Smoking leaves imprint on human genome, new study finds

Smoking leaves an imprint on the human genome, a recent study found. The results from the study demonstrate numerous differences in smokers and non-smokers, and some of those differences were still evident in people who had quit smoking up to 30 years prior to the study.

The University of Minnesota collaborated on the study, including co-authors Weihua Guan, Ph.D., associate professor with the School of Public Health, James Pankow, Ph.D., professor with the School of Public Health, and Ellen Demerath, Ph.D., professor with the School of Public Health. They conducted their research at the Minneapolis Center of the Atherosclerosis Risk in Communities Study (ARIC) which is one of four ARIC study centers in the nation. The research was published in Circulation: Cardiovascular Genetics, an American Heart Association journal.

The study focused on the epigenome, which is the aspect of the human genome that is changeable and dictates gene expression. Researchers examined one feature of the epigenome called DNA methylation, which was measured in blood samples from nearly 16,000 participants from 16 cohort studies in the Cohorts for Heart and Aging Research in Genetic Epidemiology (CHARGE) Consortium. The researchers compared DNA methylation patterns in people who smoke currently and people who quit smoking to patterns in people who never smoked.

“This is important because while cigarette smoking is widely recognized to be harmful to one’s health, the idea that smoking does this by changing particular parts of the epigenome is new. This is the largest epigenome-wide study of smoking to date, and it shows how much and how long smoking might damage the epigenome in the general population,” said Demerath.

Demerath said the information gathered in this study could be useful because it suggests a possible biomarker of smoking exposure damage over time. Existing biomarkers of smoking capture only recent smoking history. The study also highlights particular gene pathways deranged by smoking which could be theoretically “reset” with appropriate pharmaceutical intervention to prevent or treat tobacco-related diseases.

“People need to keep in mind, however, that we are comparing DNA methylation differences between different individuals with different smoking histories, and inferring from that the “effect” of smoking. Ideally, studies should begin to collect longitudinal, repeated snapshots of the epigenome within individuals followed over time before and after quitting smoking, for instance. Also, the DNA methylation patterns related to smoking that we see in blood could be different than those seen in other tissues,” said Demerath.

https://twin-cities.umn.edu/node/263121
University of Minnesota, Twin Cities
06/27/2018