Persistent tobacco smoking from childhood may cause heart damage by the mid-twenties

The study was conducted in collaboration between the Universities of Bristol and Exeter in the UK, and the University of Eastern Finland, and the results were published in the prestigious Journal of the American College of Cardiology (JACC).

In the present study, 1,931 children drawn from the University of Bristol’s Children of the 90s cohort were followed up from age 10 until 24 years. At baseline, 0.3% children smoked cigarettes at age 10 years, which significantly increased to 26% in young adults by their mid-twenties. Nearly two-thirds of children who started tobacco smoking in childhood or adolescence continued smoking in young adulthood.

Active smoking of tobacco from age 10 years through 24 years was associated with a 52% increased risk of premature heart damage, such as excessively enlarged heart, decreased relaxation of the heart, and increased pressure in blood flow to the heart by age 24 years. After accounting for other risk factors like increased blood pressure, obesity, inflammation, dyslipidemia, and sedentariness, the direct effect of tobacco smoking on increased heart size during growth from age 17 through 24 years was 30 %.

Previous studies among adults have shown that adolescent smoking increased the risk of cardiovascular death in the mid-fifties. However, no study in the world has previously examined the earliest manifestation of the consequence of long-term active tobacco smoking from childhood on the heart. This is because repeated echocardiography assessments of the heart in a large population of healthy youth are rare.

The current study is the largest and the longest follow-up of active tobacco smoking and repeated echocardiography study in the world. The participants filled out questionnaires on tobacco smoking at ages 10, 13, 15, 17, and 24 years and had echocardiography measurements of the heart structure and function at ages 17 and 24 years. Their fasting blood samples were also repeatedly measured for low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, glucose, insulin, and high-sensitivity C-reactive protein. Blood pressure, heart rate, socio-economic status, family history of cardiovascular disease, accelerometer measure of sedentary behaviour and physical activity as well as dual-energy X-ray absorptiometry measured fat mass and lean mass were accounted for in the analyses. 

“Adolescence is a critical period for initiating smoking. The recent upsurge in vaping among teenagers is a serious health concern as well. We now know that vaping and e-cigarette products contain substances that can damage the lungs, in addition to the abnormal heart rhythm that nicotine causes to the heart. This current study could be extrapolated to vaping and e-cigarette users who might unknowingly be at risk of significant and irreversible heart damage. Studies in adults have reported that the risk of heart failure continued for 30 years after tobacco smoking has been stopped,” says Andrew Agbaje, an award-winning physician and associate professor (docent) of Clinical Epidemiology and Child Health at the University of Eastern Finland.

“This study shows that teen smoking doesn’t just increase the risk of heart disease later in life – it causes early and lasting damage to heart muscle and function,” said Emily Bucholz, MD, PhD, MPH, Assistant Professor of Pediatrics at the University of Colorado School of Medicine and Associate Editor of JACC. “It’s a wake-up call for prevention efforts to protect young hearts early.”

“Parents and caregivers must lead by example and government agencies should be bold to address the preventable heart disease risk by creating a smoke and nicotine-free country. Raising tobacco taxes is insufficient because the cost of health care due to smoking-related diseases twice exceeds tobacco tax profits. Why should we pay for what is killing us softly? Let us say NO to tobacco and its fancy products in order to save the lives and future health of our children and adolescents,” Agbaje concludes.

Agbaje’s research group (urFIT-child) is supported by research grants from Jenny and Antti Wihuri Foundation, the Finnish Cultural Foundation Central Fund, the Finnish Cultural Foundation North Savo Regional Fund, the Orion Research Foundation, the Aarne Koskelo Foundation, the Antti and Tyyne Soininen Foundation, the Paulo Foundation, the Yrjö Jahnsson Foundation, the Paavo Nurmi Foundation, the Finnish Foundation for Cardiovascular Research, Ida Montin Foundation, Eino Räsänen Fund, Matti and Vappu Maukonen Fund, Foundation for Pediatric Research, Alfred Kordelin Foundation and Novo Nordisk Foundation.