ORGANOCHLORIDE PESTICIDES IN MACEDONIAN GIRLS
WITH PREMATURE SEXUAL DEVELOPMENT
Krstevska-Konstantinova M1,*, Kocova M1, Charlier C2, Bourguignon JP3
*Corresponding Author: Dr. Marina Krstevska Konstantinova, Pediatric Clinic, Department of Endocrinology and Genetics, Medical Faculty, Vodnjanska 17, 1000 Skopje, Republic of Macedonia; Tel.: +389-2-314-7474; Fax: +389-2-3225-809; E-mail: marina@lancom.com.mk
page: 43
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INTRODUCTION
Puberty is a very important phase in the process of becoming an adult, because secondary sexual characteristics appear, a growth spurt occurs, fertility is achieved and significant psychological changes occur. The mean age of menarche in several developed countries of Europe and the USA, decreased from the mid-1800s to mid-1900s [1].This effect is thought to result from improved socio-economic factors, health, nutrition, and the gains of urbanization [2]. We found a positive association between the levels of organochloride pesticides (p,p’-DDE) in precocious puberty in girls adopted from developing countries and significantly higher levels than in native Belgian girls with the same condition [3].
In premature sexual development (PSD) the appearance of secondary sexual characteristics occurs before the age of 8 years in girls. Sexual development that results from premature activation of the hypothalamic pulsatile generator-pituitary gonadotropin-gonadal axis is considered as a complete isosexual development, or true central precocious puberty. When secretion of gonadotropins or gonadal steroids occurs independently of the pulsatile gonadotropin-releasing-hormone (GNRH) generator, it is considered to be a pseudo-precocious puberty. Early puberty occurs between the age of 8 and 9 years in girls. An isolated growth of breasts in girls represents premature thelarche [4].
Although improved nutrition leads to earlier puberty [5], exposure to endocrine disruptors may contribute for earlier appearance to the puberty or other pubertal disturbances [3,6-8]. Children from developing countries adopted in Western countries often develop PSD [9-11]. Precocious puberty has been described after accidental exposure to estrogenic compounds in cosmetic products, food, or pharmaceutical products [12]. In our Belgian study, we investigated whether exposure to p,p’-DDE may lead to PSD [3].
Endocrine disruptors are synthetic chemicals that, on absorbtion into the body, either mimic or block hormones and disrupt the body’s normal functions [13]. They include certain pesticides (DDT), industrial chemicals (PCBs, dioxins), phthalates, phenols (bisphenol A, alkylphenol) and plant hormones (phytoestrogens). Delayed puberty has been associated with exposure to endocrine disruptors [7], of which some may have intrinsic estrogen activity or increase endogenous sex hormone levels [13]. These effects have been documented at extremely low doses [13], which are thought to be safe, but produce undesirable effects in animal studies. In rats, minimal doses of bisphenol A that is present in plastics, produce structural abnormalities of the vagina and uterus [14]. Some forms of DDT and other pesticides and industrial chemicals such as PCBs, increase the wet weight of the virgin mouse uterus, the classic bioassay for estrogenicity [15].
Adolescence, with its increased levels of hormones needed for sexual development, is especially vulnerable to these substances. This increase in hormone levels may cause the development of hormone-dependent cancers, especially if associated with exposure to phytoestrogens or other endocrine disruptors [16]. Girls are in greater danger because they have a larger amount of fat tissue in which the disruptors are stored. Early or delayed puberty may result from endocrine disruptors and may become a difficult emotional problem, since young girls lack the socialization and self-confidence of older children. The health effects associated with PSD in girls in later life are: increased risk of breast cancer and polycystic ovary disease (PCOS), inadequate behavior, acne and hirsutism.
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