Researchers at the Keck School of Medicine of USC found a large study involving people from different ethnic backgrounds to understand how smoking affects genes and their expression.
This study could help us to predict the risk of diseases caused by smoking better in the future. Smoking can change how genes work, leading to illnesses like lung cancer. However, we still don’t fully grasp how smoking affects genes, particularly in different racial and ethnic groups.
Brian Huang, Ph.D., is an assistant professor in the population and public health sciences department at the Keck School of Medicine of USC and the first author of the new study said, “We know that smoking affects people differently based on their race and ethnicity, but identifying epigenetic signatures of smoking would help us better predict risk for smoking-related diseases.”
Researchers from the Keck School of Medicine, funded by the National Institutes of Health, studied how smoking affects DNA methylation, a type of epigenetic change. They examined data from 2,728 people of six different racial and ethnic groups.
The study found 408 DNA methylation markers related to smoking, including two that varied depending on race or ethnicity. This research, published in the American Journal of Human Genetics, is one of the most extensive multiethnic studies on smoking and epigenetics.
Unlike previous studies that focused on one or two racial groups, this study looked at a more diverse population. The researchers measured smoking by analyzing participants’ total nicotine equivalents (TNEs), which provides a more accurate assessment of smoking dose compared to self-reported measures.
Huang said, “This study gives us some additional information about the mechanism by which smoking can affect health and how that could differ across various populations. Ultimately, that can lead to better prediction, early detection, and treatment for smoking-related conditions.”
The research team used data from the Multiethnic Cohort Study, which involves African Americans, European Americans, Japanese Americans, Latinos, and Native Hawaiians. They collected biological samples from 1,994 participants to measure smoking dose (using TNEs) and DNA methylation levels at various points across the genome (through an EWAS).
Smoking was found to be associated with DNA methylation changes at 408 sites, including 45 new areas not identified in studies relying on self-reported smoking behavior.
The research team used data from the Multiethnic Cohort Study, which involves African Americans, European Americans, Japanese Americans, Latinos, and Native Hawaiians. They collected biological samples from 1,994 participants to measure smoking dose (using TNEs) and DNA methylation levels at various points across the genome (through an EWAS). Smoking was found to be associated with DNA methylation changes at 408 sites, including 45 new areas not identified in studies relying on self-reported smoking behavior.
To confirm their findings, Huang and his team collected data on smoking dose (TNE) and DNA methylation from two other groups: 340 participants from the Singapore Chinese Health Study and 394 participants from the Southern Community Cohort Study.
They found many of the same DNA methylation sites as in the Multiethnic Cohort Study, especially those strongly linked to smoking dose. This shows that the critical markers of smoking-related epigenetic changes are consistent across different racial and ethnic groups.
Next, the researchers plan to study how epigenetic changes increase the risk of lung cancer in a new study. Understanding this mechanism could help predict lung cancer risk more accurately.
Huang’s team is also investigating epigenetic changes linked to other smoking-related biomarkers, such as levels of cadmium, a heavy metal in cigarette smoke.
This study gives us important information about how smoking affects DNA in people from different racial and ethnic backgrounds. Understanding these connections helps us learn more about why smoking causes diseases. It could help us find better ways to predict and stop these health problems caused by smoking.
Journal reference:
Brian Z. Huang, Alexandra M. Binder et al., Epigenome-wide association study of total nicotine equivalents in multiethnic current smokers from three prospective cohorts. American Journal of Human Genetics. DOI: 10.1016/j.ajhg.2024.01.012.
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