Adolescent exposures to cosmetic chemicals of concern
Teen Girls' Body Burden of Hormone-Altering Cosmetics Chemicals: Teens are vulnerable
A sudden flurry of interrelated hormone signals initiates the complex process of puberty in the body of an adolescent, triggering rapid development of the reproductive system. Alterations in an array of sex hormones, present in the body at levels as low as one part per billion (ppb), or even one part per trillion (ppt), guide this transformation to adulthood.
Subtle hormonal signals coordinate many other critical developmental processes occurring during human adolescence, including the adolescent "growth spurt" and associated rapid bone growth, maturation of the immune, blood, and adrenal hormone systems, shifts in metabolism, and key changes to brain structure and function. The dramatic changes of adolescence, all orchestrated via shifts in the minute levels of hormones present in healthy bodies, suggest a unique vulnerability of adolescents and pre-adolescents to the effects of exposures to low levels of hormone-active chemicals found in body care products and other everyday items.
Premature puberty – a warning sign
Signs of this vulnerability are evident in girls growing up all over America. Over the last 4 decades, the age at which girls begin to develop breasts has declined by 1 to 2 years (Steingraber 2007), with black girls typically developing at an earlier age than white girls. At present, about half of all U.S. girls show signs of breast development by their 10th birthday, with 14% attaining breast buds between their 8th and 9th birthdays (Herman-Giddens 1997; Lee 2001). Early breast development, as well as the appearance of pubic hair at a young age, have become so common that in 1999 the clinical definition of early-onset or precocious puberty in the U.S. was reduced from age 8 to 7 for white girls, and from age 7 to 6 for black girls (Kaplowitz 1999). By some estimates, precocious puberty currently affects as many as 1 in 5,000 children, and is 10 times more common in girls than boys (Nebesio 2005; Partsch 2001).
Over the same 40 year time period, the age at which girls in the U.S. begin menstruating has declined by a few months, with substantial variation by ethnicity (Steingraber 2007). According to the Centers for Disease Control and Prevention (CDC), the mean age of the beginning of menstruation, or menarche, in the U.S. was 12.8 years in 1970 (Harlan 1980); nearly 40 years later, it stands at about 12.6 years for white girls, 12.1 for black girls and 12.2 for Mexican American girls (Kaplowitz 2006; Herman-Giddens 1997, 2006).
Early puberty and adult disease
A girl that begins puberty at an early age is at greater risk for several adult illnesses, including breast cancer (Wang 2005; Steingraber 2007; Golub 2008) and polycystic ovary syndrome (Ibáñez 1997; Kousta 2006; Steingraber 2007; Golub 2008), a leading cause of pelvic pain and infertility. Polycystic ovary syndrome is also linked to increased risk of obesity, diabetes, and impaired glucose tolerance (Auchus 2004; Kousta 2006), and increased prevalence of risk factors associated with cardiovascular disease (Kousta 2006). In addition, girls who experience premature puberty are more likely to fail to reach normal adult height (Carel 2006; Partsch 2006). In boys, early puberty may be associated with an increased risk for testicular cancer according to some epidemiological studies (Golub 2008).
Early-maturing girls are also more prone to a variety of psychiatric or behavioral problems, including depression, eating disorders, and attempted suicide (Graber 1997; Kaltiala-Heino 2001, 2003a, 2003b), early use and abuse of drugs, alcohol, and cigarettes (Graber 1997, 2004; Kaltiala-Heino 2003b), early sexual encounters (Kaltiala-Heino 2003b), unprotected sex (Flanigan 2003), teen pregnancy (Deardorff 2005), and conduct disorders and criminal behavior (Johansson 2005; Kaltiala-Heino 2003b; Burt 2006; Celio, 2006). Early-maturing girls are also more likely to be physically and violently victimized (Haynie 2006). Women experiencing early puberties tend to have lower academic education (Johansson 2005), while late-maturing girls tend to perform better in school and are more likely to finish college (Graber 1997, 2004).
Chemical contaminants can disrupt the hormone system
While improved nutrition and increased incidence of obesity may play a role in the falling age of puberty, scientists and medical professionals increasingly identify exposures to hormone-disrupting chemicals as a potentially critical factor in unnaturally accelerating this critical period of development. Few epidemiological studies probe the association between exposures to trace levels of widely used hormone-disrupting chemicals and the timing of puberty. However, preliminary research on people suggests that exposures to phthalates (Colon 2000), the pesticide DDT and its metabolite DDE (Krstevska-Konstantinova 2001; Vasiliu 2004), and polybrominated biphenyls (PBBs; Blanck 2000), may be linked to early puberty in girls. In contrast, exposures to the pesticide endosulfan (Saiyed 2003), polychlorinated biphenyls (PCBs; Den Hond 2002), and lead (Hauser 2008) may be linked to delayed puberty in boys. The hormone-disrupting properties of these chemicals have been corroborated in numerous animal studies (e.g., ATSDR 1995, 1997, 2000, 2002).
Animal studies also indicate that exposures during puberty to hormone-disrupting contaminants may trigger unique and lasting adverse health effects unlike those seen for exposures during adulthood. For example, immature and pubertal rats appear to be more sensitive than adults to testicular toxicity induced by exposure to phthalates, perhaps due to differences in the absorption or metabolism of these compounds (Gray 1986; Sjoberg 1986; Dostal 1988). Immature male rats are also more sensitive than adults to the pesticide 1,2-dibromo-3-chloropropane (Lui 1987). This pesticide was banned after reports of infertility in occupationally exposed men. In parallel, immature rats may be more susceptible than adult rats to ovarian toxicity produced by the industrial chemical 4-vinylcyclohexene diepoxide (Flaws 1994).
Animal studies on breast cancer also indicate that the period around puberty, in which mammary glands undergo critical types of development, may be a period of special vulnerability to toxic chemicals that can provoke alterations in development that predispose the breast to cancer (Fenton 2006). Animals exposed to the extremely potent hormone disruptor dioxin experienced inhibited mammary gland development, the effects of which persisted into adulthood (Brown 1998; Lewis 2001; Fenton 2002). A study of 200 Belgian adolescents exposed to dioxin and other chemicals via pollution demonstrated a significant delay in breast development in girls associated with a doubling of serum dioxin concentrations (Den Hond 2002).
Researchers at the University of California at Davis have performed a thorough examination of the effects of hormone disruption during adolescence by exposing female rhesus monkeys to known estrogenic agents methoxychlor and diethylstilbestrol (DES) during puberty (Golub 2003, 2004). DES in particular was found to have a dramatic effect on development, triggering increased incidence of ovarian cysts, suppression of menses, premature emergence of some secondary sex characteristics and delayed emergence of others, inhibition of the adolescent growth spurt, reduced bone mass and length, and alterations to a number of blood and immune system parameters. Disruption in these systems could alter adult risk for reproductive system dysfunction, as well as osteoporosis, heart disease, and autoimmune disease.
Deficient public health policies leave teens at risk
Despite this evidence, little concerted effort has been made to evaluate the relative sensitivity to toxic assault of the breast, the male and female reproductive systems, and the brain, blood, bone, and immune systems during adolescence, as compared to adulthood. Though a recent review by government scientists of "critical windows" of vulnerability to the effects of toxic chemicals reveals an urgent need for study of exposures during puberty (Selevan 2000), standardized animal tests that probe for many of these effects have yet to be developed.
Also lacking are public health policies that recognize this unique adolescent sensitivity to chemical exposures, a sensitivity alarmingly highlighted by the dangerous side effects adolescents can experience when treated with specific antidepressants and drugs tested only on adults (Pryor 2000; FDA 2007). For example, EPA required nearly a decade of review to update its cancer risk guidelines in 2003, finally conceding the importance of general childhood exposures to toxic chemicals (EPA 2005). The new policy targets only cancer, leaving EPA with no formal policy regarding childrens' and teens' vulnerability to chemicals that damage the immune system, the brain, the hormone system, or a host of other potential targets, despite evidence that these populations face higher risks for harm.
The U.S. Food and Drug Administration (FDA), the government agency responsible for regulating both pharmaceuticals and personal care products, has recently instituted policies designed to improve pediatric drug research and treatment. In contrast, FDA provides no safety standards that protect children or adolescents from potentially harmful ingredients in body care products. Despite well-known examples of the premature appearance of pubic hair or breast buds on girls and boys following use of body care products containing high levels of estrogen, placenta, tea tree essential oil, or lavender essential oil (Zimmerman 1995; Tiwary 1998; Felner 2000; Golub 2000; Henley 2007), FDA has no authority to require premarket testing of personal care product ingredients for safety. This appalling lack of responsibility leaves all American teens at risk.