{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T14:24:18Z","timestamp":1772115858595,"version":"3.50.1"},"reference-count":60,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2016,5,26]],"date-time":"2016-05-26T00:00:00Z","timestamp":1464220800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100007036","name":"Milj\u00f8styrelsen","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100007036","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007398","name":"Strategiske Forskningsr\u00e5d","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100007398","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Andrology"],"published-print":{"date-parts":[[2016,7]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Many modern pesticides have endocrine disrupting abilities and early\u2010life exposure may affect growth and disease risk later in life. Previously, we reported associations between prenatal pesticide exposure and higher childhood body fat content measured by anthropometry. The associations were affected by child <jats:italic>PON1<\/jats:italic> Q192R genotype. We aimed to study whether prenatal pesticide exposure was still associated with body fat content and distribution in the children at puberty and the potential impact of both maternal and child <jats:italic>PON1<\/jats:italic> Q192R genotype. In this prospective cohort study of 247 children born by occupationally exposed or unexposed women (greenhouse workers and controls) two follow\u2010up examinations (age 10\u201315 and 11\u201316\u00a0years) including simple anthropometry, skinfold measurements, pubertal staging and blood sampling were performed. Total and regional fat% was determined by dual X\u2010ray absorptiometry (DXA) at age 10\u201315. Prenatal pesticide exposure was associated with increased total, android, and gynoid fat percentage (DXA) at age 10\u201315\u00a0years after adjustment for sex, socioeconomic status, and puberty (all \u03b2\u00a0=\u00a00.5 standard deviation score (SDS) <jats:italic>p<\/jats:italic>\u00a0&lt;\u00a00.05). Stratified by sex, the associations were significant in girls (total fat: \u03b2\u00a0=\u00a00.7 SDS, android\u2013gynoid ratio: \u03b2\u00a0=\u00a00.1, both <jats:italic>p<\/jats:italic>\u00a0&lt;\u00a00.05), but not in boys. Carrying the R\u2010allele (child or mother, separately, or both) augmented the differences between exposed and unexposed children (total fat: \u03b2\u00a0=\u00a01.0 SDS, \u03b2\u00a0=\u00a00.8 SDS, <jats:italic>p<\/jats:italic>\u00a0&lt;\u00a00.05, respectively, and \u03b2\u00a0=\u00a01.2 SDS, <jats:italic>p<\/jats:italic>\u00a0&lt;\u00a00.01). No exposure\u2010related differences were found if either the child or mother had the QQ wild\u2010type. At age 11\u201316, exposed children tended to have a higher total fat% estimated by skinfolds than unexposed children (<jats:italic>p<\/jats:italic>\u00a0=\u00a00.06). No significant associations between prenatal exposure and body mass index or waist circumference were found. Prenatal pesticide exposure was associated with higher adolescent body fat content, including android fat deposition, independent of puberty. Girls appeared more susceptible than boys. Furthermore, the association depended on maternal and child <jats:italic>PON1<\/jats:italic> Q192R genotype.<\/jats:p>","DOI":"10.1111\/andr.12194","type":"journal-article","created":{"date-parts":[[2016,5,27]],"date-time":"2016-05-27T05:03:40Z","timestamp":1464325420000},"page":"735-744","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Prenatal pesticide exposure and <i>PON1<\/i> genotype associated with adolescent body fat distribution evaluated by dual X\u2010ray absorptiometry (DXA)"],"prefix":"10.1111","volume":"4","author":[{"given":"J.","family":"Tinggaard","sequence":"first","affiliation":[{"name":"Department of Growth and Reproduction University Hospital of Copenhagen Rigshospitalet Copenhagen Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C.","family":"Wohlfahrt\u2010Veje","sequence":"additional","affiliation":[{"name":"Department of Growth and Reproduction University Hospital of Copenhagen Rigshospitalet Copenhagen Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.","family":"Husby","sequence":"additional","affiliation":[{"name":"Hans Christian Andersen Children's Hospital University of Southern Denmark Odense Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L.","family":"Christiansen","sequence":"additional","affiliation":[{"name":"Institute of Public Health University of Southern Denmark Odense Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"N. 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