3.9 Article

Early breast development in girls after prenatal exposure to non-persistent pesticides

期刊

INTERNATIONAL JOURNAL OF ANDROLOGY
卷 35, 期 3, 页码 273-282

出版社

WILEY
DOI: 10.1111/j.1365-2605.2011.01244.x

关键词

adrenarche; early thelarche; pesticides; prenatal exposure; puberty

资金

  1. Danish Environmental Protection Agency
  2. Danish Council for Strategic Research
  3. Program Commission on Health, Food and Welfare [2101-08-0058]
  4. Ville Heise's scholarship
  5. Jacob and Olga Madsen's Foundation
  6. Rigshospitalet's Research Foundation

向作者/读者索取更多资源

Contemporary American and European girls experience breast development at earlier ages compared with 1520 years ago. Alterations in BMI alone cannot account for these changes. Several currently used pesticides possess endocrine disrupting properties and may interfere with reproductive development, but human data are sparse. We examined girls whose mothers worked in greenhouses in the first trimester of pregnancy to assess the long-term effects of prenatal pesticide exposure on puberty. Mothers were prenatally categorized as exposed or unexposed to pesticides. We studied the offspring of these greenhouse workers, and evaluated the anthropometry, pubertal staging in the girls, and blood samples were drawn at 3 months of age (n = 90) and again once at school age (611 years, n = 83). No clinical and biochemical differences were found between the exposed and unexposed girls at 3 months of age. Mean onset of B2+ was 8.9 years (95% CI: 8.2; 9.7) in prenatally exposed girls, compared with 10.4 years (9.2; 17.6) in the unexposed (p = 0.05), and 10.0 (9.710.3) years in a Danish reference population (p = 0.001). Exposed girls had higher serum androstenedione levels (geometric means: 0.58 vs. 0.79 nmol/L, p = 0.046) and lower Anti-Mullerian Hormone (AMH) compared with the unexposed (geometric means: 16.4 vs. 21.3 pmol/L, p > 0.05) and the reference group (20.2 pmol/L, p = 0.012). Levels of testosterone, estradiol, prolactin, FSH, LH, SHBG, DHEAS, DHT, Inhibin A and Inhibin B did not differ between the groups. In conclusion, our findings suggest that prenatal exposure to currently approved pesticides may cause earlier breast development in girls. This association appeared not to be because of changes in gonadotropins, but rather to higher androgen levels, which indirectly may increase oestrogens through aromatization. In addition, lower serum AMH levels indicated a reduced pool of antral ovarian follicles. The long-term consequences of our findings with regard to establishment of future reproductive function still remain unknown.

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