Being exposed to secondhand smoke (sometimes called “passive smoking”) or actively smoking even a few cigarettes a week may harm genes in the lining of the lungs, new research shows. These genetic changes may increase the risk of developing lung diseases, including chronic obstructive pulmonary disease (COPD), which may take the form of emphysema, bronchitis, and asthma. The genetic changes are also often seen in people who develop lung cancer. The research provides further support for public smoking bans, as well as to protect children from secondhand smoke, especially during pregnancy and infancy.
The study, published online ahead of print on August 6 in the American Journal of Respiratory and Critical Care Medicine, is the first to show that gene function changes even with very low levels of exposure to cigarette smoke. Epidemiological studies – studies of diseases in populations – have long shown that secondhand smoke contributes significantly to lung disease. But up until now, there’s been no evidence showing what exposure to low levels cigarette smoke does to genes in the lining of the lungs. These genes are commonly turned on in in the cells of heavy smokers. And, it turns out, they are also turned on or off in those with very low-level exposure.
“Even at the lowest detectable levels of exposure, we found direct effects on the functioning of genes within the cells lining the airways,” said Dr. Ronald Crystal, lead author of the study and chief of the division of pulmonary and critical care medicine at NewYork-Presbyterian and Weill Cornell Medical Center and chair of the department of genetic medicine at Weill Cornell Medical College in New York City.
The research team tested 121 people from three different categories: “nonsmokers,” “active smokers” and “low exposure smokers.” To determine which category each participant fell into, the researchers tested for levels of nicotine and cotinine — markers of cigarette smoking within the body – in the urine.
The researchers used a technique called bronchoscopy to obtain samples of the cells lining the lungs. They then scanned each person’s entire genome to determine which genes were either activated or deactivated in cells lining the airways. Genetic abnormalities were found at all levels of exposure.
“This means that no level of smoking, or exposure to secondhand smoke, is safe,” says Dr. Crystal. He compares these genetic changes to a “canary in a coal mine,” warning of potential life-threatening disease, “but the canary is chirping for low-level exposure patients, and screaming for active smokers.”
These findings suggest that the overall impact of secondhand smoke and infrequent smoking may be much greater than once thought. The genetic effect was much lower for low exposure than for regular smokers in the study. But the sheer number of people who are exposed to low levels of cigarette smoke makes the public health effect of such exposure significant.
Dr. Crystal noted that his team’s findings provide further support for smoking bans in public places, where non-smokers, including employees of businesses that allow smoking, are put at risk for future lung disease. It also emphasizes the importance of protecting children, especially infants and toddlers, from secondhand smoke.