Current smokers faced nearly three times the risk of premature death from cardiovascular disease compared with people who never smoked, with the risk being higher among those who began smoking during childhood, according to new research published today in the Journal of the American Heart Association, an open access journal of the American Heart Association.
Smoking continues to cause an estimated 100,000 deaths from cardiovascular disease every year in the U.S. Currently, there are about 25 million people who smoke daily including 5 million who became regular smokers before the age of 15.
Earlier research in Cuba found a correlation between childhood smoking and a higher risk for premature death overall.
In this new study, investigators set out to determine if the findings were generalizable in other populations by conducting a similar analysis of U.S. data focused on death from cardiovascular disease.
“It was surprising to see how consistent these findings were with our earlier research and with other studies from around the world, including from the U.K., Australia and Japan, among others, both in terms of the substantial risks associated with smoking and with the health benefits of quitting smoking,” said lead study author Blake Thomson, M.Phil., D.Phil., an epidemiologist at the University of Oxford in Oxford, England.
“The age at which a person begins smoking is an important and often overlooked factor, and those who start smoking at a young age are at especially high risk of dying prematurely from cardiovascular disease.
However, quitting can substantially reduce that risk, especially for those who quit at younger ages. Getting people to quit smoking remains one of the greatest health priorities globally.”
Using data collected between 1997 and 2014, from the annual U.S. National Health Interview Survey, researchers examined the medical histories, lifestyle habits and demographics of smokers and nonsmokers.
The study included 390,929 adults, ages 25 to 74 years (average age of 47), 56% female. Occasional smokers were excluded from the study. Current smokers were grouped by the age at which they began smoking.
During the follow-up period, 4,479 people died before the age of 75 from heart disease or stroke. After adjusting for potential confounding variables, such as age, education, alcohol consumption, region and race, researchers found:
- 58% were never smokers; 23% were ex-smokers; and 19% were current smokers;
- Among current smokers, 2% had started smoking before age 10, and 19% began smoking between ages 10 and 14; and
- Those who quit smoking by the age of 40 reduced their excess risk of premature death from cardiovascular disease by about 90%.
Quitting smoking at any age offered benefits, and the earlier a person quit, the better, according to the findings. The analysis found that when compared to peers who had never smoked:
- Smokers who quit between ages 15 to 34 had about the same risk of dying from heart disease or stroke;
- Those who quit between ages 35 to 44 had about a 20% higher risk;
- Those who quit between ages 45 to 54 had about a 60% higher risk;
- Those who quit between ages 55 to 64 had about a 70% higher risk of death from heart disease or stroke; and
- Those who were current smokers had nearly three times the risk of dying prematurely from heart disease or stroke.
“Preventing the next generation from smoking can save lives, but we must also emphasize that quitting smoking can save lives now, and in the years to come,” said Thomson.
“Simply put, health policies should aim to prevent young people from smoking and should clearly communicate the benefits of quitting to those who do smoke, ideally as young as possible, and before the onset of serious illness.”
“This study adds to the body of evidence that starting to smoke at younger ages can significantly increase the risk of death from cardiovascular disease. It validates the American Heart Association’s position that smoking is a serious health hazard, that effective multi-episode counseling and medical therapies for cessation should be available to all and that stopping smoking should be an urgent priority for smokers of all ages, especially the young,” said Rose Marie Robertson, M.D., FAHA, deputy chief science and medical officer of the Association.
“This data precedes the explosion in e-cigarette use in the U.S., and similar long-term outcomes from vaping can only be assessed over time.
However, health risks have begun to emerge, and we know that vaping among teens is a precursor to smoking combustible cigarettes for many,” said Robertson, who is also co-director of the Association’s Tobacco Center of Regulatory Science.
Thomson said more research is needed to better clarify the mechanisms by which prolonged smoking from childhood affects cardiovascular risk.
Future research should also further examine the association between early smoking initiation and death from other causes, such as respiratory diseases and cancers, and in other populations.
Smoking During Adolescence and Young Adulthood: A Critical Period for Health
Since the 1994 report, the basis for concern about smoking during adolescence and young adulthood has expanded beyond the immediate health consequences for the young smoker to a deeper understanding of the implications for health of exposure to tobacco smoke across the life course, including into the next generation.
This broadened concern reflects the emergence of a body of evidence linking risk exposures in early life, even in the antenatal period, to risk for chronic disease in adulthood. The general hypothesis that has been constructed from this evidence is often called the “developmental origins of adult disease” hypothesis or the “Barker” hypothesis, in reference to David Barker, who documented associations between early-life nutrition and subsequent risk for cardiovascular disease (Barker 2004; de Boo and Harding 2006).
Research in humans that is relevant to this hypothesis has largely come from epidemiologic studies that have tied nutrition in early life to subsequent risk for hypertension and other cardiovascular diseases (Huxley et al. 2000; Barker et al. 2005; de Boo and Harding 2006).
There is also relevant experimental research (Nuyt 2008). The proposed underlying mechanisms emphasize genetic and epigenetic changes that could have lasting implications across the life span (Young 2001; Gicquel et al. 2008).
Even before conception, the sperm and oocytes of future parents who smoke are exposed to the DNA- damaging constituents of tobacco smoke (USDHHS 2004); the fetus of a mother who smokes or who is exposed to secondhand smoke will be exposed to these damaging materials, resulting most often in reduced birth weight (USDHHS 2004, 2006).
To date, however, there has been little investigation of the molecular changes as a result of these early-life exposures to tobacco smoke. One recent study, however, has demonstrated epigenetic changes in children with in utero exposure to maternal smoking (Breton et al. 2009), a finding consistent with one proposed mechanism for long-term consequences of early-life exposures.
Thus, given the numerous known carcinogens and toxins present in tobacco smoke and the known mechanism by which they cause disease, the developmental origins of adult disease is a critical concept to consider when addressing youth tobacco use.
For many of the chronic diseases caused by smoking, the risks increase with the duration and cumulative amount of this behavior. Consequently, the age of starting to smoke has consequences for the age at which the risks of smoking become manifest.
In the United States, the age of starting to smoke regularly became increasingly younger late in the twentieth century (NCI 1997), first for males and then for females, but more recently, it has been stable (Figure 2.1). By the early 1990s, the mean age of first trying a cigarette was about 16 years for those who ever smoked (see Chapter 3, “The Epidemiology of Tobacco Use Among Young People in the United States and Worldwide”).
In many other countries, the mean age of uptake is similarly young (see Chapter 3).
This earlier age of onset of smoking marks the beginning of exposure to the many harmful components of smoking. This is during an age range when growth is not complete and susceptibility to the damaging effects of tobacco smoke may be enhanced. In addition, an earlier age of initiation extends the potential duration of smoking throughout the lifespan.
For the major chronic diseases caused by smoking, the epidemiologic evidence indicates that risk rises progressively with increasing duration of smoking; indeed, for lung cancer, the risk rises more steeply with duration of smoking than with number of cigarettes smoked per day (Doll and Peto 1978; Peto 1986; USDHHS 2004).
For chronic obstructive pulmonary disease (COPD), risk varies directly with the total number of cigarettes consumed over a lifetime (USDHHS 2004), which would suggest greater risk for longer duration or higher intensity. There is little direct evidence, however, on whether the age of starting to smoke, by itself, modifies the risk of smoking-related disease later, that is, whether starting to smoke during adolescence versus young adulthood increases the subsequent risk for such disease (International Agency for Research on Cancer 2004).
This chapter has four major sections which correspond to the principal health domains that are related to smoking during adolescence and young adulthood: factors related to initiation and continuation of smoking, including nicotine addiction, smoking and body weight, respiratory symptoms, and cardiovascular effects.
Other adverse effects of smoking on adolescents and young adults have been covered in other reports during the last decade, including the effects of smoking on reproduction and on increasing risk for respiratory infections (USDHHS 2004).
This chapter was developed following the approach set out in the 2004 report of the Surgeon General (USDHHS 2004). The authors systematically searched for all relevant evidence that appeared in the scientific literature after earlier reviews on these topics; this evidence, along with the prior findings, was evaluated and classified as described in the 2004 report.
reference link : https://www.ncbi.nlm.nih.gov/books/NBK99242/
More information: Journal of the American Heart Association (2020). DOI: 10.1161/JAHA.120.018431