Exposure to even minimal levels of secondhand tobacco smoke causes significant DNA damage in human cells, according to a study using a new detection method. DNA damage plays a key role in the development of cancer and other neurodegenerative, pulmonary, cardiovascular, and aging-related diseases.

The study was published in the January 2015 Supplement to the American Journal of Preventive Medicine and supported by the Oklahoma Tobacco Research Center at the Stephenson Cancer Center. Funding for the study was provided by the Oklahoma Tobacco Settlement Endowment Trust.

The study authors developed a new, highly sensitive detection process and used it to measure damage to human cells induced by exposure to various doses of mainstream and sidestream tobacco smoke, the main components of secondhand smoke.

Using the new detection method, DNA damage was observed for tobacco smoke exposure levels equal to about one-tenth of a cigarette, ten-fold lower than previously documented. These more precise measurements of DNA damage will improve tobacco-associated disease risk assessment and could contribute to better screening and early diagnosis.

Because of its simplicity and high sensitivity, the new method has many other potential uses, including the prediction of cancer risk in individuals, treatment outcomes and prognoses, and DNA damage in aging-related changes and neurological disorders.

“Previously, technical limitations and analytical complexity have hampered this field of research,” said Lurdes Queimado, MD, PhD, the principal investigator of the study and Director of Basic and Translational Research in Otorhinolaryngology at the University of Oklahoma Health Sciences Center. “Using this new detection method, we were able to demonstrate for the first time that mainstream and secondhand smoke cause distinct types and levels of DNA damage. Most important, we found that even very low doses of secondhand smoke cause DNA damage that could lead to cancer mutations.”

Although repair of most forms of DNA damage occurs naturally in living cells, the study found that damage from very low doses of secondhand smoke persists unrepaired for at least 16 hours. This suggests that the body’s natural process for DNA repair is not activated for this level of DNA damage or is not able to fully repair the damage. Further research is needed, but this may indicate a disproportionate carcinogenic effect from exposure to very low levels of secondhand smoke.

“This landmark study builds upon earlier findings of significant risks of cancer and heart disease,” said Oklahoma Tobacco Research Center Director Robert McCaffree, MD “Too many people are still at risk every day.”

The 2014 U.S. Surgeon General’s Report on the health consequences of smoking estimated that exposure to secondhand smoke causes more than 7,300 lung cancer deaths and nearly 34,000 heart disease deaths among US nonsmokers each year. The report concluded that there is no safe level of exposure to secondhand smoke.

“With tobacco use being the top cause of cancer deaths in our state and nation, this research is fulfilling the mission of the Stephenson Cancer Center to provide patient-centered care through translational research.” said Greg Krempl, MD, the Paul and Ruth Jonas Chair in Cancer and Chairman of the Department of Otorhinolaryngology at the OU Health Sciences Center. “Improved risk assessment and early diagnosis can greatly reduce cancer deaths,” Krempl said.

To view the full study, see: www.ajpmonline.org/article/S0749-3797%2814%2900484-X/pdf.