compared with their counterparts at nonparticipating schools. They were also 32 percent less likely to have experienced menarche during the 19-month study than girls in control schools. Such programs need to be replicated widely.
The success of school-based interventions can be carried out to the community at large. Since 2005, there has been a dramatic increase in efforts to improve access to healthy foods in urban, low-income areas through the creation of farmers’ markets and community gardens. Persuading schools, neighborhood stores, and convenience markets to source with local, organic farms is a decentralized grassroots campaign whose efforts are relevant to protecting girls from early sexual maturation.
Strategies to lower rates of preterm and low-weight babies include eliminating exposure to tobacco smoke and chemical solvents as well as eliminating sources of air pollution and mercury contamination. Strategies to lower the pediatric body burden of endocrine-disruptive chemicals include phaseouts of chemicals such as bisphenol A and phthalates, to which girls have documented exposures. Supporting organic agriculture not only lowers the burden of hormonally active residues in food, it protects watersheds from contamination by pesticides, herbicides, animal hormones, and antibiotics, which flow from farms, ranches, and manure lagoons into rivers and streams. Buying organic thus protects drinking water, another potential source of exposure. The Healthy Schools Network has spearheaded the effort to bring non-chemical pest-control practices into schools and daycare centers.
Ongoing ignorance about the extent to which chemical exposures are altering the timing of sexual maturation in children is directly attributable to a lack of basic data on the ability of common chemicals to act as endocrine disruptors. (The U.S. Environmental Protection Agency’s Endocrine Disruptor Screening Program was initiated in response to a 1996 directive from Congress to develop a basic screening assay for such chemicals, but the program has been crippled by funding problems and the repeated disbanding of its advisory panel.) Right-to-know laws about toxic exposures must be expanded. In order to prevent children’s exposures to endocrine-disrupting chemicals, physicians and public-health researchers need to know more about the sources, emissions, and fate of such chemicals in commercial use.
Chemical ingredients in consumer products and their sources should be fully disclosed. Inventories of emissions and monitoring of important routes of exposure — such as air, food, and drinking water — should be comprehensive.
Strategies to lower the combined burden of psychosocial, socioeconomic, and environmental stressors — which disproportionately affect poor and minority communities, especially African-American communities — require community-based solutions, as identified by the National Environmental Justice Advisory Board.
Because it arises from a combination of many different stressors in several different aspects of the environment — psychosocial, nutritional, behavioral, chemical — early puberty in girls is not a trend that will be reversed by single actions by single-purpose agencies. It is a multi-causal threat to the well-being of girls and women that ultimately requires a comprehensive, integrated, unified response.
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