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Francesca Castiello and Carmen Freire

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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Carmen Freire, Rosa Ramos, Esperanza Amaya, Mariana F Fernández, Piedad Santiago-Fernández, Maria-Jose Lopez-Espinosa, Juan-Pedro Arrebola, and Nicolas Olea


An association between thyroid function during pregnancy or infancy and neurodevelopment in children has been demonstrated. We aimed to investigate whether newborn TSH concentrations are related to subsequent neurocognitive development.


We conducted a longitudinal study on 178 children from a general population birth cohort in Granada (Spain) born in 2000–2002.


TSH concentrations were measured in umbilical cord blood, and cognitive functions were assessed at 4 years of age using the McCarthy's scales of children's abilities (MSCA). Organochlorine (OC) compound concentrations and the combined oestrogenicity (total effective xeno-oestrogenic burden (TEXB)) were also determined in the placentae.


Mean newborn TSH was 3.55 mU/l (range=0.24–17 mU/l). In multivariate regression analyses, adjusting for maternal and child characteristics, higher newborn TSH concentrations showed a decrease of 3.51 and 3.15 points on the MSCA general cognitive and executive function scores respectively and were associated with a higher risk of scoring below the 20th percentile (P20) on the quantitative score (odds ratio (OR)=2.64). Children with TSH in the upper quartile (4.19–17.0 mU/l) were at higher risk of scoring <P20 on span memory (OR=5.73), whereas children with TSH in the second quartile (2.05–2.95 mU/l) were at lower risk of scoring <P20 on the verbal scale (OR=0.24). Neonatal TSH status was also associated with general cognitive and executive function outcomes when controlling for prenatal exposure to OCs or placental TEXB.


Newborn thyroid hormone status expressed by TSH in cord blood may adversely affect later cognitive function. A more thorough screening for neonatal thyroid deficiency is warranted.