Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/30775
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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