Early puberty is associated with numerous negative mental health and physical health outcomes over the life course for girls and women, including obesity, type II diabetes, depression, conduct problems, substance use, teen pregnancy, and breast and other reproductive cancers [1
]. Timing of pubertal onset among girls varies widely, with secondary sexual characteristics - the first observable signs of puberty - usually appearing around ages 10 to 11 years [8
]. However, epidemiologic evidence confirms that certain pubertal markers are occurring earlier among girls in the U.S. than in the past, particularly onset of breast and pubic hair development [8
]. In addition, there are marked disparities in pubertal timing across ethnic groups. Recent epidemiological research shows that at age 8 years approximately 43% of black girls, 31% of Hispanic girls and 18% of white girls have experienced onset of breast development [13
This documented trend of earlier pubertal onset has prompted a cascade of research focused on potential antecedents that may explain variability in girls' timing of puberty. A variety of environmental and genetic factors have been identified that influence pubertal timing [14
] with a recent enhanced focus on behavioral and environmentally-related factors, including overweight and obesity [15
], family stressors [16
], and environmental toxins [20
] as potentially important determinants. No known studies, however, have examined the influence of neighborhood factors, nor how neighborhood effects might operate through girls' overweight, to influence pubertal onset. The current study addresses these gaps in the scientific literature.
Neighborhoods are complex entities encompassing culture, economics, history, governance, and the built and natural environments [21
]. The neighborhoods in which children live have been shown to influence their behaviors and health outcomes [22
]. There are conceivably two potential pathways through which a neighborhood environment might influence a girl's pubertal timing: (1) through reduced access to healthful foods and physical activity, which may lead to overweight and, in turn, earlier pubertal onset, and (2) through exposure to acute and chronic stress, which may trigger hormonal stress responses that prompt pubertal onset. An extensive body of literature supports the first proposed pathway. Research shows that body composition and physical activity levels are influenced by neighborhood environments and are also related to timing of girls' pubertal development [25
]. Limited availability of fresh foods and poor access to safe recreational outlets may negatively influence girls' eating habits and physical activity patterns, which can lead to overweight and increased adiposity. In turn, hormonal changes related to increases in adiposity can subsequently accelerate pubertal maturation [34
]. In addition, ample research suggests that exposure to stressful environmental conditions, particularly within the family realm, confers risk for earlier pubertal development [14
] ostensibly by influencing hormonal pathways that trigger puberty [19
]. As such, neighborhood stressors may operate in a similar manner to stress in the family and directly influence pubertal maturation. A combination of these two pathways may also exist, whereby neighborhood stressors and poor psychological functioning lead to emotional eating, reduced physical activity and overweight, which in turn may promote earlier puberty.
Past studies examining environmental determinants of pubertal timing have exhibited methodological limitations. One such limitation is that many studies have focused on menarche as an outcome, which occurs relatively late in the pubertal transition. Other studies have examined overall pubertal development without distinguishing between onset of breast development (thelarche) and onset of pubic hair (pubarche) development. Thelarche and pubarche represent observable markers of underlying hormones that are dependent on the maturation of unique endocrine axes, i.e., the hypothalamic-pituitary-gonadal (HPG) and hypothalamic-pituitary-adrenal (HPA) axis, respectively. Neighborhood factors might conceivably act on these hormonal pathways differentially. For instance, neighborhood conditions that lead to increases in body fat, which is associated with estrogen production, are likely to trigger the HPG axis resulting in accelerated breast development. Alternatively, environmental stress and resulting cortisol release (a measure of stress response) may awaken the HPA axis and accelerate pubic hair development [19
]. As such, it is important to examine these early pubertal markers (thelarche and pubarche) separately in an effort to better understand potential hormonal responses to neighborhood environments. Moreover, these systems may play differential roles in the etiology of downstream health outcomes, such as breast cancer and other reproductive cancers.
In addition to the aforementioned limitations, studies of environmental determinants of pubertal onset have often been limited by study design. Many were cross-sectional, therefore limiting causal inference. Of those that were longitudinal, often participants were recruited after pubertal onset occurred, i.e., when girls were already peri-pubertal. As such, there is a need for longitudinal research that recruits girls at younger ages and follows them through the pubertal transition.
The current study aims to address these gaps in the extant literature. We utilized 5 waves of data from a larger ongoing study of ethnically-diverse girls and their parents/caregivers. Using direct observations of neighborhood environment and clinic-based Tanner stage assessments, we investigated the contribution of neighborhood factors to timing of onset of breast and pubic hair development, while adjusting for family income. Because girls and their families may be differentially affected by their neighborhoods depending on their contextual and cultural backgrounds, we also examined the modifying (moderating) effect of girls' ethnicity on the associations between neighborhood factors and pubertal outcomes. Moreover, in order to understand potential mechanisms, we investigated whether BMI operated in the causal pathway (i.e., mediated the relationship) between neighborhood factors and onset of puberty.