Paternal tobacco smoke correlated to offspring asthma and prenatal epigenetic programming

Chih Chiang Wu, Te Yao Hsu, Jen Chieh Chang, Chia Yu Ou, Ho Chang Kuo, Chieh An Liu, Chih Lu Wang, Hau Chuang, Chie Pein Chen, Kuender D. Yang*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

34 Scopus citations


Rationale: Little is known about effects of paternal tobacco smoke (PTS) on the offspring's asthma and its prenatal epigenetic programming. Objective: To investigate whether PTS exposure was associated with the offspring's asthma and correlated to epigenetic CG methylation of potential tobacco-related immune genes: LMO2, GSTM1 or/and IL-10 genes. Measurements and Main Results: In a birth cohort of 1,629 newborns, we measured exposure rates of PTS (23%) and maternal tobacco smoke (MTS, 0.2%), cord blood DNA methylation, infant respiratory tract infection, childhood DNA methylation, and childhood allergic diseases. Infants with prenatal PTS exposure had a significantly higher risk of asthma by the age of 6 than those without (p = 0.026). The PTS exposure doses at 0, <20, and ≧20 cigarettes per day were significantly associated with the trend of childhood asthma and the increase of LMO2-E148 (p = 0.006), and IL10_P325 (p = 0.008) CG methylation. The combination of higher CG methylation levels of LMO2_E148, IL10_P325, and GSTM1_P266 corresponded to the highest risk of asthma by 43.48%, compared to other combinations (16.67-23.08%) in the 3-way multi-factor dimensionality reduction (MDR) analysis. The LMO2_P794 and GSTM1_P266 CG methylation levels at age 0 were significantly correlated to those at age of 6. Conclusions: Prenatal PTS exposure increases CG methylation contents of immune genes, such as LMO2 and IL-10, which significantly retained from newborn stage to 6 years of age and correlated to development of childhood asthma. Modulation of the LMO2 and IL-10 CG methylation and/or their gene expression may provide a regimen for early prevention of PTS-associated childhood asthma.

Original languageEnglish
Article number471
JournalFrontiers in Genetics
Issue numberMAY
StatePublished - 2019

Bibliographical note

Publisher Copyright:
Copyright © 2019 Wu, Hsu, Chang, Ou, Kuo, Liu, Wang, Chuang, Chen and Yang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.


  • Asthma development
  • CG methylation
  • GSTM1
  • IL-10
  • LMO2
  • Paternal tobacco smoke
  • Prenatal tobacco smoke exposure


Dive into the research topics of 'Paternal tobacco smoke correlated to offspring asthma and prenatal epigenetic programming'. Together they form a unique fingerprint.

Cite this