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BioMed Research International
Volume 2016 (2016), Article ID 4515928, 10 pages
http://dx.doi.org/10.1155/2016/4515928
Research Article

Infant’s DNA Methylation Age at Birth and Epigenetic Aging Accelerators

1Institute of Pediatrics, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Jinsui Road 9, Tianhe District, Guangzhou, Guangdong 510623, China
2Department of Cardiac Surgery, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Jinsui Road 9, Tianhe District, Guangzhou, Guangdong 510623, China

Received 13 August 2016; Revised 1 November 2016; Accepted 6 November 2016

Academic Editor: Heide Schatten

Copyright © 2016 Ruheena Javed et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Knowing the biological age of the neonates enables us to evaluate and better understand the health and maturity comprehensively. However, because of dearth of biomarkers, it is difficult to quantify the neonatal biological age. Here we sought to quantify and assess the variability in biological age at birth and to better understand how the aging rates before birth are influenced by exposure in intrauterine period by employing a novel epigenetic biomarker of aging (epigenetic clock). We observed that the methylation age at birth was independent of the infant’s sex but was significantly influenced by race. Partial correlation analysis showed a significant negative relationship between maternal socioeconomic status and infants’ methylation age (, = 0.005). A significant association with the risk of fast aging was observed for prenatal exposure to tobacco smoke with OR (95% CI) of 3.17 (1.05–9.56). Both estimated cell abundance measures and lymphocyte subpopulations in cord blood showed that tobacco exposed group exhibit an altered T cell compartment, specifically substantial loss of naive T cells. Present study provides the first evidence that common perinatal exposure (such as maternal smoking and lower socioeconomic status) may be important aging accelerators and substantial loss of naive T cells may play a role in the smoking-related fast aging phenomenon.