Not only does cigarette smoke severely harm the body, it also leaves behind long-lasting damage on DNA, according to a recent study. An unwanted surplus of chemical marks are added to specific spots on the genome of a smoker, which may give rise to diseases such as a cancer, cardiovascular and lung disorders, and osteoporosis.
A group of international researchers conducted a large scale meta-analysis of genome-wide DNA methylation, pulling data from nearly 16,000 people. Around 15% of participants were active smokers and the rest were split almost evenly between those who were former smokers or had never smoked. Their analysis uncovered a distinct “fingerprint” on the DNA of those who smoked tobacco.
They detected a pattern of persistent changes in methylation on smokers’ DNA. For some, this epigenetic signature was present even 30 years after they kicked the habit.
“By analyzing this large volume of data we were able to show that smoking leaves a type of epigenetic fingerprint behind that can still be detected years later,” said Dr. Melanie Waldenberger, a group leader in the Research Unit of Molecular Epidemiology at the German Research Center for Environmental Health who was a part of the investigation.
Epigenetics involves turning genes on or off without changing the gene sequence. Chemical tags such as methyl groups can be added to different locations on DNA, suppressing the expression of genes in a process known as DNA methylation.
“Seen at the molecular level, this fingerprint involves methyl groups that are added to individual bases where they can influence the activity of the genes below,” explained Waldenberger.
They found that more than 7,000 genes were linked to smoking, or roughly one-third of known human genes. Many of the genes were related to pulmonary function, cancer, inflammation, and cardiovascular disease. They even noticed some were linked to arthritis.
“Given the widespread impact of smoking on disease outcomes across many organ systems and across the life span, the identification of a large number of genes at genome-wide significance is not surprising,” the researchers reported.
“Some of these had already been associated with smoking, while others were new in this context,” said Professor Annette Peters, Director of the Institute of Epidemiology. “Our hope is that it will be possible to derive disease mechanisms and consequently to create new treatments.”
Dr. Rui Wang-Sattler, a group leader in the Research Unit of Molecular Epidemiology, commented: “Five years after smoking cessation, the majority of the methylation signals return to the levels of those who have never smoked.”
According to the CDC, cigarette smoking kills more than 480,000 Americans every year, with more than 41,000 of these deaths from exposure to secondhand smoke. Could it be possible that second-hand smoke is even affecting the DNA of non-smokers? These and many other questions may arise as additional studies are conducted to tease out the mechanisms underlying smoking-related diseases.
Decades ago, nearly half of adults in the U.S. smoked cigarettes, according to the CDC. At one point, it was even endorsed by doctors. Although tobacco use has since declined, it still remains the single largest preventable cause of death and disease in the U.S.
Previous studies have shown that there are epigenetic warning signs of cancer which can be found in the cheek cells of smokers. Others have shown that nicotine may cause epigenetic changes that negatively impact fertility or maternal smoking epigenetically harms child development. Hopefully, as more details are revealed by epigenetic research, we can get closer to understanding the precise disease mechanisms and begin to develop new treatments.
Source: Joehanes, R. et al. (2016). Epigenetic Signatures of Cigarette Smoking. Circulation: Cardiovascular Genetics, 9(5): 436-447.
Reference: Smoking leaves historical ‘footprint’ in DNA. Health Canal. 17 Oct 2016.
