Year : 2017 | Volume
: 30 | Issue : 3 | Page : 653--656
Puberty disorders and environmental disruptors
Mostafa G El Nagar1, Alaa A Dawood1, Marwa G Elsayed2,
1 Department of Internal Medicine, Faculty of Medicine, Menoufia University, Shebin Elkom, Egypt
2 Department of Internal Medicine, Shebin Elkom Teatching Hospital, Shebin Elkom, Egypt
Marwa G Elsayed
Shebin El-Kom, Menoufia, 32511
The aim of this study was to perform review studying the effect of different environmental disruptors on normal puberty and occurrence of its disorders.
PubMed, Web of science, Wiley Online Library, Central Authentication Service, and Astrophysics Data System were searched. The search was performed from 1 September 2016 to 15 October 2016.
The initial search presented 250 articles. The researches that met the inclusion criteria were six articled. The articles included physiology of puberty in male and female individuals, puberty disorders, endocrinal disruptors, and effects of endocrinal disruptors on puberty.
Data from each eligible study were independently abstracted in duplicate using a data collection form to capture information on study characteristics, interventions, and quantitative results reported for each outcome of interest.
There was heterogeneity in the collected data. It was not possible to perform meta-analysis. Significant data were collected. Thus, a structured review was performed.
Puberty marks a transition between childhood and the adult reproductive stage. It is a vulnerable stage of life, and deregulation has been linked to increased health and psychosocial problems. Puberty development is a multifaceted process that is under the control of different hormonal regulatory mechanisms. Both steroid and nonsteroid hormones were vulnerable to disruption by environmental chemicals. It had also become clear that although the initial focus was on synthetic chemicals such as pesticides and industrial pollutants in the environment that disrupted endocrine activity, a wide variety of chemicals, including those in food, could alter endocrine signaling. Evidence is accumulating that exogenous hormone disruptors may advance or sometimes delay puberty.
|How to cite this article:|
El Nagar MG, Dawood AA, Elsayed MG. Puberty disorders and environmental disruptors.Menoufia Med J 2017;30:653-656
|How to cite this URL:|
El Nagar MG, Dawood AA, Elsayed MG. Puberty disorders and environmental disruptors. Menoufia Med J [serial online] 2017 [cited 2018 Dec 16 ];30:653-656
Available from: http://www.mmj.eg.net/text.asp?2017/30/3/653/218294
Puberty is the life period when pituitary-gonadal maturation leads to a series of physical changes and, ultimately, results in achievement of reproductive capacity. A central event in the onset of puberty is an increase in frequency and amplitude of gonadotropin-releasing hormone (GnRH) secretion in the hypothalamus. This event is controlled by redundant inhibitory or excitatory mechanisms that respectively disappear or appear at the onset of puberty .
It is generally agreed that variations in pubertal timing within a physiological 5-year period are predominantly determined by genetic factors, whereas environmental factors play a comparatively minor role .
A robust landmark of environmental effects on pubertal timing arose through the secular advance in menarcheal age. As this observation was made between the mid-19th and the mid-20th centuries in both the USA and Western Europe and more recently in developing countries , the likely explanation was thought to be improvement in health and nutritional status with industrialization. Accordingly, the end or slowdown of this process seen between 1960 and 2000 was expected. Around the year 2000, however, two large American studies provided evidence of earlier onset of puberty . Initial signs such as onset of breast development were more affected than subsequent signs such as menarcheal age .
Age distribution showed skewing toward earlier ages for initial signs and toward later ages for final signs .
Endocrinal disruptors (EDs) are environmental chemicals, which may be either natural or synthetic. EDs accumulate in the environment in the long term and are introduced into the human body through water, air, and foodstuffs or through equipments used in the office and home. Additionally, it has been demonstrated that EDs can be transferred from the mother to the fetus by placenta or to the baby by breast milk . Studies have shown that several environmental chemical pollutants including dichlorodiphenyltrichloroethane/dichlorodiphenyldichloroethylene, polychlorinated biphenyls, polybrominated bisphenyl, hexachlorobenzene, endosulfan, dioxins, heavy metals, and phthalates affect puberty in humans .
Materials and Methods
The guideline for conducting this review was according to the guidance developed by the center for review and dissemination . It was used to assess the methodology and outcome of the studies.
Search was performed in several databases. It included PubMed, Web of science, Wiley Online Library, CAS, and ADS. The search was performed from 1 September 2016 to 15 October 2016, and included all articles published.
All researches were assessed to be included in the review by two researchers. They were included if they satisfied the following criteria:
Physiology of pubertyPuberty disordersEnvironmental disruptors and puberty
Participants were persons exposed to EDs
Intervention included stop use and substitution of environmental disruptors
Comparative constituents were puberty disorders
Outcome was proper health.
The article title and abstract were initially screened. Then the selected articles were read in full and further assessed for eligibility. All references from the eligible articles were reviewed to identify additional studies.
Data from each eligible study were independently abstracted in duplicate using a data collection form to capture information on study characteristics, interventions, and quantitative results reported for each outcome of interest. Conclusion and comments for each study were made.
There was heterogeneity in the collected data. It was not possible to perform meta-analysis. Significant data were collected. Thus, a structured review was performed.
Overall, four studies were selected. The studies were deemed eligible by fulfilling the inclusion criteria. There was a high degree of heterogeneity regarding the effect of environmental disruptors on puberty.
Puberty is characterized by rapid physiological changes such as growth spurt and maturation of the gonads and the brain. It entails the individual's transition period from a nonreproductive to a reproductive state. Moreover, it is an acknowledged period of emotional stress and vulnerability to socioenvironmental factors . This vulnerable period of transition into adulthood is fine-tuned by endocrine-regulatory mechanisms .
During the past decades, secular trends of earlier age at onset of puberty have been reported .
Endocrine-disrupting chemicals have been implicated in numerous physiological processes affecting normal reproductive health in human beings and animals . Monitoring changes in pubertal onset and development may function as early warning signs for reproductive capacity, both individually and at the population level. The physiological processes that regulate onset of puberty and transit through adolescence are not yet fully understood. Next to a genetic component, environmental factors influence the timing of puberty onset .
The improvement of the nutritional and health status between mid-19th century and the mid-20th century has been associated with an overall decrease in menarcheal age on an average of 3 years in the USA and some countries of Western Europe . The importance of the nutritional status has been demonstrated also in children migrating from developing countries. A Danish study showed that adopted children from developing countries have a 15–20 times higher risk of developing precocious puberty compared with Danish-born children .
Puberty is a multifaceted process that may be monitored by different markers. External signs such as the development of breasts in girls, the increase in testicular volume in boys, and pubic hair growth are staged in adolescents according to criteria defined in the pioneering work by Marshall and Tanner ,. In girls, breast development, pubic hair growth, age at menarche, and regular menstrual cycles are used as markers for pubertal development. In boys, the increase in testicular volume, pubic hair growth, spermaturia, age at first ejaculation, fundamental voice frequency, growth and height spurt, and increased bone density are markers of puberty development . Breast development ('thelarche', the onset of breast development) follows the secretion of ovarian estrogen, whereas the development of female pubic hair ('adrenarche' or 'pubarche', the onset of pubic hair development) is caused by androgens from both the adrenal glands and ovaries. Menarche occurs in response to the gonadotropins such as follicle-stimulating hormone (FSH) and luteinizing hormone (LH) that are released by the pituitary. Menarche occurs generally in late puberty, ~2.0–2.5 years after breast budding. In boys, testicular enlargement and the secretion of testicular androgen (both are called 'gonadarche') usually, but not always, precede pubic hair development .
As the onset of puberty and pubertal progression is under hormonal control, monitoring endocrine status may offer useful biomarkers of puberty. The main hormone involved in the regulation of puberty onset is GnRH in the hypothalamus that stimulates the release of both LH and FSH from the pituitary gland . LH stimulates the production and release by the gonads of testosterone (boys) and estrogens (girls) that can be measured in early puberty as elevated concentrations in morning urine samples . The secretion of adrenal androgens starts in the earliest stages of puberty under control of the hypothalamus–pituitary–adrenal axis. These hormones cause pubic and axillary hair growth and sensitize the androgen receptors of the hypothalamus pituitary. Inhibins are peptides of gonadal origin that suppress FSH production. .
Prepubertal changes in weight and height have been associated with puberty development, and thus, it has been suggested that markers for energy balance and metabolic status may be early biomarkers for puberty development. More recently, leptin has been suggested to be the metabolic messenger between the fat cell and the hypothalamus that stimulates the onset of puberty . Furthermore, insulin levels may stimulate hypothalamic neuronal cells to express and secrete GnRH .
Insulin itself is known to affect the central nervous system functions including the reproductive axis. Normal serum insulin level mediates the normal functions of the hypothalamic–pituitary–gonadal axis. Thus, low levels of insulin are considered to delay the function of this axis, with the subsequent delayed release of GnRH, leading to pubertal delay . Leptin is an adipocyte hormone that signals to the hypothalamus and the reproductive system as it stimulates GnRH release . Insulin like growth factor-1, which stimulates and promotes growth and puberty, has been proved to be a direct regulator of GnRH .
Many reports have suggested a role of exogenous endocrine-disrupting chemicals in timing and development of puberty. Few epidemiological studies have addressed this hypothesis. ,.
EDs are environmental chemicals, which may be either natural or synthetic. EDs accumulate in the environment in the long term and are introduced into the human body through water, air, and foodstuffs or through equipments used in the office and home. Additionally, it has been demonstrated that EDs can be transferred from the mother to the fetus by placenta or to the baby by breast milk .
Natural endocrine disruptors are found in several nutrients that are frequently consumed in daily life (i.e., carrots, garlic, apple, coffee, cherry, parsley, and legumes). Phytoestrogens have estrogenic effects when consumed in huge amounts and antiestrogenic effects at low concentrations .
Synthetic endocrine disruptors include pesticides, fungicides, and herbicides used in agriculture; cleaning substances used in daily life; contents of cosmetic products; dyes; plastic substances; and solvents .
As neutralization or inactivation is difficult and most of these substances often accumulate in fat tissue, they may persist in the body for long periods of time and cause harmful effects .
The dose and duration of exposure to EDs are important in terms of potential negative consequences. The negative effects may become more serious as the duration of exposure and dose increase .
Although puberty is an important developmental interval, the effect of endocrine disruptors on all aspects of human puberty is not extensively represented. Nevertheless, there is considerable evidence in laboratory animal models that many estrogenic endocrine disruptors are associated with, or are indeed causal to, early puberty in female rodents, whereas males are less frequently affected .
Puberty marks a transition between childhood and the adult reproductive stage. It is a vulnerable stage of life, and deregulation has been linked to increased health and psychosocial problems. Puberty development is a multifaceted process that is under the control of different hormonal regulatory mechanisms. Evidence is accumulating that exogenous hormone disruptors may advance or sometimes delay puberty. Considering that most endocrine disruptors act as estrogen mimics or may exhibit antagonistic effects to estrogen or androgen receptors, such exposures have been implicated as provoking pubertal abnormalities in humans by interrupting normal hormonal activity.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
|1||Bourguignon JP. Control of the onset of puberty. In: Pescovitz OH, Eugster E, editors. Pediatric endocrinology: mechanisms, manifestations and management: Lippincott Williams and Wilkins; 2004. pp. 285–298.|
|2||Parent AS, Teilmann G, Juul A, Skakkebaek NE, Toppari J, Bourguignon JP. The timing of normal puberty and the age limits of sexual precocity: variations around the world, secular trends, and changes after migration. Endocr Rev 2003; 24:668–693.|
|3||Lee PA, Guo SS, Kulin HE. Age of puberty: data from the United States of America. APMIS 2001; 109:81–88.|
|4||Aksglaede L, Sørensen K, Petersen JH, Skakkebaek NE, Juul A. Recent decline in age at breast development: the Copenhagen puberty study. Pediatrics 2009; 123:e932–e939.|
|5||Roelants M, Hauspie R, Hoppenbrouwers K. References for growth and pubertal development from birth to 21 years in Flanders, Belgium. Ann Hum Biol 2009; 36:680–694.|
|6||Buck Louis GM, Gray LE, Marcus M, Ojeda SR, Pescovitz OH, Witchel SF, et al. Environmental factors and puberty timing: expert panel research needs. Pediatrics 2008; 121 (Suppl 3): S192–S207.|
|7||Jacobson-Dickman E, Lee MM. The influence of endocrine disruptors on pubertal timing. Curr Opin Endocrinol Diabetes Obes 2009; 16:25–30.|
|8||Patton GC, Viner R. Pubertal transitions in health. Lancet 2007; 396:1130–1169.|
|9||Terasawa E, Fernandez DL. Neurobiological mechanisms of the onset of puberty in primates. Endocr Rev 2001; 22:111–161.|
|10||McLachlan JA. Environmental signaling: what embryos and evolution teach us about endocrine disrupting chemicals. Endocr Rev 2001; 22:319–360.|
|11||Teilmann G, Pedersen CB, Skakkebæk NE, Jensen TK. Increased risk of precocious puberty in internationally adopted children in Denmark. Pediatrics 2006; 118:e391–e400.|
|12||Marshall WA, Tanner JM. Variations in pattern of pubertal changes in girls. Arch Dis Child 1969; 44:291–303.|
|13||Marshall WA, Tanner JM. Variations in the pattern of pubertal changes in boys. Arch Dis Child 1970; 45:13–23.|
|14||Rockett JC, Lynch CD, Buck GM. Biomarkers for assessing reproductive development and health: Part 1 – Pubertal development. Environ Health Perspect 2004; 112:105–117.|
|15||Styne DM. Puberty, obesity and ethnicity. Trends Endocrinol Metab 2004; 15:472–480.|
|16||Wu FC, Brown DC, Butler GE, Stirling HF, Kelnar CJ. Early morning plasma testosterone is an accurate predictor of imminent pubertal development in prepubertal boys. J Clin Endocrinol Metab 1993; 76:26–31.|
|17||Gamba M, Pralong FP. Control of GnRH neuronal activity by metabolic factors: the role of leptin and insulin. Mol Cell Endocrinol 2006; 254–255:133–139.|
|18||Schoeller EL, Scion S, Molty KH. The effect of type I diabetes on the hypothalamic, pituitary and testes axis. Cell Tissue Res 2012; 349:839–847.|
|19||Watanobe H. Leptin directly acts within the hypothalamus to stimulate Gonadotropin-releasing hormone secretion in vivo in rats. J Physiol 2002; 545:255–268.|
|20||Hiney JK, Srivastava VK, Pine MD, Dees WL. Insulin-like growth factor-I activates KiSS-1 gene expression in the brain of the prepubertal female rat. Endocrinology 2009; 150:376–384.|
|21||Klein KO. Precocious puberty: who has it? Who should be treated? J Clin Endocrinol Metab 1999; 84:411–415.|
|22||Rasier G, Toppari J, Parent A-S, Bourguignon J-P. Female sexual maturation and reproduction after prepubertal exposure to estrogens and endocrine disrupting chemicals: a revxiew of rodent and human data. Mol Cell Endocrinol 2006; 254–255:187–201.|
|23||Roy JR, Chakraborty S, Chakraborty TR. Estrogen-like endocrine disrupting chemicals affecting puberty in humans-a review. Med Sci Monit 2009; 15:137–145.|
|24||Dickerson SM, Gore AC. Estrogenic environmental endocrine-disrupting chemical effects on reproductive neuroendocrine function and dysfunction across the life cycle. Rev Endocr Metab Disord 2007; 8:143–202.|