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Title: | Early life tobacco exposure and children’s telomere length: The HELIX project | Authors: | Osorio-Yanez, Citlalli CLEMENTE BATALHA PARDAL, Diana Maitre, Lea Vives-Usano, Martha Bustamante, Mariona Martinez, David Casas, Maribel Alexander, Jan Thomsen, Cathrine Chatzi, Leda Gutzkow, Kristine B. Grazuleviciene, Regina MARTENS, Dries PLUSQUIN, Michelle Slama, Remy McEachan, Rosemary C. Wright, John Yang, Tiffany C. Urquiza, Jose Tamayo, Ibon Sunyer, Jordi Vafeiadi, Marina NAWROT, Tim Vrijheid, Martine |
Issue Date: | 2020 | Publisher: | ELSEVIER | Source: | SCIENCE OF THE TOTAL ENVIRONMENT, 711 (Art N° 135028) | Abstract: | Telomere length and mitochondrial DNA content are considered biomarkers of cellular aging, oxidative stress, and inflammation, but there is almost no information on their association with tobacco smoke exposure in fetal and early life. The aim of this study was to assess whether prenatal and childhood tobacco exposure were associated with leukocyte telomere length (LTL) and mitochondrial DNA (mtDNA) content in children. As part of a multi-centre European birth cohort study HELIX (Human Early-Life Exposome) (n = 1396) we assessed maternal smoking status during pregnancy through questionnaires, and through urinary cotinine levels that were then used to classify women as not exposed to smoking (<10 mu g/L), exposed to secondhand smoke (SHS) (10-50 mu g/L) and active smokers (>50 mu g/L). When the children were around 8 years of age (range: 5.4-12.0 years), childhood SHS tobacco smoke exposure was assessed through an extensive questionnaire and through measurements of urinary cotinine (<3.03 mu g/L non-detected, >3.03 mu g/L detected). Leukocyte mtDNA content and LTL were measured in the children at 8 years employing real time polymerase chain reaction (qPCR). Effect estimates were calculated using multivariate linear regression models for prenatal and childhood exposures adjusted for potential confounders. Maternal cotinine levels indicative of SHS exposure during pregnancy were associated with a decrease of 3.90% in LTL in children (95% CI: -6.68, -0.91), compared with nonsmoking, whereas the association for maternal cotinine levels indicative of active smoking did not reach statistical significance (-3.24%; 95% CI: -6.59, 0.21). Childhood SHS tobacco exposure was not associated with LTL in children. Global SHS exposure during childhood was associated with an increase of 3.51% (95% CI: 0.78, 6.27) in mtDNA content. Our findings suggest that tobacco smoke exposure during pregnancy, even at SHS levels, may accelerate telomere shortening in children and thus induce biological aging from an early age. (C) 2019 Elsevier B.V. All rights reserved. | Notes: | Vrijheid, M (reprint author), Inst Global Hlth, ISGlobal, Barcelona 08003, Spain. martine.vrijheid@isglobal.org |
Other: | Vrijheid, M (reprint author), Inst Global Hlth, ISGlobal, Barcelona 08003, Spain. martine.vrijheid@isglobal.org | Keywords: | Tobacco exposure;Leukocyte telomere length;Mitochondrial DNA content;Pregnancy;HELIX | Document URI: | http://hdl.handle.net/1942/30775 | ISSN: | 0048-9697 | e-ISSN: | 1879-1026 | DOI: | 10.1016/j.scitotenv.2019.135028 | ISI #: | WOS:000509344700052 | Rights: | 2019 Elsevier B.V. All rights reserved. | Category: | A1 | Type: | Journal Contribution | Validations: | ecoom 2021 |
Appears in Collections: | Research publications |
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