Teen boys who vape risk having children who suffer from obesity, asthma and low lung function, a new study reveals.
Scientists at Southampton University called for a clampdown on vaping after they discovered that boys who smoke risk passing on harmful epigenetic traits to future children.
Researchers found that men who smoked before the age of 15 could alter up to 14 genes in their offspring associated with asthma, obesity and lung function.
They believe that it is nicotine that is driving these changes, making vapes just as dangerous as cigarettes to future children.
Study co-author Professor John Holloway, from the University of Southampton and the NIHR Southampton Biomedical Research Centre said: “Some animal studies suggest that nicotine may be the substance in cigarette smoke that is driving epigenetic changes in offspring.
“So it’s deeply worrying that teenagers today, especially teenage boys, are now being exposed to very high levels of nicotine through vaping.
“The evidence from this study comes from people whose fathers smoked as teenagers in the 60s and 70s, when smoking tobacco was much more common.
“We can’t definitely be sure vaping will have similar effects across generations, but we shouldn’t wait a couple of generations to prove what impact teenage vaping might have. We need to act now.”
The University of Southampton’s LifeLab program engages with young people to show how lifestyle choices can impact their health and the health of any children they may have in the future.
Dr. Kath Woods-Townsend, LifeLab Program manager said: “Parents, teachers and young people themselves are concerned about the impact of vaping.
“We’re working with our Youth Panel to understand the role vaping plays in their lives and to co-create resources that will help inform young people about the risks.”
The study, published in the journal Clinical Epigenetics, revealed that biomarkers in kids associated with paternal preconception smoking were different from those associated with maternal or personal smoking.
It is the first human study to reveal the biological mechanism behind the impact of fathers’ early teenage smoking on their children.
Along with colleagues from the University of Bergen in Norway, the team investigated the epigenetic profiles of 875 people, aged seven to 50, and the smoking behaviors of their dads.
They found epigenetic changes at 19 sites mapped to 14 genes in the kids of dads who smoked before the age of 15.
These changes in the way DNA is packaged in cells, regulate gene expression switching them on and off and are associated with asthma, obesity and wheezing.
Dr. Negusse Kitaba, Research Fellow at the University of Southampton said: “Changes in epigenetic markers were much more pronounced in children whose fathers started smoking during puberty than those whose fathers had started smoking at any time before conception.
“Early puberty may represent a critical window of physiological changes in boys.
“This is when the stem cells are being established which will make sperm for the rest of their lives.”
They also compared the paternal preconception smoking profiles with people who smoked themselves and those whose mothers smoked before conception.
Dr. Gerd Toril Mørkve Knudsen from the University of Bergen and co-lead author of the study said: “Interestingly, we found that 16 of the 19 markers associated with fathers’ teenage smoking had not previously been linked to maternal or personal smoking.
“This suggests these new methylation biomarkers may be unique to children whose fathers have been exposed to smoking in early puberty.”
Professor Cecilie Svanes from the University of Bergen and Research Director of the RHINESSA study added: “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 are parents – in particular for boys in early puberty and mothers/grandmothers both pre-pregnancy and during pregnancy.
“It is really exciting that we have now been able to identify a mechanism that explains our observations in the cohorts.”
Produced in association with SWNS Talker
Edited by Suparba Sil and Newsdesk Manager
