A study of nearly 500,000 people has shown that smoking shortens the end fragments of chromosomes in the white blood cells of our immune systems. The length of these end fragments, called telomeres, is an indicator of how quickly we age and our cells’ ability to repair and regenerate.
“Our study shows that smoking status and cigarette quantity can result in the shortening of leucocyte telomere length, which is an indicator of tissue self-repair, regeneration, and aging. In other words, smoking can accelerate the process of aging, while quitting may considerably decrease the related risk,” says Siyu Dai, PhD, in her presentation at the European Respiratory Society International Congress in Milan, Italy. Dai is an assistant professor at the School of Clinical Medicine, Hangzhou Normal University, and also an honorary postdoctoral researcher in the department of pediatrics at The Chinese University of Hong Kong.
Telomeres are like the plastic or metal sheathes at the end of shoelaces, which prevent the shoelaces from fraying. They are lengths of repetitive DNA sequences that protect the ends of chromosomes. Each time a cell divides, the telomeres become slightly shorter, eventually becoming so short that the cell can no longer divide successfully, and it dies. This is part of the aging process. Telomere length in white blood cells (called leucocytes) has been linked previously to smoking, but, until now, there has been little research into whether smoking status and the quantity of cigarettes smoked actually caused the shortening in telomere length.
Researchers analyzed data from UK Biobank, which contain genetic and health information from half a million UK participants. They looked at whether a person was a current smoker, previous smoker or had never smoked, level of addiction to smoking, how many cigarettes they smoked (the pack years of cigarette consumption), as well as information on leucocyte telomere length taken from blood tests.
They used Mendelian randomization, which uses the variations in genes (known as single nucleotide polymorphisms or SNPs) that are inherited from our parents, to infer how exposure to a modifiable environmental factor (such as smoking) is causally related to a disease or health condition (such as shorter leucocyte telomeres).
The researchers used data from 472,174 UK Biobank participants and 113 SNPs relating to smoking status (15 SNPs for current smokers, 78 SNPs for never-smokers, and 20 SNPs for people who had smoked previously).
“We found that current smoking status was statistically significantly associated with shorter leucocyte telomere length, whereas previous smokers and people who had never smoked didn’t show significantly shorter leucocyte telomere length. Among people who used to smoke, there was a trend towards shorter telomere length, but this was not statistically significant. People who smoked the greater number of cigarettes had significantly shorter leucocyte telomere length. In summary, smoking may cause the shortening of leucocyte telomere length, and the more cigarettes smoked, the stronger the shortening effect,” says Dai in a release.
Researchers will carry out further research to validate the current findings. They are also interested in exploring further the effect of passive smoke exposure on tissue self-repair, regeneration, and aging, particular in the way that it could affect children.
Jonathan Grigg, MD, chair of the European Respiratory Society Tobacco Control Committee who was not involved with this research, says in a release, “Dr Dai and her colleagues, in a study of half a million adults, show a clear association between smoking and reduced telomere length. This study applied Mendelian randomization, a well-known method for providing good levels of evidence and being able to show causal relationships, to support previous, observational studies suggesting that smoking causes aging, while quitting may reverse this effect.”
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