The work makes a case for how male germ cells particularly may be used to transfer epigenetic processes of pubertal paternal smoking to enhance the risk of respiratory health across generations.
This epigenome-wide association study (EWAS), which was published in Clinical Epigenetics1, is to the researcher’s knowledge the first of its sort to look at the effects of dads’ smoking throughout their adolescent years on their kids.
“Our studies in the large international RHINESSA, RHINE and ECRHS studies have shown that the health of future generations depends on the actions and decisions made by young people today – long before they become parents – in particular for boys in early puberty and mothers/grandmothers both pre-pregnancy and during pregnancy,” said Cecilie Svanes, MD, PhD, of the University of Bergen and Research Director of the RHINESSA study.2 It is quite exciting that we have now been able to pinpoint a mechanism that accounts for our cohort data.
The epigenetic profiles of 875 people between the ages of 7 and 50 were included in the RHINESSA cohort’s EWAS research, along with information on their fathers’ smoking habits. The study was carried out at the Universities of Southampton and Bergen in Norway. 304 of the dads in this cohort started smoking while they were less than 15 years old.
Using 1 g of DNA taken from peripheral blood using a straightforward salting out process, DNA methylation in kids was assessed. Analyses of replication and sensitivity were both carried out. Asthma, obesity, and wheeze are all correlated with these methylation alterations, which are known to control gene expression.
Using robust multiple linear regression models, the research took into account EWAS on the father’s smoking exposure before to conception and DNA methylation. The researchers also took into account the age of the kids, one’s own smoking, and one’s mother’s smoking. Maternal smoking was determined by reports of mothers smoking during their children’s youth and during pregnancy. Personal smoking was characterized as now smoking, never smoking, or never having smoked.
Following examination, the researchers discovered that the father’s use of tobacco products before to conception was linked to the methylation of two cytosine-phosphate-guanine (CpG) sites in the PRR5 and CENPP regions of the offspring’s blood DNA (false discovery rate [FDR] 0.05).
Additionally, among the offspring of men who smoked before the age of 15 years, 19 epigenetic alterations were discovered at 19 locations linked to 14 genes (TLR9, DNTT, FAM53B, NCAPG2, PSTPIP2, MBIP, C2orf39, NTRK2, DNAJC14, CDO1, PRAP1, TPCN1, IRS1, and CSF1R). Some of these sites, such as ever-asthma (NTRK2), ever-wheezing (DNAJC14, TPCN1), weight (FAM53B, NTRK2), and BMI (FAM53B, NTRK2), were connected to the outcomes of the children (P .05).
The impacts of second-hand smoke exposure, self-reported smoking bias, and the possibility that reporting of fathers’ smoking behaviors is independent of DNA methylation seen in kids are some of the study’s shortcomings, according to the researchers.
Despite these drawbacks, the researchers maintain that the study demonstrates how dads smoking while still adolescents has substantial health consequences for their offspring and that this relationship may evolve into additional health issues as teen vaping and nicotine usage rises.
The National Institute for Research Health Southampton Biomedical Research Centre, the University of Southampton, and John Holloway, PhD, FHEA, said in a statement that the study’s evidence came from people whose fathers smoked when they were teenagers in the 1960s and 1970s, when tobacco use was much more prevalent.2 “While we can’t say for certain that vaping will have the same consequences across generations, we shouldn’t wait a few generations to demonstrate the potential repercussions of teenage vaping. We must move right away.