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Exposure to non-persistent pesticides and puberty timing: a systematic review of the epidemiological evidence

Journal

EUROPEAN JOURNAL OF ENDOCRINOLOGY
Volume 184, Issue 6, Pages 733-749

Publisher

BIOSCIENTIFICA LTD
DOI: 10.1530/EJE-20-1038

Keywords

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Funding

  1. Instituto de Salud Carlos III (ISCIII)
  2. 'Fondo Europeo de Desarrollo Regional' (ISCIII/FEDER) [FIS-PI17/01526]

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Exposure to different types of pesticides has been associated with altered puberty timing in girls and/or boys in several studies, such as atrazine, organophosphate pesticides, and pyrethroids. Most studies describe a relationship between pesticide exposure and changes in the age of puberty onset or sex hormone levels, although the quality of evidence is generally low.
Endocrinology Background: Numerous modern non-persistent pesticides have demonstrated estrogenic/anti-androgenic activity and have been classified as endocrine-disrupting chemicals (EDCs). Processes involved in puberty development are vulnerable to EDCs, such as compounds that interfere with the metabolism or activity of sex steroids. Objective: To conduct a systematic review of epidemiological studies on the relationship between early-life exposure to non-persistent pesticides and puberty timing and/or sexual maturation in girls and boys. Methods: A systematic search was carried out using MEDLINE and SCOPUS databases, including original articles published up to November 2020. Results: Thirteen studies were selected after excluding non-original and non-human studies. Exposure to different types of pesticides has been associated with altered puberty timing in girls and/or boys in eight studies. In utero exposure to atrazine has been related to earlier age of menarche in girls; exposure to organophosphate (OP) pesticides has been related to delayed sexual development in boys and girls; childhood pyrethroid exposure has been associated with pubertal delay in girls and pubertal advancement in boys; and prenatal/childhood exposure to multiple pesticides has been linked to earlier puberty onset in girls and pubertal delay in boys. Conclusions: Most of the reviewed studies describe a relationship between pesticide exposure and changes in the age of puberty onset or sex hormone levels, although the quality of the evidence is generally low. Further well-designed longitudinal studies are warranted on specific classes of pesticides and on possible interactions between different types of compounds.

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