Lower placental telomere length may be attributed to maternal residential traffic exposure; a twin study Esmée Bijnens a,b , Maurice P. Zeegers b , Marij Gielen b , Michal Kicinski a , Geja J. Hageman c , Daniëlle Pachen c , Catherine Derom d , Robert Vlietinck d , Tim S. Nawrot a,e, ⁎ a Centre for Environmental Sciences, Hasselt University, Agoralaan Building D, 3590 Diepenbeek, Belgium b Department of Complex Genetics, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands c Department of Toxicology, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands d Centre of Human Genetics, University Hospitals Leuven, Herestraat 49, 3000 Leuven, Belgium e Department of Public Health, Leuven University (KU Leuven), Kapucijnenvoer 35, 3000 Leuven, Belgium abstract article info Article history: Received 27 August 2014 Received in revised form 9 January 2015 Accepted 13 February 2015 Available online xxxx Keywords: Telomeres Traffic Placenta Twin Background: High variation in telomere length between individuals is already present before birth and is as wide among newborns as in adults. Environmental exposures likely have an impact on this observation, but remain largely unidentified. We hypothesize that placental telomere length in twins is associated with residential traffic exposure, an important environmental source of free radicals that might accelerate aging. Next, we intend to unravel the nature-nurture contribution to placental telomere length by estimating the heritability of placental telomere length. Methods: We measured the telomere length in placental tissues of 211 twins in the East Flanders Prospective Twin Survey. Maternal traffic exposure was determined using a geographic information system. Additionally, we estimated the relative importance of genetic and environmental sources of variance. Results: In this twin study, a variation in telomere length in the placental tissue was mainly determined by the common environment. Maternal residential proximity to a major road was associated with placental telomere length: a doubling in the distance to the nearest major road was associated with a 5.32% (95% CI: 1.90 to 8.86%; p = 0.003) longer placental telomere length at birth. In addition, an interquartile increase (22%) in maternal residential surrounding greenness (5 km buffer) was associated with an increase of 3.62% (95% CI: 0.20 to 7.15%; p = 0.04) in placental telomere length. Conclusions: In conclusion, we showed that maternal residential proximity to traffic and lower residential surrounding greenness is associated with shorter placental telomere length at birth. This may explain a significant proportion of air pollution-related adverse health outcomes starting from early life, since shortened telomeres accelerate the progression of many diseases. © 2015 Published by Elsevier Ltd. 1. Introduction Telomeres consist of TTAGGG tandem repeats and cap chromosomes (Blackburn, 2001). They undergo progressive attrition in somatic cells because DNA polymerase is unable to fully replicate the ends of DNA caused by the unidirectional growth and the requirement for a primer to initiate synthesis (Levy et al., 1992). This is referred to as the end-replication problem. As a result telomeres progressively shorten in somatic cells and a mean leukocyte telomere length has been observed to diminish with age (Benetos et al., 2001; Slagboom et al., 1994). As aging starts before birth, not only establishing the telomere length at birth is a prerequisite, but also investigating environmental and genetic factors influencing telomere length is needed. The placenta plays a pivotal role in fetal development and functions as a barrier be- tween fetal and maternal circulation. In utero telomere attrition is prevented by telomerase activity but as pregnancy progresses its activity in placental tissue declines making telomeres more sensitive to degradation (Chen et al., 2002; Gielen et al.; Kyo et al., 1997). Maternal stress (Class et al., 2011; Lee et al., 2011; Torche, 2011), under nutrition (Schulz, 2010), exposure to cigarette smoke (Ko et al., 2014; Wahabi et al., 2013) and air pollution (Ballester et al., 2010; Brauer et al., 2008; Dadvand et al., 2013; Liu et al., 2003; Pedersen et al., 2013) have been linked to fetal growth retardation, with compro- mised fetal cerebral development, and might be linked with early onset of insulin resistance (Entringer et al., 2012). It has been suggested that telomere length underlies this fetal programming (Entringer et al., 2012). For instance, exposure to maternal psychosocial stress during intrauterine life has been associated with shorter leukocyte telomere length in young adulthood (Entringer et al., 2011). In adults telomere Environment International 79 (2015) 1–7 ⁎ Corresponding author at: Agoralaan Building D, 3590 Diepenbeek, Belgium. E-mail address: tim.nawrot@uhasselt.be (T.S. Nawrot). http://dx.doi.org/10.1016/j.envint.2015.02.008 0160-4120/© 2015 Published by Elsevier Ltd. Contents lists available at ScienceDirect Environment International journal homepage: www.elsevier.com/locate/envint