Adolescent smokers appear to be more susceptible to long-term DNA damage associated with lung cancer than people who start smoking as adults, according to a study led by a UC San Francisco researcher that examined DNA damage in former smokers who have lung cancer.
The study, published in the April 6 issue of Journal of the National Cancer Institute, indicates that ex-smokers with lung cancer who began smoking in adolescence had higher levels of chemically altered DNA in their lungs and blood than ex-smokers who started smoking later in life. The study accounted for numerous variables, including the number of years ex-smokers smoked and the amount they smoked.
"Our finding suggests that young smokers incur more severe or persistent DNA damage than adult smokers do," said the lead author of the study," John K. Wiencke, PhD, associate professor of epidemiology at UCSF.
"Smoking during adolescence may produce physiologic changes that lead to persistent increased DNA damage, or young smokers may be markedly susceptible to DNA damage formation and have higher burdens of damage after they quit smoking than those who started smoking later in life," said Wiencke.
All smokers develop some level of DNA damage, which is a known risk factor for lung cancer, and all people who quit experience some level of DNA repair. The current finding suggests that less repair - or less successful repair - occurs in people who smoked as adolescents.
The finding was drawn from a broader investigation that sought to parse out correlations between the various possible factors contributing to lung cancer - such as years and intensity of smoking--and DNA damage in the lungs.
"The ability to identify those current and former smokers with the highest risk
of developing cancer has substantial preventive implications," said Wiencke.
The damaged, or chemically altered segments of DNA, known as DNA adducts, are
physical complexes in genes that are known to result from expos
Contact: Jennifer O'Brien
University of California - San Francisco