Precocious Puberty: A Comprehensive Review of Literature

IN REVIEW

Precocious Puberty: A Comprehensive Review of Literature Sandra K. Cesario and Lisa A. Hughes

Context: Precocious puberty currently affects 1 in 5,000 children and is 10 times more common in girls. Statistics indicate that girls in the United States are maturing at an earlier age than they did 30 years ago and the number of girls with diagnosed precocious puberty (the appearance of secondary sex characteristics before 8 years of age or the onset of menarche before age 9) is on the rise. A summary of the growing body of literature on this topic is necessary to inform nurses and other health care providers of the current trends and incidence of precocious puberty to better meet the physical and psychosocial needs of these girls and their families. Methods: EBSCOhost Research Databases that included CINAHL Plus, Health Source: Nursing Edition, MEDLINE, PsycINFO, and Women’s Studies International were searched for journal articles published in the past 10 years (1997-2006) that explicitly examined precocious puberty in females and proposed theories to describe the phenomenon. Search terms included precocious puberty, sexual maturation, menarche, and secondary sex characteristics. These terms were searched individually and in combination with proximate determinants such as endocrine disruptors, environmental toxins, phthalates, stress, skin care, genetics, age, ethnicity, obesity, and assisted reproduction. The search yielded 947 articles addressing this issue. Results: Eighty-two studies or case reports met the criteria for inclusion in this literature review that captured six attributable causes of early sexual maturation in female children. These included genetic, ethnic, and pediatric obesity, as well as environmental toxins that disrupt endocrine function (chemicals, toxins, plasticizers, infant feeding methods, skin and hair products, assisted reproductive technologies),

psychosocial stress, and early exposure to a sexualized society. The robustness of the reports varied and few of the studies were widely generalizable but did offer suggestions for assessment and nursing care. Conclusions: Precocious puberty has health and social implications that are complex and influenced by multiple factors. Further research is needed to expand and elucidate theoretical relationships between the early development of secondary sex characteristics in young girls and the proposed causative factors. JOGNN, 36, 263-274; 2007. DOI: 10.1111/ J.1552-6909.2007.00145.x Keywords: Endocrine disruptors—Menarche— Precocious puberty Accepted: March 2007 Girls in the United States appear to be maturing at an earlier age and documented incidence of precocious puberty is on the rise. Earlier body changes of these girls present the appearances of mature physiological readiness for sexuality and childbearing while retaining immature psychosocial characteristics that signal a lack of preparedness for intimate relationships and decision making. Studies indicate that girls who become sexually mature at earlier ages are more likely to engage in risk-taking behaviors such as smoking, using alcohol or drugs, and engaging in unprotected sex (American Academy of Pediatrics [AAP], Committee on Adolescence, & American College of Obstetricians and Gynecologists [ACOG], Committee on Adolescent Health Care, 2006; Flanigan, 2003; Zuckerman, 2001). The purpose of this article was to examine the various theories believed to contribute to the early appearance of puberty in girls in global society and

© 2007, AWHONN, the Association of Women’s Health, Obstetric and Neonatal Nurses

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suggest strategies that may be employed by health care providers to address the issues that arise as a result of this phenomenon. A description of the special needs of girls experiencing precocious or early puberty will also be discussed. Nursing care that recognizes the unique needs of this population is directed toward decreasing risk-taking behaviors, incorporating age-specific assessment techniques, and supporting developmentally appropriate sex education. A comprehensive review of the literature published in the past 10 years (1997-2006) has been completed via EBSCOhost Research Databases that included CINAHL Plus, Health Source: Nursing Edition, MEDLINE, PsycINFO, and Women’s Studies International. Search terms included precocious puberty, sexual maturation, menarche, and secondary sex characteristics. These terms were searched alone and in combination with other terms such as endocrine disruptors, environmental toxins, phthalates, stress, skin care, genetics, age, ethnicity, obesity, and assisted reproduction. A substantial, multidisciplinary list of references was generated and is presented in this article to serve as a resource for health care providers serving this population. The need for further research in this area will also be addressed.

pubic and axillary hair. Precocious puberty has a prevalence of 1 in 5,000 children and exists in girls more than boys by a ratio of 10:1 (Nebesio & Pescovitz, 2005; Partsch & Sippell, 2001). Early menarche has been linked to greater risk of breast cancer as an adult; therefore, precocious onset would seem to increase that risk (Wang, Needham, & Barr, 2005; Zuckerman, 2001). Though girls who experience premature puberty grow faster than their peers due to accelerated bone growth, they fail to reach the normal adult height (Carel, 2006; Partsch & Sippell). While the overall age at menarche is not significantly different (0.34 years earlier) than that reported for U.S. girls in 1973, it is noted that menarche of non-Hispanic Black girls is significantly earlier than that of the White or Mexican American girls (Chumlea et al., 2003; Parent et al., 2003).

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he age of menarche for Black girls is significantly earlier than the age for White or Mexican American girls.

Precocious Puberty and Early Sexual Maturation Puberty is a complex developmental process that begins in late childhood and is characterized by maturation of the hypothalamic-pituitary-gonadal axis, the appearance of secondary sexual characteristics, acceleration of growth, and ultimately the capacity for fertility (Kakarla & Bradshaw, 2003). There is evidence that girls are maturing at an earlier age and that precocious puberty is on the rise (Egli, 2003; Gillis & Schenker, 2002). Precocious puberty, seen more frequently in girls, traditionally has been defined as the appearance of secondary sex characteristics before the age of 8 years or the onset of menarche before age 9 (Colaco, 1997; Massart et al., 2005). This age was determined more than 30 years ago based on a study conducted by Marshal and Tanner (1969) upon examination of 192 English girls. However, in 1997, Herman-Giddens et al. analyzed data collected from 17,077 U.S. girls between the age of 3 and 12 by the Pediatric Research in Office Settings (PROS) network. In 1999, the Lawson Wilkins Pediatric Endocrine Society recommended lowering the normal age of the onset of puberty from 8 to 7 in White girls and to 6 years in African American girls based largely on this study (Kaplowitz, Oberfield, & The Drug and Therapeutics and Executive Committees of the Lawson Wilkins Pediatric Endocrine Society, 1999). The results of this study precipitated the work of the health care community to seek answers for the declining age of puberty and the early appearance of secondary sex characteristics such as breast development and growth of 264 JOGNN

These findings were consistent with those of Wu, Mendola, and Buck (2002) in their analysis of data extracted from the Third National Health and Nutrition Examination Survey. This study found that 49.4% of Black girls at 9 years of age had breast development compared with 24.5% of Mexican American girls and 15.8% of White girls. The mean age for menarche, however, was not as varied with Black girls beginning menses at 12.1 years, Mexican American girls at 12.2 years, and White girls at 12.7 years. It has also been noted that the age of menarche is slightly lower in Mexican immigrant children (Bona & Marinello, 2000). There is evidence that the age of menarche has been gradually getting lower for more than 30 years. Anderson, Dallal, and Must (2003) suggested that the 4-month drop in the average age of menarche observed during the time period between 1988 and 1994 was not significantly different than the drop of approximately 2.5 months seen from the time period of 1963 to 1970. Davison, Susman, and Birch (2003) found that higher relative weight was strongly associated with increased likelihood of having reached menarche after controlling for age and race. Black girls had a lower average age at menarche than did White girls, which was independent of the effect of relative weight. Therefore, girls with higher weight status in early childhood were more likely to exhibit earlier pubertal development relative to peers at 9 years of age, indicating that weight status preceded pubertal timing in girls. Volume 36, Number 3

The PROS is a practice-based research network established by the AAP in 1986. It consists of approximately 2,000 pediatric practitioners in 49 states, Puerto Rico, and Canada who work with the American Academy of Pediatricians and research consultants from around the country (PROS, 2005). The PROS network has been instrumental in determining if earlier sexual development could be attributed to increased prevalence of obesity in young girls, and if African American girls might mature earlier due to a greater degree of obesity (Kaplowitz, Slora, Wasserman, Pedlow, & Herman-Giddens, 2001). The study found that obesity, measured by body mass index, was significantly associated with signs of early puberty in White girls at 6 to 9 years of age, but in African American girls, obesity only attained significance by age 9. Researchers have also noted that African American girls have higher leptin levels than White girls. The adipocyte hormone leptin, levels of which correlate with body fat stores, has been recognized as a factor in the neuroendocrine control of puberty (Ong, Ahmed, & Dunger, 1999). It remains unclear, however, whether the hormonal changes of puberty in girls are more often the cause of increased body fat rather than the result (Egli, 2003). Maternal malnutrition during pregnancy and girls considered to be small for gestational age (SGA) at the time of birth exhibited menarche at an early age, while infants and young girls who experience prolonged bouts of malnutrition show stunted growth during preschool years and have a delay in the onset of menarche (Adair, 2001). In addition to the genetic, ethnic, and pediatric obesity explanations for the earlier onset of sexual maturation, three other broad theories have been proposed. These include exposure to environmental toxins that disrupt endocrine function, psychosocial stress, and early exposure to an increasingly sexualized society, the latter being most provocative and not well supported in the literature. This speculation is rooted in the notion that early exposure to sexual images via the media and in real life triggers the complex neuroendocrine process that results in puberty (Lemonick, 2000).

Endocrine Disrupting Chemicals Synthetic and naturally occurring substances in the environment that affect the normal function of the endocrine system are referred to as endocrine disrupting chemicals (EDCs). An EDC is a chemical that either mimics or blocks hormones, thereby altering the normal hormone levels and endocrine function of the body (National Resources Defense Council, 1998; Wu, Buck, & Mendola, 2003). They can either accelerate or delay puberty due to their interruption in normal hormonal activity. Exposure to EDCs in utero can alter the growth of mammary glands and the age of onset of puberty of the offspring many years later (Wang et al., 2005). Studies have shown several environmental chemicals, such as chlorinated hydrocarbons May/June 2007

act as EDCs in laboratory animals, wildlife and specific human cases (DiDiego, Eggert, Pruitt, & Larcom, 2005; Wang et al.). Pesticides such as dichlorodiphenyltrichloroethane (DDT) are known to have estrogenic effects and its metabolites have an antiandrogen effect. DDT was developed during World War II to combat mosquitoes spreading malaria, typhus, and other insect-borne human diseases among both military and civilian populations, and as an agricultural insecticide. There exists controversy regarding the use of “persistent” chemicals such as DDT because they linger or accumulate in the environment. This accumulation effect was seen in male alligators from Lake Apopka in Florida that had small phallus size, low testosterone levels, and abnormal gonad structure (Nebesio & Pescovitz, 2005). Another example of persistent estrogenic effect was seen in fish in the Great Lakes when they developed swollen thyroid glands and reproductive abnormalities due to pollution from polychlorinated byphenyls (PCBs). There are no known natural sources of PCBs. They are commercially produced mixtures of up to 209 individual chlorinated compounds (known as congeners) used as coolants and lubricants in transformers, capacitors, and other electrical equipment. The manufacture of PCBs was stopped in the United States in 1977 because of evidence they build up in the environment and can cause harmful health effects. Products made before 1977 that may contain PCBs include old fluorescent lighting fixtures and electrical devices containing PCB capacitors, and old microscope and hydraulic oils. Industrial wastes disposed of in the Great Lakes resulted in contamination of fish and other wildlife. Birds, humans, and other animals that eat these contaminated fish have developed similar health, reproductive, and development problems (DiDiego et al., 2005). Contact with substances not generally considered to be toxic such as certain soy, plastics, and beauty products can also disrupt endocrine balance within the body (Barrett, 2005; Chen & Rogan, 2004; Sanghavi, 2006). Isoflavones, natural substances in soy that act as a weak form of estrogen, have been shown to increase the rate at which breast cells reproduce leading to premature breast development in young girls. In addition, isoflavones bind with estrogen receptors and disrupt thyroid function causing iodine deficiency and alteration in physical development (Doerge & Sheehan, 2002). Phthalates found in plastics and chemicals found in many cosmetics and beauty products similarly mimic estrogen causing hormonal and physical growth alterations. Even prescribed medications such as those used in assisted reproductive techniques can have untoward effects in fetal or early childhood development of the offspring resulting from the therapy (Andersson, 2006; RojasMarcos, David, & Kohn, 2005). Further discussion of each of these implicated causative agents follows. JOGNN 265

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any factors, including environmental toxins and psychosocial stress, may contribute to the phenomenon of early sexual development.

Environmental Toxins and Pollutants The theoretical explanation of increasingly early development of female secondary sex characteristics that has the greatest biologic plausibility is its well-documented relationship with chemicals and toxins found in the environment (Blanck et al., 2000; Denham et al., 2005; Ojeda & Heger, 2001). This has been tested repeatedly in laboratory animal experiments and seen in wildlife with relatively high exposures to a variety of substances. While endocrine disruption by pollutant chemicals in humans is more difficult to demonstrate, the underlying science is sound and the potential for such effects is real (Rogan & Ragan, 2003). A limited number of reports in the scientific literature (Mocarelli, Brambilla, Gerthous, Patterson, & Needham, 1996) described the accidental exposure of humans to EDCs such as lindane and other organochlorine pesticides, dioxins, and PCBs with known endocrine disrupting properties (Staessen et al., 2001). A retrospective study of 145 children in Belgium seen for precocious puberty over a 9-year period found a relationship to dichlorodiphenyldichloroethylene (DDE), a metabolite of DDT, in foreign-born children. The foreign children had 80 times the prevalence of precocious puberty as native Belgian children. These children came from various countries where the pesticide DDT was widely used (Krstevska-Konstantinova et al., 2001; Nebesio & Pescovitz, 2005; Solomon & Schetter, 2000). Vasiliu, Muttineni, and Karmaus (2004) investigated the effect of DDE in the offspring of fisherman’s wives living on Lake Michigan who were known to have high levels of DDE during pregnancy. The cohort consisted of 151 women born between 1973 and 1991. A linear regression analysis indicated that in utero exposure of fetuses to DDE was strongly associated with a 1-year reduction in the age of menarche. Massart et al. (2005) studied the prevalence of precocious puberty in a region of northwest Tuscany using medical records of girls with a diagnosis of precocious puberty who received prescriptions for gonadotropin-releasing hormones (GnRHs) (treatment for very young precocious puberty) from January 1997 to December 2003. They found a prevalence of precocious puberty in more than 161 cases per 100,000 children with a mean age of 266 JOGNN

menarche of 8.2 years. These children resided in agricultural areas of the country where inhalation, ingestion, and transdermal exposures to pesticides were common.

Increased Use of Plastics and Preservatives Other substances such as phthalate esters, alkyl phenols, and surfactants present in commercial products that are commonly used for packaging, storing, and preserving food are also classified as EDCs. That the environmental and developmental effects of plasticizers vary by country is, for the most part, unknown. However, in developing countries, the effect is assumed to be significant because of the high level of consumption of dietary products sold or stored in plastic containers (Rastogi, 1998). Because contact with or consumption of these substances in the general population is believed to be widespread, exposure of human fetuses, newborns, and young girls to these exogenous estrogenic chemicals may lead to premature and adverse effects in sexual development (Colon, Caro, Bourdony, & Rosario, 2001; Valentin-Blasini et al., 2005). Phthalates are compounds used as plasticizers to add flexibility to hard plastics. They are not a persistent chemical and are widely used in a number of products from nail polish to children’s toys (Jobling, Reynolds, White, Parker, & Sumpter, 1995). They are used in medical equipment such as IV bags and lines. They can be found in adhesives, caulk, paint, solvents, fixatives, detergents, lubricating oils, cosmetics, and even sex toys made of “jelly rubber” (Colborn, Dumanoski, & Meyers, 1996). The smell of a new car, especially after sitting in the sun, is the phthalates from the plastic dashboard volatilizing in the heat. When the car cools down, those same phthalates condense to cause the oily film on the inside of the window (Colborn et al., 1996). Many brands of nail polish, hair spray, deodorants, and body fragrances are also high in phthalates. A report published by Houlihan, Brody, and Schwan (2002) in collaboration with environmental working group provides a comprehensives list of specific products containing large amounts of this substance. The many uses of phthalates allow many routes of exposure, including oral, dermal, inhalation, and intravenous. Certain phthalates have proven to be disruptive to development and reproduction in laboratory animals (Blount et al., 2000). Particularly alarming is the study performed by Gray et al. (1999) that found certain phthalates have low-dose toxicity for fetuses during critical windows of development. The focus had been on high exposure levels prior to this discovery. Blount et al. (2000) from the National Center for Environmental Health at the Centers for Disease Control and Prevention performed a study on 289 adult humans analyzing urine samples for phthalate levels. Their study found that exposures to phthalates were higher and more common than previously believed and had a significant Volume 36, Number 3

effect on development and reproduction of both males and females. Females tended to grow more rapidly, reach puberty at an earlier age, but have adult heights that are shorter than average. The estrogenic effects have the opposite effect on males who exhibit delays in puberty. The strongest evidence implicating phthalates as a cause of precocious puberty came from a well-known study of young Puerto Rican girls from the ages of 6 months to 8 years from 1994 to 1998 (Colon, Caro, Bourdony, & Rosario, 2000). They analyzed 41 serum samples from girls diagnosed with precocious puberty and 35 control samples. High levels of phthalates (average concentration of 450 ppb) were found in 28 (68%) of the 41 samples from patients with premature breast development. This is in comparison to an average of 70 ppb in the control group suggesting a strong association between phthalates and precocious puberty. Phthalates are abundant in Puerto Rico in the form of plastic containers used in dietary products imported to the island. However, the accuracy of the measurement of phthalates in human blood is questioned due to the phthalates found in the plastic blood collection or storage devices that can contaminate the specimen (Food and Drug Administration [FDA], 2001).

A Link to Infant Feeding The environment and diet of breastfeeding mothers can impact pubertal development of offspring. Studies have shown the association of polybrominated biphenyls (PBBs) to early onset of thelarche (breast development) in girls who were breastfed by mothers with serum levels of PBB >7 ␮g/L (Wang et al., 2005). Residual hormones in meat and milk were commonly associated with accelerated sexual development 20 to 30 years ago, but tighter industry standards have reduced the amounts of these substances currently consumed by the U.S. population (Egli, 2003). This phenomenon can still be observed in countries where meat and dairy industries are not as well regulated. There has been expressed concern that phytoestrogen exposure in infants fed soy formulas, soy milk, or cereals has the potential to alter endocrine function in later life. Up to 25% of bottle-fed infants in North America receive soy-based formulas. The Woman, Infants and Children (WIC) program, a major supplier of infant formulas to low-income women, often recommends soy formula for African Americans because of a higher incidence of milk allergy in this population. The more frequent use of soy products by WIC infants may, in part, account for the higher rates of precocious puberty in African American girls. Klein (1998) reported that the daily exposure of infants to isoflavones in soy infant formula is 6 to 11 times higher on a body weight basis than the dose that has hormonal effects in adults consuming soy foods. Circulating concentrations of isoflavones in infants fed soy-based formula were 13,000 to 22,000 times higher than plasma May/June 2007

estradiol concentrations in infants on cow’s milk formula (Setchell, Zimmer-Nechimias, Cai, & Heubi, 1998). To date there has been no definitive evidence reported to support this concern. Chen and Rogan (2004) were able to document that exclusively soy-fed infants have the highest exposure to a nonpharmacologic source of exogenous estrogen compounds, but they could not document that this form of phytoestrogen ingestion results in precocious puberty. In a retrospective study, soy formula–fed men and women were compared to adults who were fed cow’s milk–based formulas and no differences were found in age of menarche or breast development of the women in the study (Strom et al., 2001). The researchers did note that soy formula–fed women did report significantly longer duration of menstrual bleeding and greater discomfort with menstruation.

Skin and Hair Care Products Premature development of secondary sex characteristics has also been associated with the systemic absorption of certain cosmetic and hair care products, most commonly used by African Americans. B&B Super Gro, marketed in the United States since 1994, is an example of a product that contains 1.6 g of estrogen per 100 g. As evidenced by the delivery of hormone therapy via skin patches, estrogen is readily absorbed by the skin. Products containing estrogen or placenta, when unintentionally ingested or inhaled, applied to the breast area, or used as a topical treatment for diaper rash or scalp conditions, have resulted in the early development of sexual characteristics (Golub, 2000; Tiwary, 1998; Zimmerman, Francis, & Poth, 1995). Even after discontinuation of an estrogen- or placenta-containing preparation, the sexual development may persist up to 36 months. The U.S. FDA does not regulate estrogen-containing cosmetic or skin care products, many of which contain placental extracts and estrogen in amounts high enough to cause precocious puberty, gynecomastia in men, or postmenopausal bleeding in women (Nebesio & Pescovitz, 2005). Disrupted sex hormone action is also believed to be involved in the increased occurrence of genital abnormalities among newborn boys as well as precocious puberty in girls (Andersson, 2006).

Assisted Reproductive Technology Another area under investigation is that of hormone use during the implementation of a variety of assisted reproductive technologies (ART). There are clinical accounts of infants born with developed breasts or pubic hair, or both, when their mothers had become pregnant using ART (Rojas-Marcos et al., 2005). No safe threshold for estrogen use has been determined so caution should be taken to avoid unnecessary exposure of fetuses and young children to exogenous sex steroids (Andersson, 2006). As a relatively new phenomenon, no data are available to JOGNN 267

describe the long-term effects of ART on pubertal development in children who were the products of this method of conception. While little is known about pubertal development in these children, it is theorized that fetal exposure to high hormone levels has an effect on health later in life. Placental weight is considered to be a biomarker that reflects hormone levels during pregnancy. Women who have two pregnancies with placental weights greater than 700 g are twice as likely to develop breast cancer as women whose placentas each weighed less than 500 g (Cnattingius et al., 2005).

Overweight and Obesity Influences on Endocrine Function The number of overweight children aged 6 to 11 has more than doubled in the past 20 years (7% in 1980 to 18.8% in 2004) and the rate has more than tripled among adolescents aged 12 to 19 (5% in 1980 to 17.1% in 2004) (Ogden et al., 2006). The role of obesity is often cited in association with the earlier onset of puberty and has been a source of debate since the Lawson Wilkins Society recommendation to amend the definition of precocious puberty in U.S. girls (AAP & ACOG, 2006). The height to weight ratio is also affected when endocrine function is disrupted, which may also contribute to the number of persons defined as obese in adulthood. Girls with precocious puberty have rapid physical growth early in life but shorter height later in life (Brown & Warne, 2006). While obesity is often cited as being associated with precocious puberty, there is no well-designed research to support this supposition.

Stress as an Endocrine Disruptor Psychosocial stress may be a stimulant of, as well as a response, to puberty. A study of preteen girls who were sexually abused suggested that the abuse may have served as a stressor that stimulated the hypothalamus to activate the process of puberty (Ge, Conger, & Elder, 1996; Herman-Giddens, Sandler, & Friedman, 1998). These studies dispute the reverse assumption that abuse is more prevalent in girls who appear sexually mature and, in some way, provoke the abuse. Other stressors such as low socioeconomic status, peer pressure, violence, bullying, or performance pressure have also been implicated as factors that trigger the onset of puberty. Also, it is believed that regular exposure to unrelated adult males may serve as a link to early sexual development. This theory is based on the role of pheromones, a known trigger for sexual development in other mammalian species. Therefore, stepfather presence, not biological father absence, appears to be a better predictor for earlier pubertal maturation in young girls (Ellis & Garber, 2000). These researchers also reported that a history of mood disorders in mothers was associated with earlier onset of 268 JOGNN

puberty in female children. The early puberty observed in adopted girls may be associated with previous life stressors and exacerbated by pheromone exposure (Mul, Oosdiijk, & Drop, 2002b).

Assessment of the Prepubertal and Pubertal Child A comprehensive biopsychosocial assessment of the preteen girl experiencing early onset of puberty or pregnancy is of utmost importance. In addition to the usual components of a comprehensive examination, the assessment should include anatomic and physical markers as well as molecular and cellular biomarkers (Ritzen, 2003; Rockett, Lynch, & Buck, 2004; Traggiai & Stanhope, 2003). The evaluation of a girl demonstrating signs of precocious puberty requires a complete clinical history with an emphasis on pubertal progression, graphing height and weight on a growth chart, discussion of developmental milestones of parents and siblings, neurologic events, and ingestion or exposure to gonadal steroids. A thorough examination of the color of the vaginal mucosa, vaginal discharge, density of breast tissue, pattern of body hair, presence of acne, and muscle development are essential components of the physical examination. Diagnostic tests should include radiography of the left hand and wrist to determine bone density, cranial magnetic resonance imaging (MRI), ultrasound of the ovaries and uterus, basal hormone functions (serum follicle-stimulating hormone, leutenizing hormone, human chorionic gonadotropin, gonadal steroid levels, and thyroid function studies), and a GnRH stimulation test (Diaz & Danon, 2000). Girls with early development of secondary sex characteristics should have a cranial MRI to rule out intracranial pathology such as central nervous system tumors or head trauma that may cause a disruption in endocrine function. In a study by Ng, Kumar, Cody, Smith, and Didi (2003), intracranial abnormalities were present in 15% of patients presenting with precocious puberty. The differentiation between gonadotropin-dependent and gonadotropin-independent precocious puberty is an important step in the proper diagnosis and prompt treatment of patients with precocious puberty (Kakarla & Bradshaw, 2003). Gonadotropin-dependent precocious puberty, also referred to as central precocious puberty, is characterized by premature activation of the GnRH pulse generator. Gonadotropin-independent precocious puberty, or peripheral precocious puberty, is present when the GnRH pulse generator is suppressed (Massart et al., 2005).

Anatomic Markers Used to Stage Pubertal Development One of the standards used most often to stage the normal development of puberty in females is a system described Volume 36, Number 3

by Marshall and Tanner in 1969 (Table 1). In table format, the physical changes that result from body chemistry changes are used as a guide to the “normal” process of puberty usually completed over a period of approximately 4.5 years. In recent years, limitations have been cited in the use of this tool resulting in alternative methods of assessment. Because visual examination of a nude child or adolescent by a trained examiner is necessary to use the Tanner method, many clinicians have proposed the use of self-assessment techniques to obtain this information (Rockett et al., 2004). These techniques utilize a variety of photos or line drawings in which the child or adolescent selects the example that most closely depicts their own development, usually with great accuracy.

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he diagnosis of precocious puberty can be a distressing finding for families and a challenge for health care providers.

The diagnosis of precocious puberty can be a distressing finding for families and a challenge for health care providers (Clark, 1998). The early occurrence of these physical changes often leads to psychosocial distress and an alteration in the developmental tasks of this age group. Being viewed as “different” from their peers, these girls have difficulty developing social relationships and a positive

self-concept. Body image, expressions of sexuality, and self-esteem can be easily altered at this time in a child’s life. These young girls are more likely to be depressed, aggressive, socially withdrawn, or moody (Zuckerman, 2001). In addition to the psychosocial disturbances associated with precocious puberty, the premature pubertal growth spurt and the accelerated bone maturation result in reduced adult height (Partsch & Sippell, 2001). Continuing to graph height and weight can alert the provider to such patterns of growth. The early onset of puberty also places the girl at higher risk of developing breast cancer later in life (Zuckerman, 2001). The hereditary and genetic component must also be explored with a detailed history of puberty onset of the parents as well as height, weight, and growth patterns of other family members (AAP, 2006). Although there is a trend toward earlier puberty in American children, a study by Midyett, Moore, and Jacobson (2003) concluded that signs of puberty in 6- to 8-year-old girls should not be considered normal or benign. In their study, 12.3% (n = 223) of the girls exhibiting signs of puberty at this age were found to have an endocrine disorder such as congenital adrenal hyperplasia, pituitary adenoma, and neurofibromatosis. The researchers fear that implementation of lowering the prevailing standard for puberty from 8 to 7 in White girls and 6 in Black girls will result in the failure to identify conditions that respond to early intervention.

Nursing Care and Interventions The ACOG (ACOG, Committee on Adolescent Health Care, 2006) recommends that the initial visit to the

TABLE 1

Tanner Stages of Female Puberty Stage

Breast

1 Preadolescent

Only papillae are elevated.

2

Breast bud and papilla are elevated and a small mount is present; areola diameter is enlarged. Further enlargement of breast mound; increased palpable glandular tissue. Areola and papilla are elevated to form a second mound above the level of the rest of the breast.

3 4 5 Adult

Adult mature breast; recession of areola to the mound of breast tissue, rounding of the breast mound, and projection of only the papilla are evident.

Pubic Hair Vellus hair only and hair is similar to development over anterior abdominal wall (i.e., no pubic hair). There is sparse growth of long, slightly pigmented, downy hair or only slightly curled hair, appearing along labia. Hair is darker, coarser, more curled, and spreads to the pubic junction. Adult-type hair; area covered is less than that in most adults; there is no spread to the medial surface of thighs. Adult-type hair with increased spread to medial surface of thighs; distribution is as an inverse triangle.

Note. Reproduced with permission from the BMJ Publishing Group from Tanner, J., & Whitehouse, R. (1976). Clinical longitudinal standards for height, weight, height velocity, weight velocity, and stages of puberty. Archives of Disease in Childhood, 51, 170-179.

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TABLE 2

Web Sites for Additional Information www.med.umich.edu/1libr/yourchild/puberty.htm Informational Web site for parents and professionals sponsored by the University of Michigan Health Systems. http://www.magicfoundation.org/www/docs/146/ The Magic Foundation provides information on precocious puberty, as well as webcasts and online networking opportunities for parents and health professionals. www.cincinnatichildrens.org/health/info/endocrine/diagnose/precocious.htm A concise descriptions and summary of potential causes, symptoms, and treatment of precocious puberty that is provided by Cincinnati Children’s Hospital Medical Center. http://www.safecosmetics.org/index.cfm The campaign for safe cosmetics is a coalition dedicated to protecting health by identifying cosmetic products that contain chemicals that may be linked to cancer, birth defects, and reproductive and developmental problems. www.nottoopretty.org Up-to-date information on women’s cosmetics, fragrances, and other products containing phthalates.

gynecologist for health guidance, screening, and provision of preventive services should take place by age 13. Girls who demonstrate precocious development should be referred at an earlier age whenever secondary sex characteristics begin to appear. At these visits, nurses can furnish information about menstrual hygiene, menstrual protection, sexual activity, contraception, and sexually transmitted diseases through private discussion, printed materials, and suggested reputable Web sites (Adams-Hillard, 2002). Written educational materials can be prepared for the cognitive perception of the 9- to 12-year-old age group and at the appropriate level of reading comprehension (Gallager, 1999). Barriers to health care such as poverty, low level of educational attainment of the head of household, substance abuse, depression, and sexual, physical, or domestic violence are risk factors that require screening, assessment, and intervention when necessary. Appropriate local and governmental assistance programs should be offered and explored when warranted. Consider enlisting the assistance of a social worker to help with public assistance, medical costs, and counseling needs. Short and Rosenthal (2003) suggested that clinicians can influence the sexual decisions of children who exhibit early pubertal changes through education, open discussion of feelings in a nonthreatening manner, and the encouragement of parental or adult role modeling. It is important, however, to maintain the child’s right to confidential care. Parents can be provided with age-appropriate guidelines for supervision and what constitutes developmentally appropriate limit setting (Gallager). Support parents of the sexually precocious child in developing their skill in discussing sexuality or advise them to find other family members with similar values with whom the child feels comfortable. The social context of a child’s life, including peer and societal norms, influences the child’s decision making processes. In general, young girls believe that intercourse should happen in a committed relationship. However, 270 JOGNN

sometimes teens find themselves having sex with people they do not know well (Bruckner & Bearman, 2003). The type of relationship impacts whether or not condoms are used (Short & Rosenthal, 2003). This results in more than three million new cases of sexually transmitted diseases and almost one million pregnancies in teens and preteens every year (Martin, Hamilton, Ventura, Menacker, & Park, 2002). Bacterial vaginosis, chlamydia, gonorrhea, cytomegalovirus, herpes simplex viruses, human immunodeficiency virus, and syphilis occur at extremely high rates for this age group (Conrad & Blythe, 2003). An appropriate method of contraception for the very young or preadolescent should be considered if it is found that the child is sexually active (Camillo, 2003). A positive and accepting attitude of the nurse in providing care to the young girl experiencing early development of secondary sexual characteristics facilitates a healthy rapport between the patient, her family, and the health care system. Health care that is perceived by the recipient as caring and supportive is instrumental in aiding the school-age child in establishing or maintaining a positive self-concept and body image (Connelly, 1998). Recognizing the importance of a support person, regardless of who the child selects for this role, demonstrates respect. This person should be encouraged to accompany the child on health care visits and be included in the teaching plan. Preadolescents, just as adults, desire their caregivers to be respectful, caring, and supportive. They want to feel accepted and valued and are sensitive to comments and behaviors that communicate the belief that they are different than their peers, creating additional stress. Care should also emphasize health promotion and include diet, exercise, and age-appropriate activities. Encouraging the child and her family to eat a well-balanced diet that is based on the recommended daily allowances for preadolescents is essential for optimal growth and development. Body image issues or eating disorders may keep her from consuming an Volume 36, Number 3

adequate diet. Programs that help girls with precocious puberty discover their inner strength and create environments for coping with physical differences assist the child in successful mastery of the developmental tasks appropriate for chronologic age. Sellman (2004) recommended the following parent teaching points: • Avoid using pesticide, herbicides, or insecticides that young children could come in contact with • Be aware of practices in the community that require the spraying of EDCs for insect control • Thoroughly cleanse nonorganic fruits and vegetables • Read the labels on personal care products and check Web sites for phthalates and other toxic or hormonemimicking chemicals • Beware of soft plastic toys to which phthalates may have been added to soften polyvinyl chloride (PVC) plastic toys • Teach and remind children of good hand washing practices • Do not cook foods packaged in plastics in the microwave oven • Use of a high-grade water filter aids in removing impurities from water sources • Encourage children to get plenty of exercise to maintain appropriate weight and promote elimination of contamination through perspiration • Avoid PVC products, including vinyl shower curtains and toys and packaging that bear the number “3,” indicating they are made with PVC.

Conclusions Precocious puberty has physical, psychological, and social implications that are complex and influenced by many factors. A young girl exhibiting extremely early sexual development faces tremendous social stigma with probable negative effects on her health and well-being (Mul, Oostdiijk, & Drop, 2002a). Health care providers play an integral role in coordinating services to these young patients and have the potential to influence society’s view of the developmental needs of this portion of the population. Early screening, identification, and intervention will ensure optimal health and sexuality outcomes for these girls. REFERENCES Adair, L. (2001). Size at birth predicts age of menarche. Pediatrics, 107, E59. Adams-Hillard, P. (2002). Menstruation in young girls: A clinical perspective. Obstetrics and Gynecology, 99, 655662. American Academy of Pediatrics, Committee on Adolescence, & American College of Obstetricians and Gynecologists, Committee on Adolescent Health Care. (2006). Menstrua-

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nal of the International Society of Gynecological Endocrinology, 16, 163-171. Golub, M. (2000). Adolescent health and the environment. Environmental Health Perspectives, 108, 355-362. Gray, E., Wolf, C., Lambright, C., Mann, P., Price, M., Cooper, R. L., et al. (1999). Administration of potentially antiandrogenic pesticides (procymidone, linuron, iprodione, chlozolinate, p, p’-DDE, and ketoconazole) and toxic substances (dibutyl- and diethlhexyl phthalate, PCB 169, and ethane dimethane sulphonate) during sexual differentiation produces diverse profiles of reproductive malformations in the male rat. Toxicology and Industrial Health, 15, 94-118. Herman-Giddens, M., Sandler, A., & Friedman, N. (1998). Sexual precocity in girls: An association with sexual abuse. AJDC, 142, 431-433. Herman-Giddens, M., Slora, E., Wasserman, R., Bourdonoy, C., Bhapkar, M., Koch, G., et al. (1997). Secondary sexual characteristics and menses in young girls seen in office practice: A study from the Pediatric Research in Office Settings Network. Pediatrics, 99, 505-512. Houlihan, J., Brody, C., & Schwan, B. (2002). Not too pretty: Phthalates, beauty products, and the FDA. Environmental Working Group. Retrieved December 30, 2006, from http://www.safecosmetics.org/docUploads/NotTooPretty_ r51.pdf Jobling, S., Reynolds, T., White, R., Parker, M., & Sumpter, J. (1995). A variety of environmentally persistent chemicals, including some phthalate plasticizers, are weakly estrogenic. Environmental Health Perspective, 103, 582-587. Kakarla, N., & Bradshaw, K. (2003). Disorders of pubertal development: Precocious puberty. Seminars in Reproductive Medicine, 21, 339-351. Kaplowitz, P., Oberfield, S., & The Drug and Therapeutics and Executive Committees of the Lawson Wilkins Pediatric Endocrine Society. (1999). Re-examination of the age limit for defining when puberty is precocious in girls in the United States. Pediatrics, 104, 936-941. Kaplowitz, P., Slora, E., Wasserman, R., Pedlow, S., & HermanGiddens, M. (2001). Earlier onset of puberty in girls: Relation to increased body mass index and race. Pediatrics, 108, 347-353. Klein, K. (1998). Isoflavones, soy-based infant formulas and relevance to endocrine function, Nutrition Reviews, 56, 193-204. Krstevska-Konstantinova, M., Charlier, C., Craen, M., Du Caju, M., Heinrichs, C., & de Beaufort, C. (2001). Sexual precocity after immigration from developing countries to Belgium: Evidence of previous exposure to organochlorine pesticides. Human Reproduction, 16, 1020-1026. Lemonick, M. (2000). Teens before their time. Time Magazine, 156, 66-74. Marshall, W., & Tanner, J. (1969). Variations in patterns of pubertal changes in girls. Archives of Disease in Childhood, 44, 291-303. Martin, J., Hamilton, B., Ventura, S., Menacker, F., & Park, M. (2002). Births: Final data for 2000 [Online]. National Vital Statistics Reports, 50. Retrieved January 15, 2007, from http://www.cdc.gov/nchs/data/nvsr/nvsr50/nvsr50_05. pdf

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Massart, F., Seppia, P., Pardi, D., Lucchesi, S., Meossi, C., Gagliardi, L., et al. (2005). High incidence of central precocious puberty in a bounded geographic area of northwest Tuscany: An estrogen disrupter epidemic? Gynecological Endocrinology, 20, 92-98. Midyett, L., Moore, W., & Jacobson, J. (2003). Are pubertal changes in girls before age eight benign? Pediatrics, 111, 47-51. Mocarelli, P., Brambilla, P., Gerthous, P., Patterson, D., & Needham, L. (1996). Change in sex ratio with exposure to dioxin. Lancet, 348, 409. Mul, D., Oostdiijk, W., & Drop, S. (2002a). Early puberty in girls. Best Practice and Research: Clinical Endocrinology and metabolism, 16, 153-163. Mul, D., Oostdiijk, W., & Drop, S. (2002b). Early puberty in adopted children. Hormone Research, 57, 1-9. National Resources Defense Council. (1998). Health & the environment health effects of air & water pollution endocrine disruptors. Retrieved December 15, 2006, from http:// www.nrdc.org/health/effects/qendoc.asp Nebesio, T., & Pescovitz, O. (2005). Historical perspectives: Endocrine disruptors and the timing of puberty. The Endocrinologist, 15, 44-48. Ng, S., Kumar, Y., Cody, D., Smith, C., & Didi, M. (2003). Cranial MRI scans are indicated in all girls with central precocious puberty. Archives of Disease in Childhood, 88, 414-418. Ogden, C., Carroll, M., Curtin, L., McDowell, M., Tabak, C., & Flegal, K. (2006). Prevalence of overweight and obesity in the United States, 1999-2004. Journal of the American Medical Association, 295, 1549-1555. Ojeda, S., & Heger, S. (2001). New thoughts on female precocious puberty. Journal of Pediatric Endocrinology and Metabolism, 14, 245-256. Ong, K., Ahmed, M., & Dunger, D. (1999). The role of leptin in human growth and puberty. Acta Paediatrics Supplement, 433, 95-98. Parent, A., Teillmann, G., Juul, A., Shakkebaek, N., Toppari, J., & Bourguignon, J. (2003). The timing of normal puberty and the age limits of sexual precocity: Variations around the world, secular trends, and changes after migration, Endocrine Review, 24, 668-693. Partsch, C., & Sippell, W. (2001). Pathogenesis and epidemiology of precocious puberty. Effects of exogenous estrogens. Human Reproduction Update, 7, 292-302. Pediatric Research in Office Settings. (2005). Earlier sexual development attributed to increased prevalence of obesity. Retrieved December 30, 2006, from http://www.aap.org/ pros/abtpros.htm Rastogi, S. (1998). Gas chromatographic analysis of phthalate esters in plastic toys. Chromatographia, 47, 724-726. Ritzen, E. (2003). Early puberty: What is normal and when is treatment indicated? Hormone Research, 60(3 Suppl.), 31-34. Rockett, J., Lynch, C., & Buck, G. (2004). Biomarkers for assessing reproductive development and health: Part 1—Pubertal development. Environmental Health Perspectives, 112, 105-112. Rogan, W., & Ragan, N. (2003). Evidence of effects of environmental chemicals on the endocrine system in children. Pediatrics, 112, 247-252.

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Rojas-Marcos, P., David, R., & Kohn, B. (2005). Hormonal effects in infants conceived by assisted reproductive technology. Pediatrics, 116, 190-194. Sanghavi, D. (2006). Preschool puberty, and a search for the causes. New York Times, 156, D1, D6. Sellman, S. (2004). The problem of precocious puberty. Retrieved December 30, 2006, from http://www.oasisadvancedwellness.com/learning/precocious-puberty.html Setchell, K., Zimmer-Nechimias, L., Cai, J., & Heubi, J. (1998). Exposure of infants to phyto-estrogens from soy-based infant formula. Lancet, 350, 23-27. Short, M., & Rosenthal, S. (2003). Helping teenaged girls make wise sexual decisions. Contemporary OB/GYN, 48, 84-95. Solomon, G. M., & Schetter, T. (2000). Environment and health: 6. Endocrine disruption and potential human health implications. CMAJ, 163, 1471-6. Available: www.cmaj.ca/ cgi/content/full/163/11/1471[Free Full Text] https://owa. twu.edu/cgi/ijlink? linkType=FULL&journalCode=cmaj&resid=136/11/1471 Staessen, J., Nawrot, T., Den Hond, E., Thijs, L., Fagard, R., Hoppenbrouwers, K., et al. (2001). Renal function, cytogenetic measurements, and sexual development in adolescents in relations to environmental pollutants: a feasibility study of biomarkers. Lancet, 357, 1660-1669. Strom, B., Schinnar, R., Ziegler, E., Barnhart, K., Sammel, M., Macones, G., et al. (2001). Exposure to soy-based formula in infancy and endocrinological and reproductive outcomes in young adulthood. Journal of the American Medical Association, 286, 807-814. Tanner, J., & Whitehouse, R. (1976). Clinical longitudinal standards for height, weight, height velocity, weight velocity, and stages of puberty. Archives of Disease in Childhood, 51, 170-179. Tiwary, C. (1998). Premature sexual development in children following the use of estrogen-or placenta-containing hair products. Clinical Pediatrics, 37, 733-739. Traggiai, C., & Stanhope, R. (2003). Disorders of pubertal development. Best Practice and Research: Clinical Obstetrics and Gynaecology, 17, 41-56. Valentin-Blasini, L., Sadowski, M., Walden, D., Caltabiano, L., Needham, L., & Barr, D. (2005). Urinary phytoestrgen concentrations in the U.S. population (1999-2000). Journal of Exposure Analysis and Environmental Epidemiology, 15, 509-523. Vasiliu, O., Muttineni, J., & Karmaus, W. (2004). In utero exposure to organochlorines and age at menarche. Human Reproduction, 19, 1506-1512. Wang, R., Needham, L., & Barr, D. (2005). Effects of environmental agents on the attainment of puberty: Considerations when assessing exposure to environmental chemicals in the National Children’s Study. Environmental Health Perspectives, 113, 1100-1107. Wu, T., Buck, G., & Mendola, P. (2003). Blood lead levels and sexual maturation in US girls: The Third National Health and Nutrition Examination Survey, 1988-1994. Environmental Health Perspectives, 111, 737-741. Wu, T., Mendola, P., & Buck, G. (2002). Ethnic differences in the presence of secondary sex characteristics and menarche among US girls: The Third National Health and

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Nutrition Examination Survey, 1988-1994. Pediatric, 110), 752-757. Zimmerman, P., Francis, G., & Poth, M. (1995). Hormonecontaining cosmetics may cause signs of early sexual development. Military Medicine, 160, 628-630. Zuckerman, D. (2001). When little girls become women: Early onset of puberty in girls. The Ribbon: A Newsletter of the Cornell University Program on Breast Cancer and Environmental Risk Factors in New Your State (BCERF), 6, 6-9. Retrieved November 22, 2005 from http://envirocancer.cornell.edu/Newsletter/Newsletter.cfm

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Sandra K. Cesario, RNC, PHD, is a doctoral program coordinator and an associate professor at the College of Nursing, Texas Woman’s University, Houston. Lisa A. Hughes, MEd, is a research coordinator at the University of Texas School of Nursing, Houston. Address for correspondence: Sandra K. Cesario, RNC, PHD, College of Nursing, Texas Woman’s University, 6700 Fannin Street, Houston, TX 77030-2343. E-mail: [email protected].

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